2004 - 05

Karol Bagh New Delhi – 110005

(University of Delhi)

Directed By :-

Dr. P.K. Chaudhary (M.S.)Presented By :-

Monika Sharma

PEPTIC ULCER DISEASE(PUD)

An ulcer is defined as disruption of the mucosal integrity so ‘peptic ulcer’ refers to an ulcer in the lower oesophagus, stomach or duodenum, in jejunum after surgical anastomosis to stomach or rarely in the ileum adjacent to muckel’s diverticulum leading to local defect or excavation due to active inflammation.

DEFINITION

Although the prevalence of peptic ulcer is decreasing in many western countries it still affects approximately 10% of all adults at some time in their lives. The male to female ratio for duodenal ulcers varies from 5:1 to 2:1 whilist for gastric ulcers is 2:1 or less.

INCIDENCE

Despite the constant attack on gastroduodeual mucosa by a host of noxious agents (acid, pepsin, bile, acids, pancreatic enzymes, drugs & bacteria) integrity is maintained by an intricate system that provides mucosal defense & repair.

GASTRIC PHYSIOLOGY

GASTRIC ANATOMY Gastric epithelium

consists of rugae with microscopic gastric pits haring each four - five branching gastric glands.

Majority of gastric glands (75%) found with in oxyntic mucosa & contain mucous neck, parietal, chief endocrine & entero chromaffin cells.

Pylori glands contain mucous & endocrine cells & are found in antrum.

GASRIC MUCOSAL DEFENSE Defense system consistof 3 level barriers:

1. Pre – epithelial2. Epithelial 3. Sub-epithelial

elements  Figure : Components involved in providing gastroduodenal mucosal defense and repair.

First line of defense Consist of mucous – bicarbonate layer. Some as a physiochemical barrier.

Mucous secreted from surface epithelial cells

Act as non-stirred water layer

Impend diffusion of ions & molecules Bicarbonate :-

Secretes by surface epithelial cells into mucons gel.

Raise the PH gradient at gastric luminal surface.

II line of defense Epithelial element defense by :

Mucous production. Epithelial cell ionic transport maintains intra cellular pH.

Bicarbonate production. Intra cellular tight junctions.

On breaching of first line of defense gastric epithelial calls bordering a site of injury can migrate to restore a damaged region.

III rd line of defense :- An elaborate microvascular system with in gastric sub mucosal layer key component of sub epithelial defense system.

Rich submucosal circulatory bed.

Provide HCO3 - + provide micronutrients + O2

Neutralizes acid remove toxic metabolic by – product PROSTA GLANDIS

plays important role in defense system regulate release of mucosal bicarbonate & mucus, inhibit parietal cells secretion & epithelial cell restitution.

AETIOLOGY & PATHOGENESIS

PUD encompasses both gastric and duodenal ulcers.

Acute peptic ulcer Ingestion of Aspirin or butazolidin. By stress (Stress ulcer):- May be following endotoxic shock :

Hypotension,Haemorrhage or

Cardiac infarction.

Sepsis. After trauma or neurosurgical operations (Curling’s ulcers). After burns (curling’s ulcers). Patient on steroids (Steroids ulcers). The size of peptic ulcer

Acute peptic ulcer

CHRONIC PEPTIC ULCERS GASTRIC ULCERS 1. Decrease mucosal resistance.

2. Pyloroduodenal reflex.

3. Deficient mucous barriers.

4. Mucosal trauma.

5. Local Ischaemia.

6. Antral stasis.

7. NSAIDs.

8. Helicobacter pylori.

DUODENAL ULCER 1. Acid hyper secretion. 2. Genetics factor. 3. Endocrine organ

dysfunction. 4. Liver abscess. 5. Emotional factors. 6. Diet & smoking. 7. Helicobacter pylori. 8. Decrease in

bicarbonate production.

CHRONIC PEPTIC ULCERS

Pathogenesis

NSAIDs migrate across lipid membrane of epithelial cells.

Trapped in an ionized form.

Related with NSAIDs

Cell injury.

Topical NSAIDs.

Alter surface mucous layer.

Peronits back diffusion of H+ & Pepsin.

Further cell damage.

Figure shows machanisms by which NSAIDs may induce nucosal injury :

Risk factors for NSAID – induced Gastroduodenal ulcers

Established

Advanced age. History of ulcer.Concomitant use of glucocorticoids.High dose of NSAIDs. Multiple NSAIDs.Concomitant use of anticoagulants serious or multi system disease.

Possible

Concomitant infection with H. pylori. Cigarette smoking.Alcohol consumption.

Related to H. Pylori

Factors predisposing to higher colonization rate includes :-

Poor socio – economic status.

Less education.

Transmission :-

Oral-oral. Fecal-oral route.

Bacterial factors

Produces surface factors chemo tactic for neutrophils & monocytes contributing to epithelial cell injury.

Make proteases & phospholipase one breaking down glycoprotein of mucous gel, reducing efficacy of first line of defense.

Expresses adhesions facilitating attachment of bacteria to gastric epithelial cells.

LPS of bacteria help in infection.

Host Factors Inflammatory response contributing epithelial cell damage. H. Pylori antral infection.

Increase acid production.

Increase duodenal acid & mucosal injury. H. pylori infection.

Increase Basal & stimulated gastrin.

Decrease somatostain – secreting D-cells. It associates with decrease duodenal mucosal bicarbonate

production.

Clinical feature Symptoms :-Acute peptic ulcers

Symptoms of short duration.

