Adult Medical-Surgical Nursing Gastro-intestinal Module: Gastritis and Peptic Ulcer
Gastritis
Gastritis Gastritis is an acute or chronic inflammation of the gastric mucosa Risk factors include: Spicy food Overuse of Aspirin, NSAIDs Excessive alcohol and caffeinated drinks Smoking; stressful lifestyle Helicobacter pylori or other pathogen
Gastritis: Pathophysiology The gastric mucosa is protected from the high acidity of hydrochloric acid in the stomach by mucus secretion Mucosal damage occurs through: Interference with the amount of acid: hypersecretion or achlorhydria Reduction of mucus production Generalised inflammation results. Where acute can lead to necrosis, scarring or perforation
Helicobacter Pylori H pylori is an organism which has been closely related to gastritis and peptic ulcer It can be detected in blood and breath tests Where present, treatment includes antibiotics in addition to control of peptic acid content
Gastritis: Clinical Manifestations Anorexia Heartburn after eating Flatulence (belching) Nausea/ vomiting Sour taste in mouth
Gastritis: Diagnosis Clinical symptoms and dietary history Breath test, stool or serological test for H pylori Endoscopy: Inspection Gastric washings for H. pylori Biopsy Serum B12 (may be ↓ if intrinsic factor affected)
Gastritis: Treatment/ Counselling Dietary changes ↓ smoking Less stressful lifestyle Antibiotics Acid reduction through: H2 receptor inhibitors (Ranitidine) Proton pump inhibitors (Lanzoprazole)
Peptic Ulcer
Peptic Ulcer The gastric and intestinal wall layers are: mucosa → sub-mucosa → muscle→ serosa→ peritoneum A peptic ulcer is an erosion of the mucosa of the stomach, pylorus, duodenum or oesophagus in a circumscribed area. It may pass through all layers and eventually perforate to the peritoneum Multiple ulcers may be present at once
Gastric Ulcers (15% of total): Main Features Later onset: usually after 50 years of age Similar occurance in male : female (1:1) Normal, ↑ HCl or ↓ HCl (achlorhydria) Epigastric pain occurs after a meal (within the following hour), relieved by vomiting Associated with weight loss Risk of haemorrhage Long-term risk for gastric malignancy
Duodenal Ulcers (80% of total): Main Features Affect younger age group (30-60 years) Occurence in male: female is 2-3 :1 Related to hyperacidity (↑ HCl secretion) Epigastric dull, gnawing pain occurs 2-3 hours after food, often awakens the patient, relieved by food Vomiting not common Increased risk of perforation Less risk of malignancy
Peptic Ulcer: Aetiology Risk factors for peptic ulcer include: H pylori (70% in gastric; 95% in duodenal) Genetic link: blood group “O” Spicy food; also milk and cream Smoking Stressful lifestyle Use of aspirin, NSAIDs, corticosteroids Excessive alcohol and caffeinated drinks
Peptic Ulcer: Stress Ulcers Stress ulcers are usually found in ICU patients (prophylaxis given routinely) Related to physiological stress Also related to corticosteroid therapy Usually preceded by shock (severe trauma, burns, sepsis) → reduced blood flow to the mucosa and reflux of duodenal contents to the stomach → outpouring of HCl and pepsin on less protected mucosa → ulceration
Peptic Ulcer: Pathophysiology Peptic ulcer is largely related to: Increased concentration and action of HCl on the mucosa (stress, spicy foods, smoking, caffeine, alcohol) Reduced mucus secretion: ↓ mucosal resistance and protection from the digestive action of HCl (stress, aspirin, NSAIDs, corticosteroids, H pylori)
Peptic Ulcer: Clinical Manifestations Dull, gnawing epigastric or back pain (thought to be the effect of acid on exposed nerve endings) Relieved by vomiting (gastric) or by food (duodenal) Tenderness over the epigastrium Possible weight loss Anaemia if acute or chronic haemorrhage Haematemesis or malaena (“tarry” stool)
Peptic Ulcer: Diagnosis History and physical examination CBC (anaemia) Stool: Guiac test for occult blood Breath test, stool or serum (antibodies) for Helicobacter pylori Endoscopy: Inspection Biopsy of mucosa for histology Gastric washings for culture of H pylori
Peptic Ulcer: Medical Management Lifestyle changes Medical treatment: Antibiotics (Flagyl and one other antibiotic) H2-receptor antagonist (Ranitidine) or Proton-pump inhibitor (Lanzoprazole) Mucosal protection (Misoprostol) (Usually avoid antacids as interfere with treatment)
Peptic Ulcer: Surgery Surgery is less used now. Mainly for: Ulcers not healing after 12 – 16 weeks Life-threatening complications: Haemorrhage Perforation/ penetration Pyloric obstruction
Peptic Ulcer: Surgery Types of surgical procedure: Vagotomy (resection of the vagus, parasympathetic nerve: ↓ HCl secretion) Pyloroplasty (with or without vagotomy) Gastro-enterostomy (bypass from stomach to jejunum)
Peptic Ulcer Complications: Haemorrhage Haemorrhage: ulcer has eroded a blood vessel Haematemesis, especially gastric ulcer: fresh blood or “coffee-ground” vomit Malaena (more obvious if duodenal ulcer) May be an emergency → hypovolaemic shock GXM, IV fluids, vital signs, NG tube, NPO Rest, mouth care, surgical prep (if needed)
Peptic Ulcer Complications: Perforation Ulcer has perforated layers to the peritoneum Acid contents leaking into peritoneum Patient in severe shock from extreme pain of chemical peritonitis Rigid, board-like abdomen, extremely tender Hypotension: emergency requiring immediate resuscitation and preparation for surgery to repair
Peptic Ulcer: Nursing Care Pre-operative care: (may well be emergency) General physical check-up, chest Xray, ECG Blood profile, IVI, group and cross-match (GXM) Breathing exercises to prepare for post-op Thrombo-embolic stockings/ prophylactic heparin Explanation of operation, consent and emotional support
Peptic Ulcer: Nursing Care Post-operative care: Pain relief Monitor vital signs, pulse oximetry, IV fluids, urine output and fluid balance Semi-sitting position once recovered Breathing and leg exercises NPO initially→ graduated intake (mouth care) NG tube aspirations, wound, drain care