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Peptic Ulcer
Disease
Muzaffar khan Alam khan
Department of Paediatric surgery
Student of TSMU
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..
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
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
Patho
physiology
• Major
causes
• Gastric
acid
• Gastric
emptying
increasddecreased
rapiddelayed
Bicarbonate
secretion
remarkably
decreased
H.pylori & NSAID H.pylori & NSAID
Abnormal resting
& stimulated
Pyloric sphincter
pressure
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
• 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
• Gram –ve
• S-shaped , flagellate
• Lies b/w mucous layer &
gastric epithelium
• 1st antrum then proximal
segments.
• Dormant state – coccoid
form
• Genome—1500 proteins
H.pylori
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.
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.
• 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
proliferation
ULCER
erosions
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
Mucosal Protective Agents
•Sucralfate -Sucralfate – 1gm qid
•Prostaglandin Analogue -Misoprostol - 200μg qid
•Bismuth Containing Compounds
Regimens for Eradication
Of H.Pylori
Triple Therapy
1.Bismuth Subsalicylate +
Metronidazole +
Tetracycline
-2 tablets qid
-250mg qid
-500mg qid
2 . Ranitidine Bismuth Citrate +
Tetracycline +
Clarithromycin / Metronidazole
-400mg bid
-500mg bid
-500mg bid
Regimens for Eradication
Of H.Pylori
3. Omeprazole +
Claithromycin +
Metronidazole /
Amoxicillin
- 20mg bid
-250/500mg bid
-500mg bid
- 1gm bid
•Quadruple therapy
•Treatment of
complications
•Therapy for NSAID
injury
•Surgical Therapy
Surgical Therapy
Duodenal Ulcer
1. Vagotomy & Drainage (By Pyroloplasty ,
Gastrodudenostomy ,
Gastrojejunostomy)
2.Highly Selective Vagotomy (does not require
drainage
procedure)
3.Vagotomy with Antrectomy
Surgical Therapy
Gastric Ulcer
1. Antral Ulcer – Antrectomy with Billroth I
Anastomosis
Ulcer Excision with
Vagotomy & Drainage
2.High GU –
• Csende’s Procedure
Subtotal Gastrectomy with a Roux-en-Y
Oesophagogastrojejunostomy
• Kelling Madlener Procedure antrectomy +
intraop. ulcer biopsy + vagotomy
Surgical complications
•Recurrent ulceration
•Afferent loop syndromes
•Dumping syndromes
•Post vagotomy diarrhea
•Bile reflux gastropathy
•Maldigestion & malabsorption
•Gastric adenocarcinoma
THANK
YO

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Peptic ulcer disease-child surgery

  • 1. Peptic Ulcer Disease Muzaffar khan Alam khan Department of Paediatric surgery Student of TSMU
  • 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
  • 5. Gastric ulcer Duodenal ulcer Patho physiology • Major causes • Gastric acid • Gastric emptying increasddecreased rapiddelayed Bicarbonate secretion remarkably decreased H.pylori & NSAID H.pylori & NSAID Abnormal resting & stimulated Pyloric sphincter pressure
  • 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
  • 8. • Gram –ve • S-shaped , flagellate • Lies b/w mucous layer & gastric epithelium • 1st antrum then proximal segments. • Dormant state – coccoid form • Genome—1500 proteins H.pylori
  • 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
  • 15. D/D OF EPIGASTRIC PAIN • Gastric • Duodenal • Gall bladder • Pancreas • Colon • Superficial / radicular pain • Nervous dyspepsia
  • 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
  • 21. Mucosal Protective Agents •Sucralfate -Sucralfate – 1gm qid •Prostaglandin Analogue -Misoprostol - 200μg qid •Bismuth Containing Compounds
  • 22. Regimens for Eradication Of H.Pylori Triple Therapy 1.Bismuth Subsalicylate + Metronidazole + Tetracycline -2 tablets qid -250mg qid -500mg qid 2 . Ranitidine Bismuth Citrate + Tetracycline + Clarithromycin / Metronidazole -400mg bid -500mg bid -500mg bid
  • 23. Regimens for Eradication Of H.Pylori 3. Omeprazole + Claithromycin + Metronidazole / Amoxicillin - 20mg bid -250/500mg bid -500mg bid - 1gm bid
  • 25. Surgical Therapy Duodenal Ulcer 1. Vagotomy & Drainage (By Pyroloplasty , Gastrodudenostomy , Gastrojejunostomy) 2.Highly Selective Vagotomy (does not require drainage procedure) 3.Vagotomy with Antrectomy
  • 26. Surgical Therapy Gastric Ulcer 1. Antral Ulcer – Antrectomy with Billroth I Anastomosis Ulcer Excision with Vagotomy & Drainage 2.High GU – • Csende’s Procedure Subtotal Gastrectomy with a Roux-en-Y Oesophagogastrojejunostomy • Kelling Madlener Procedure antrectomy + intraop. ulcer biopsy + vagotomy
  • 27. Surgical complications •Recurrent ulceration •Afferent loop syndromes •Dumping syndromes •Post vagotomy diarrhea •Bile reflux gastropathy •Maldigestion & malabsorption •Gastric adenocarcinoma