Gastritis

Gastritis Definition Histological presence of gastric mucosal inflammation Causes Common Causes Others Stress/mucosal ischemia Alcohol misuse H. pylori Autoimmune Most common HIV and immunocompromise Can cause both acute and chronic Prior gastric surgery NSAIDs Drug induced Critically ill patients Classification Duration Sudden Acute Short term Gradual Chronic Long term – weeks -> months -> years Erosion More common and more severe Erosive Ulcers in the stomach lining Damage is limited to the mucosal layer Non-erosive No ulcers Specific Subtypes H. pylori Most common Immune system attacks parietal cells Acid loss and decreased intrinsic factor Autoimmune B12 deficiency and iron deficiency Pernicious anaemia Loss of gastric liming and glands Metaplasia Atrophic Usually due to H. pylori or autoimmune disease Poor B12 and iron absorption Rare Eosinophilic Eosinophil buildup Rare Severe infection Severe invasion Phlegmonous gastritis Usually by streptococcus infection Usually in older and immunocompromised people 14-day course of broad-spectrum antibiotics may be curative May require surgical management Reactive/chemical Presence of irritants such as chemicals, medications, bile and alcohol Key Info Not a clinical diagnosis The antrum is the most common location Clinical Features Dyspepsia and epigastric discomfort Non-specific Epigastric discomfort/pain is the most common No suspicious features of malignancy Nausea and vomit Acute abdominal pain Fever Altered reflexes or sensory deficits Chronic gastritis -> B12 deficiency Cognitive impairment Chronic gastritis -> B12 deficiency Glossitis Due to B12 deficiency Co-existing autoimmune disease Severe emesis Investigations FBC Leucocytosis H. pylori urea breath test Can also monitor response to therapy First line test H. pylori faecal antigen test H. pylori rapid urease test Gastric mucosa histology Serum vitamin B12 Normal or low Blood cultures Positive for infectious agents Parietal cell antibodies Present in 90% of patients Intrinsic factor antibodies Positive in autoimmune gastritis Very sensitive for pernicious anaemia Endoscopy Consider if not responsive to treatment Gold standard Biopsy Histological assessment and classification Findings: Inflammatory cells -> lymphocytes, plasma cells and neutrophils Acute/active -> neutrophils Chronic -> lymphocytes/plasma cells PPIs, bismuth, antibiotics and PCABs may interfere with test results Management At risk of stress gastritis -> risk of causes bleeding 1 st line -> antisecretory agents -> prevention strategy Critically ill patients Risk factors: Mechanical ventilation for more than 48 hours Coagulopathy Low platelets Management with H2 antagonists or PPI Sucralfate and misoprostol are alternatives H. pylori induced H. pylori eradication therapy Erosive Discontinuation of trigger e.g. NSAIDs H2 antagonist or PPI Autoimmune Cyanocobalamin (vitamin b12) Bile reflux -> if symptomatic 1 st line: Rabeprazole or sucralfate 2 nd line Roux-en-Y diversion surgery Phlegmonous gastritis Rare but a life-threatening infection of gastric submucosa and muscularis propria in debilitated patients Admission to intensive acre unit Central line placement Volume resuscitation IV fluids to replace losses Vasopressors NGT tube Decompression Provides relief and provides fluid for culture Complications Peptic ulcers Most common complication Significant bleeding Anaemia From blood loss or malabsorption (B12 or iron) Intestinal metaplasia -> increased risk of gastric cancers Gastric polyps Perforation Gastric outlet obstruction