Gastritis PDF - A Conceptual Approach

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 3: Inflammation and Tissue Repair Module 4: Clinical Models Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology Lec...

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 3: Inflammation and Tissue Repair Module 4: Clinical Models Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology Lecture Series Copyright © 2017 Wolters Kluwer Health | Lippincott Williams &Wilkins  Acute and Chronic Gastritis Clinical Pathophysiology Diagnosis Treatment manifestations  Acute Gastritis Inflammation in the gastric mucosa Cause: Ingestion of irritating substances (medications, alcohol, microorganisms) Develops over short period Reversible if causative agent removed Role of gastric acid hypersecretion is not clear (too much stomach acid)  Acute Gastritis Pathophysiology Ingestion of irritating substances and/or poor gastric perfusion results in acute inflammation of the gastric mucosa Mild erythema Gastric acid escapes and corrodes nearby tissue Severe gastric perforation Gastric epithelial cell become necrotic Gastric acid erodes underlying tissue Kumar, Robbins & Cotran: Pathophysiological basis of disease. 8th ed. Philadelphia: Saunders;2010  Acute Gastritis Clinical Manifestations Dependent on severity: Mild to severe abdominal pain Indigestion (heartburn) Loss of appetite Nausea Vomiting Hematemesis (vomiting blood) Anemia (due to mild hemorrhage) Severe hemorrhage and perforation: lead to shock and medical emergency  Acute Gastritis Diagnosis History and physical examination Medication taking (aspirin/NSAID), alcohol, contaminated food Other potential causes of ischemia Abdominal tenderness Endoscopic examination: presence ulcers in the mucosa Stool analysis (presence of blood in stool) Hemoglobin/hematocrit level, complete blood count (anemia) http://library.med.utah.edu/WebPath/GIHTML/GI018.html  Acute Gastritis Treatment Discontinue ingestion of irritating substance Buffer or decrease production of gastric acid Prognosis is good  Chronic Gastritis Unrelenting injury Chronic infection: Helicobacter pylori Autoimmunity Helicobacter Pylori most prevalent: Asia Developing countries 50% of world’s population is infected (yes, we can call it : pandemic) Pathological effect occur in 10-20% of infected individuals  Chronic Gastritis HelicobacterPylori Pathophysiology H. Pylori: gram-negative bacteria Person-to-person: saliva, stool Ingested and multiplies on epithelial surface and mucus barrier Produce enzyme that neutralizes the pH 1.5-3.5 gastric acid H. Pylori survives and produce toxins Toxin destroys mucosal barrier >> injury Intense inflammation triggered H. Pylori is contained in the epithelial cells No erosion of the gastric mucosa Epithelial cells and glands adapt and atrophy Gastric acid production and secretion is impaired Marieb EN, Hoehn KN. Human Anatomy & Physiology. 9th ed. Boston, Pearson Education; 2013  Chronic Gastritis Autoimmune Pathophysiology Parietal cell secrete HCl Marieb EN, Hoehn KN. Human Anatomy & Physiology. 9th ed. Boston, Pearson Education; 2013 Antibodies against parietal cells: gastric acid secretion impaired Intrinsic Factor (IF) is needed for B12 absorption Antibodies against IF: B12 absorption is impaired B12 required to promote DNA synthesis in RBCs Impaired DNA synthesis >> decrease in RBCs Low haemoglobin levels Pernicious Anaemia T-cells infiltrate gastric mucosa  Chronic Gastritis Clinical Manifestations Helicobacter Pylori infection: Most infected: asymptomatic carrier Pathological effect occur in 10-20% of infected individuals Dyspepsia: vague epigastric discomfort Nausea Heartburn Loss of appetite Vomiting Autoimmune: Can be asymptomatic First sign: Pernicious anemia (deficiency in intrinsic factor, unable to absorb B12, abnormal RBCs production) Weakness, fatigue, light-headedness Dyspepsia, vague abdominal pain, nausea, vomiting, anorexia  Chronic Gastritis Diagnosis Helicobacter Pylori Endoscopic examination Biopsy of gastric tissue Urea breath test to detect H. pylori H. Pylori breaks urea into NH3 and CO2 CO2 content measured Presence of antibodies in blood Autoimmune http://www.helikit.com/en/helikit-urea-breath-test/ Biopsy of gastric tissue and histologic examination Antiparietal or anti-Intrinsic Factor antibodies in blood Existing autoimmune process Low B12 level in blood  Chronic Gastritis Treatment Helicobacter Pylori infection: Multiple antibiotics for chronic infectious processes Proton pump inhibitors (raise pH) to help healing H. pylori can lead to chronic ulcers and gastric cancer Autoimmune: Immunosuppressive drugs to block autoimmune attack against parietal cells B12 intramuscular injections (antibodies are produced against intrinsic factor), B12 absorption is impaired Autoimmune gastritis can lead to gastric cancer