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Peptic Ulcer Disease

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What is Peptic Ulcer Disease (PUD) Epidemiology

Gastric Ulcers

Duodenal Ulcers

Agents Etiology Clinical Manifestation of PUD

Diagnostic Plan Images

Endoscopy

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A chronic disease with multiple complaints(dyspeptic syndrome) located in stomach(gastric ulcer) and or duodenum (duodenalulcer), characterised by an circumscribedulcerous crater which penetrates themuscularis mucosa.

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Higher prevalence in developing countries. DU 8-10% and annual incidence of 0,2%

GU 3 times more rare

Decrease in incidence since 1970

Decrease of DU principally in men M/F 3-4/1, 2/1and even 1/1

GU no significant modifications in incidence.

Decreased incidence principally in young and

middle aged men; is becoming a disease of oldage.

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Common in late middle age incidence increases with age

Male to female ratio2:1 More common in patients with blood group A Use of NSAIDs - associated with a three- to

four-fold increase in risk of gastric ulcer Less related to H. pylori than duodenal ulcers

about 80%

10 - 20% of patients with a gastric ulcer havea concomitant duodenal ulcer

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Duodenal sites are 4x as common as gastricsites

Most common in middle age peak 30-50 years

Male to female ratio4:1 Genetic link: 3x more common in 1st degree

relatives More common in patients with blood group O Associated with increased serum pepsinogen

H. pylori infection common up to 95%

Smoking is twice as common

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Helicobacter Pylori + ulcer NSAID (aspirin) induced ulcer Stress induced ulcer Ulcer which accompanies genetic diseases

and syndromes Helicobacter negative ulcer. Smoking Ethanol Bile acids Steroids

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A peptic ulcer is a mucosal break, 3 mm or greater, thatcan involve the stomach or duodenum. The most important contributing factors are H pylori,

NSAIDs, acid, and pepsin. The most important aggressive factors implicated in ulcer

Acid hypersecretionIncrease in parietal cell mass

Increase in vagus toneIncrease in parietal cellular sensibility to gastrinAntral G cells hyper functionNocturnal acid hypersecretionDeterioration in inhibitory mechanism of acid secretionsMotility disturbances: Duodenal ulcer-rapid gastric emptying, gastriculcer- gastric hypomotility

Pepsin hypersecretionHiperpepsinogenemia I-Helicobacter pylori Duodenogastric reflux

Biliary acids, lisolecitin and proteolytic enzymes.

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Factors of defence Pre-epithelial factors

Bicarbonate and mucus barriers

Tensioactive phospholipids

Epithelial factorsCellular resistance (normal cellular metabolism)Intra-cellular PH maintenance

Growth factors (epithelial growth factors,Prostaglandins, NO)

Mechanism of repair of epithelial lesions Post-epithelial factors

Abnormal mucous blood flow

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Individual factors Genetic factors: group 0 & A, Lewis and non-

secretory factor (a-b-)

Familial Hyperpepsinogenemia type I

Studies: 39% genetic factors and 61% averagepredisposing factors Associated diseases : ZE syndrome, MEN I,

systemic mastocytosis, alfa 1 antitrypsindeficiency, hepatic cirrhosis, chronic pancreatitis,

Crohns disease, COPD, polycythemia vera,basophilic leukemia, amyloidosis

Personality changes : anxiety, neuralgia

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80-90% of ulcers after excluding AINS Increased risk 4x duodenal ulcer and 3x gastric

ulcer Decreased risk of recurrence if eradication is

successful: 6% 1 yr and 17% > 1 yr, superiorsupraselective vagotomy.

Reversible gastrine hypersecretionpredominant postprandial

Increase in acid secretion if gastritis is antral Hipersecretion of pepsinogen Changes in adherent mucus Changes in appearance of gastroduodenal

mucus.

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Mucus, bicarbonate secretion, microcirculation(mucosal appearance depends upon PG (PGE)

NSAIDS inhibits COX1 and COX2 by decreasingphysiological and pathological prostaglandins

(systemic effect ) Some of NSAID (weak acids) have mucosal

irritant effect (local effect ) NSAID and HP are independent factors in

ulcerogenesis but have additional effects (toeradicate HP before starting treatment withNSAID)

Mucosal adaptation

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Zollinger Ellison Syndrome (gastrinoma)

isolated or in association with MEN I (0,5%)

Stress Ulcer Acid hypersecretion Systemic arterial hypotension Stress coagulopathy Ischemic induced mucosal defects.

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Signs and symptoms

Early

Satiety

NauseaVomitin

gAbdominalEpigastric

Pain

Pancreati

tis

Bleedin

g

Peritonitis(Perfor

ation)

PEPTICULCER

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Stool for fecal occult blood Labs: CBC, liver function test, amylase, and

lipase.

H. Pylori can be diagnosed by urea breath test,blood test, stool antigen assays, & rapid ureasetest on a biopsy sample.

Upper GI Endoscopy: Any pt >50 yo with newonset of symptoms or those with alarm

markings including anemia, weight loss, or GIbleeding. Preferred diagnostic test b/c its highly sensitive for dx

of ulcers and allows for biopsy to rule out malignancyand rapid urease tests for testing for H. Pylori.

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EndoscopyEndoscopy

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EndoscopyEndoscopy

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EndoscopyEndoscopy

Typical radiographic features of benign gastric ulcer (a)

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Typical radiographic features of benign gastric ulcer (a)

Typical radiographic features of benign gastric ulcer (c)

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Typical radiographic features of benign gastric ulcer (c)

Typical radiographic features of benign gastric ulcer (d)

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Typical radiographic features of benign gastric ulcer (d)

Typical radiographic features of benign gastric ulcer (e)

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Typical radiographic features of benign gastric ulcer (e)

Benign gastric ulcer (b)

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Benign gastric ulcer (b)

Typical radiographic features of duodenal ulcer (b)

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Typical radiographic features of duodenal ulcer (b)

Typical radiographic features of duodenal ulcer (c)

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Typical radiographic features of duodenal ulcer (c)

Duodenal ulcer (a)

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uode a u ce (a)

Duodenal ulcer (b)

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( )

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Stigmata of recent hemorrhage (a)

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g g ( )

Stigmata of recent hemorrhage (b)

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g g ( )

Stigmata of recent hemorrhage (c)

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Stigmata of recent hemorrhage (d)

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Stigmata of recent hemorrhage (e)

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Stigmata of recent hemorrhage (f)

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Stigmata of recent hemorrhage (g)

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Stigmata of recent hemorrhage (h)

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Perforated peptic ulcer

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Pyloric outlet obstruction and peripyloric ulcer disease (b)

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Pyloric outlet obstruction and peripyloric ulcer disease (c)

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Pyloric outlet obstruction and peripyloric ulcer disease (d)

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Pyloric Stenosis ParaclinicPyloric Stenosis Paraclinic

InvestigationInvestigation

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