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
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Peptic Ulcer Disease Muzaffar khan Alam khan Department of Paediatric surgery Student of TSMU
What is PEPTIC ULCER????? »Breaks in mucosal surface »>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..
SIT E S » Gastric and duodenal – 98 % » Ratio of 1:4 » Duodenum:1 st part >95% :ant & post walls » Gastric :junctn b/w antrum &acid secr. mucosa :lesser curvature
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
Gastric ulcer Duodenal ulcer P at ho physiology Major c a u s e s G astri c acid Gastric e m p t y i ng i nc r e a sd decreased r a p i d delayed B i c arbo n a t e secretion remarkably decreased H.pylori & NSAID H.pylori & NSAID Abnormal resting & stimulated Pyloric sphincter pressure
E T I O L OGY Predisposing factors Age :young in DU and peak inc. at 6 th decade in GU. Sex :GU commoner in males Causes H.Pylori NSAID Infection: CMV,herpes simplex,etc.. Other drug/toxin: bisphosphonates, chemo, cl opidogrel , glucocorticoids Misc.:crohn,neoplasm,ashemia,infiltrating
Smoking G e n e ti c : i n c rea s e d f r e q o f b l oo d gro up O a nd n on 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
Gram –ve S-shaped , flagellate Lies b/w mucous layer & gastric epithelium 1 st antrum then proximal segments. Dormant state – coccoid form Genome—1500 proteins H.pylori
Pathophysiology 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. Peptic ulcer disease in children is the result of an imbalance between mucosal defensive and aggressive factors.
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.
Gastric metaplasia Increased acid production Decreased duodenal mucosal bicarbonate production Then how does it cause Ulcers in duodenum?????
Endothelial defects Stasis--ischemia HCL mucin bicarbonate Epi. cell p r o l i f e rati o n UL C ER e r o s i o n s Healing (spontaneous Or therapeutic) NSAID induced PUD Pathophysiology Direct toxicity by Ion trapping Epithelial effects due to PG depletion
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
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
D/D OF EPIGASTRIC PAIN Gastric Duodenal Gall bladder Pancreas Colon Superficial / radicular pain Nervous dyspepsia
Diagnostic Evaluation
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
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
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