To know basic etiology of this disease and difference between duodenal ulcer and peptic ulcer as well as how we can approach if children having peptic ulcer disease. By conservative and surgical means
2. What is PEPTIC ULCER?????
»Breaks in mucosalsurface
»>5mm in size
»Depth till submucosa
»In any part of GI tract exposed to
aggressive action of acid pepsin
juices.
»Can be acute or chronic
»Both can penetrate muscularis
mucosae..
3. SITES
» Gastric and duodenal – 98 %
» Ratio of 1:4
» Duodenum:1st part >95%
:ant & post walls
» Gastric :junctn b/w antrum &acid secr. mucosa
:lesser curvature
4. Pathomorphology
•Round
•Punched out craters
•2 to 4 cm diameter
Mild oedema of immediate adj.
mucosa
Margins – Perpendicular
- No Elevatn or Beading
Surrounding Mucosal folds Radiate
like Wheel Spokes
Base Remarkably Clean
6. ETIOLOGY
Predisposing factors
– Age :young in DU and peak inc. at 6th decade in
GU.
– Sex :GU commoner in males
Causes
– H.Pylori
– NSAID
– Infection: CMV,herpes simplex,etc..
– Other drug/toxin: bisphosphonates, chemo,clopidogrel ,
glucocorticoids
– Misc.:crohn,neoplasm,ashemia,infiltrating
7. • Smoking
• Genetic : increased freq of blood group O and non
secretor status
• Stress
• Diet : alcohol and caffeine
Associations
• Systemic mastocytosis
• CRF, nephrolithiasis
• Hyperparathyroidism
• Cirrhosis
• Alpha antitrypsin deficiency
• CAD, pancreatitis, polycythaemia vera
Pathogenetic factors not related to h.pylori &NSAID
9. Pathophysiology
1. the host factors that serve to protect the GI
mucosa from ulceration and the inflammatory
mediators and aggressive factors that
contribute to mucosal inflammation and
ulceration.
2. Peptic ulcer disease in children is the result
of an imbalance between mucosal defensive
and aggressive factors.
10. 1. An overlying physiochemical barrier provides
cytoprotection of the gastric mucosa.
• water-insoluble gastric mucus,
• gastrically produced bicarbonate,
• an unstirred water layer,
• phospholipids,
• rapid shedding of cells resulting from epidermal
growth factor,
• normal mucosal blood flow,
• prostaglandin-stimulated bicarbonate,
• mucus production,
• and inhibited acid secretion.
11. • Gastric metaplasia
• Increased acid production
• Decreased duodenal mucosal bicarbonate
production
Then how does it cause
Ulcers in duodenum?????
12. Endothelial defects
•Stasis--ischemia
• HCL
• mucin
• bicarbonate
• Epi. cell
proliferation
ULCER
erosions
Healing(spontaneous
Or therapeutic)
NSAID induced PUD
Pathophysiology
Direct toxicity by
Ion trapping
Epithelial effects
due to PG depletion
13. Clinical features
Abdominal pain*
•Epigastric
•Burning or gnawing discomfort*
•90 min to 3 h after meal
•Frequently relieved by antacids or food in DU.*
•Awakes the pt from sleep b/w midnight & 3 am.
Nausea
Weight loss
Dyspepsia
if not relieved by food antacids ,
radiates to back—penetrating ulcer
14. • NUD : non ulcerative dyspepsia
• D/D OF ULCER LIKE SYMPTOMS
• Proximal GI tumors
• Gastro esophageal reflux
• Vascular disease
• Pancreaticobiliary disease
• Crohn’s disease
Differential diagnosis
17. • Barium studies of proximal GI
• Endoscopy
• Tests for detection of H.Pylori
• Occasionally serum gastrin level
• gastric acid analysis
• screen for NSAIDs
Non invasive:
• serology Urea breath test
• Stool antigen
Invasive :
• rapid urease histology culture
Duodenal ulcer Gastric ulcer
18. Medication
Histamine H2-receptor antagonists
Ranitidine (Zantac)
Neonates: 2-4 mg/kg/d PO divided q8-12h or 2 mg/kg/d IV divided q6-8h
Infants and children: 6-9 mg/kg/d PO divided q8-12h or 2-4 mg/kg/d IV divided
q6-8h
Continuous infusion: Administer daily IV dose over 24 h
Proton pump inhibitors
Omeprazole (Prilosec, Zegerid)
0.6-0.7 mg/kg/d PO initially, may increase to 0.6-0.7 mg/kg/dose PO bid;
reported effective dose range 0.7-3.3 mg/kg/d
19.
20. Antacids
Aluminum and magnesium hydroxide (Mylanta,
Maalox)
5-15 mL PO q3-6h or q1-3h pc and hs
Alternative: 1-2 chewable tab PO q1-3h pc and hs
Antibiotics
Amoxicillin (Amoxil, Trimox)
50 mg/kg/d PO divided bid; not to exceed 2-3 g/d
Clarithromycin (Biaxin)
7.5 mg/kg PO bid for 2 wk (with omeprazole and metronidazole or with omeprazole
only) or for 10 d (with amoxicillin and omeprazole)
GI agents
Sucralfate (Carafate)
Not established; 40-80 mg/kg/d PO divided q6h have been used