Ulcers recognized when they cause haematemesis.

May perforate particularly when all in wall of duodenum.

May progress to an ulceration.

Chronic Peptic ulcers

Main symptom :- Pain in upper abdomen.

Chronic gastric ulcers

Age - Usually middle aged. Sex - Males more.

ConstitutionThin & anaemic patient with ‘J’ shaped hypotonic stomach.

Periodicity Less marked

Attack lasts for several weeks followed by interval

of freedom from symmetrical for 2 –

6 months.

Chronic Duodenal ulcers

Chronic Duodenal ulcersMales but not so much.

Healthy males with steer-horn stomach, which is high in position.

Well markedAttack lasts for several wks with interval of freedom from 2 – 6 months usually appears in spring & antrum. Continued….

Chronic gastric ulcers

Pain Strictly epigastric. Boring /pricking natures pain.On ulcer penetration pain radiate to back.

Site

Mid – epigastrium / slightly to its left.

Chronic Duodenal ulcers

Pain more severe & spasmodic innature.

Pain on transpyloric plane about 1 inch to right of midline.

Continued…..

Chronic gastric ulcers

Relation with food Almost immediately or any time up to 1½ hr. after meal as food irritates ulcer.

Pain not felt empty stomach.

Pain not felt at night.

Food aggravates pain.

Chronic Duodenal ulcers

Starts usually 2½ - 3 hr. after food.When stomach pushes chyme into duodenum & irritate ulcer.

Felt empty stomach ‘Hunger – Pain’.

At dead of night, pain is characteristic. Food relieves pain.

Continued…

Chronic gastric ulcers

Vomiting Noticeable in half cases. Occur after food. Relieves pain. May be self induces. Appetite Good. Patient afraid to take food.

Diet Patient avoids fried & spicy

food.

Chronic Duodenal ulcers

Rare.

Quite good. Eat frequently to around pain.

No particular food initiates pain. Continued…

Chronic gastric ulcersWeight Patient Losses weight. Hemorrhage Less common. Haematemesis is more –

than malena.

On Examination Tenderness in midepigastric /

slightly to left of it.

Chronic Duodenal ulcers

Patient gains the weight

More common. Malena more common than

haematemesis.

Tenderness at ‘duodenal pt’ situated on transpyloric with plane 1 inch to midline.

SPECIAL INVESTIGETIONS

1) Examination of blood. 2) Examination of stool. 3) Gastric function test 4) Radiological investigations. 5) Endoscopy. 6) USG.

USG, Endoscopy and radiology examination of PUD :

Treatment Basic Treatment

Rest. Diet (avoid spicy food, use balance

diet, no alcohol and smoking).

Medical Treatment Antacids. H2 receptor antagonistic. Proton pump inhibitors. Cytoprotective agents. Bismuth – containing preparations. Prostaglandin analogues.

Drugs used in Treatment of PUD

Drug Eg. Dose Acid suppressing drug ‘Antacids’.

Mylanta 100 – 140 mg / L/

Maalox, Tums,

3 hr. after meal.

Gaviscon Hs.

H2 receptor antagonists.

Cimetidine 800 mg hs.

Renitidine 300 mg hs.

Famotidine 400 mg hs.

Nizatidine 300 mg hs.

Drugs used in Treatment of PUDDrug Eg. Dose

Proton pump inhibitors.

Omeprazol 20 mg / d

Lansoprazol 30 mg / d Rabeprazol 20 mg / d Pantoprazol 40 mg / d

Mucosal protective agents. Sucralfate. Sucralfatet 1g qid. Prostaglandis analogus.

Misoprostol 200 mcg. qid.

Bismuth – containing compounds.

Bismuth subsalicylate (BSS)

2 tablet qid.

Regimens recommended for eradication of H. pylori :

Drug Dose

Triple therapy 1. Bismuth sub salicylate plus. 2 tab qid

Metronidagole plus. 250mg qidTetracycline. 500mg qid

2. Ranitidine Bismuth Citrate plus. 400mg bdTetracycline plus. 500mg bdClarithromycin or Metronidazole. 500mg bd

3. Omeprazole plus. 20mg bdClarithromycin plus. 250mg bdMetronidazole or 500mg bdAmoxicillin. 1g bd

Quadruple therapy :

Drug

Omeprazole. Bismuth subsalicylate. Metronidazole. Tetracyline.

Dose

20mg daily 2 Tab qid

250mg qid 500mg qid

Regimens recommended for eradication of H. pylori :

RECOMMENDED TREATMENT FOR NSAID – RELATED MUCOSAL INJURY :

Active ulcer

NSAID discontinued. NSAID Continued. Prophylactic therapy.

H. Pylori infection.

H2 receptor antagonist or PPI. Misoprostol. PPI Selective Cox – 2 inhibitor.

Eradication if active ulcer present or there is a past history of PUD.

Surgical therapy Indications

When ulcer fails to heal with medical management (2 months for gastric ulcer

& 6 month for duodenal ulcers). Patient in need of quick relief. Long-standing non – healing ulcer. Ulcer producing obstruction. Haemorrhagic ulcers. Perforation of ulcers. Suspicion of malignancy.

Continued…

Surgical therapySurgical procedures • HSV - (Highly selective

vagetomy)• Billroth I • Billroth II

Continued…

Surgical therapyComplications

• Perforation. • Haemorrhage (Haematemesis, Maloena).• Stenosis. • Penetration into neighboring viscera. • Carcinoma. • Residual absence.