Peptic ulcer disease 1

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PEPTIC ULCER disease PEPTIC ULCER disease (PUD) (PUD) Sara Elzeiny

Transcript of Peptic ulcer disease 1

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PEPTIC ULCER disease (PUD)PEPTIC ULCER disease (PUD)

Sara Elzeiny

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* Definition:

Ulceration of any part of the G.I.T exposed to the gastric juice.

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*Types

Acute Superficial erosion

Minimal erosion

ChronicMuscular wall erosion with formation of fibrous tissue

Present continuously for many months or intermittently

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I.I. ACUTE PEPTIC ULCERS ACUTE PEPTIC ULCERS (STRESS ULCERS)(STRESS ULCERS)

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* Etiology: I. Infective: Salmonellosis & staph. Food poisoning.II. Non infective:•Drugs; NSAI, cytotoxic drugs and cortisone.•Alcoholism.•Cigarette smoking.•Uremia.•Severe stress.•Chemical irritation: by strong alkalis, acids.•Mechanical trauma; during endoscopic examination.

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* Sites: stomach & 1st part of duodenum.

* Pathology: hemorrhagic inflammation and

superficial ulceration.

* Fate: usually heal by regeneration.

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Chronic peptic ulcer diseaseChronic peptic ulcer disease

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* Sites of peptic ulcer:• Duodenum: (25 times more commoner than

gastric ulcer ) usually toward the anterior wall is more often affected.

• Stomach: Usually antrum toward the Lesser curvature.

• At the margins of a gastroenterostomy (stomal ulcer)

• In the duodenum, stomach or jejunum of patients with Zollinger-Ellison syndrome.

• Within Meckel’s diverticulum that contains ectopic gastric mucosa.

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Duodenal ulcerDuodenal ulcer

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* Pathogenesis of Duodenal ulcer: Duodenal ulcer: •Due to increased gastric juice secretion + Rapid emptying of stomach into duodenum * Causes:•Increased vagus nerve stimulation.•Increased number of parietal cell (as in tall thin patient).•Increase hormonal stimulation (Z.E syndrome) Gastrinoma Gastrin.•Increase the responsiveness of parietal cells to secretory stimuli.• psychosomatic stimuli.

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Duodenal ulcerDuodenal ulcer

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Gastric ulcerGastric ulcer

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Types

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* Pathogenesis of Gastric ulcer. Gastric ulcer.•Due to decreased mucosal defense mechanisms or increasing damaging forces…

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Causes of decrease mucosal resistant

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H. Pylori infection

• H. pylori is the etiologic factor in most patients with

peptic ulcer disease and may predispose individuals to

the development of gastric carcinoma. H. pylori

colonizes in the human stomach.

• H. pylori infection is present in almost all patients with

duodenal ulcers and 70% of cases with gastric ulcers.

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* Mechanism:

1. H. pylori secretes urease (generates ammonia), protease

(breaks down glycoprotein in the gastric mucus) and

phospholipases.

2. Bacterial lipopolysaccharide attracts inflammatory cells to the

mucosa. Chronically inflamed mucosa are susceptible to injury.

3. A bacterial platelet-activating factor promotes thrombotic

occlusion of surface capillaries.

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* Gross features:* Gross features:

• Site: Gastric ulcers are located at the antrum

toward the lesser curvature. The duodenal ulcer

is usually located at the 1st part anteriorly.

• Shape: Round, oval.

• Size: Usually less than 4 cm in diameter.

PATHOLOGY OF PUD

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• Edge:

- Sharp edge.

• Floor:

- Clean

• Base of ulcer:

- Firm (formed of bundles of muscles and fibrous tissue).

• Margin (Surrounding gastric mucosa):

- Edematous and reddened due to gastritis.

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• Depth of the ulcer:

- Superficial ulcer penetrate the mucosa reaching up to

the muscularis mucosa.

- Deeply excavated ulcers having their bases on the

muscularis propria.

- When the entire wall is penetrated, the base of the

ulcer may be formed by adherent pancreas, omental

fat, or liver. Free perforation into the peritoneal

cavity may occur.

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GU

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Gastric ulcerGastric ulcer

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Biopsy of peptic ulcerBiopsy of peptic ulcer• Biopsy is necessary to distinguish between benign and

malignant ulcers.• Biopsy should be taken from the ulcer edge, at least from

each quadrant.• Up to 10-12 biopsies may be taken to exclude cancer.

* Microscopic features:

• Active peptic ulcer shows;

1. Superficial zone: fibrinoid necrosis & neutrophils.

2. Intermediate zone: chronic inflammatory cells & granulation tissue.

3. Deep zone: fibrous tissue, muscle remnants.

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*SYMPYOMS OF PUD

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* Complications of PUD :

1. Hemorrhage: hematemesis or melena.

2. Perforation

3. Healing by fibrosis causing gastric or duodenal

obstruction.

4. Malignant transformation: rare (0.5% of gastric

peptic ulcer).

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Functional dyspepsia: By Endoscopy Zollinger Ellison Syndrome (Gastrinoma) Gastric Malignant Ulcer: Endoscopy + Biopsy Biliary or pancreatic diseases: Ultrosonography, MRCP, ERCP

*Differential Diagnosis

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INVISTIGATION OF PUD

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*Laboratory analysisCBC : chronic blood loseUrinalysisLiver enzyme studiesSerum amylase determinationStool examination : occult blood

*Endoscopy procedure most often used

Determines degree of ulcer healing after treatment

Tissue specimens can be obtained to identify H. pylori and to rule out gastric cancer

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*Tests for H. pylori*Tests for H. pyloriNoninvasive testsNoninvasive tests

Serum or whole blood antibody testsSerum or whole blood antibody tests Immunoglobin G (IgG)Immunoglobin G (IgG)

Urea breath testUrea breath testInvasive testsInvasive tests

Biopsy of stomach Biopsy of stomach Rapid urease test Rapid urease test

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*RADIOLOGICAL Barium contrast studiesBarium contrast studies

Widely usedWidely used X-ray studiesX-ray studies

Ineffective in differentiating a peptic Ineffective in differentiating a peptic ulcer from a malignant tumorulcer from a malignant tumor

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TREATMENT

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CONSERVATIVE TREATMENT*GENERAL MEASURE

- Rest -Diet: -small frequent meals -avoid irritant food,drugs

&smoking -milk give some reliefDRUG THERAPY

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Establish the diagnosis (endoscopy or UGI)

Gastric ulcerbiopsy, R/O cancer

Duodenal ulcerAssess pathogenesis:H.pylori NSAIDsSmoking Family historySerum gastrin

Therapy:Treat H.pyloriAcid suppressionEnhance mucosa defense

Document H.pylori eradication

Complications -Surgery (obstruction, perforation, intractable bleeding, malignant transformation)

Endoscopic follow-upto healing

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References:Robbins and Cotran’s:

Pathologic Basis of Disease. Seventh

edition.

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