Peptic Ulcer
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Transcript Peptic Ulcer
Adult MedicalSurgical 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 Protonpump 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
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