Peptic Ulcer Disease

Done by:PROF/GOUDA ELLABBAN

SUEZ CANAL UNIVERSITY / EGYPT

ContentDefinitionIncidence & epidemiologyCausesNormal physiologyPathogenesisClinical presentationDifferentialsInvestigationsTreatmentprevention

what is a Peptic Ulcer?

A peptic ulcer is a hole in the gut lining of the Stomach (Gastric ulcer)Duodenum (duodenal ulcer)Esophagus (esophageal ulcer). An ulcer occurs when the lining of these organs is corroded by the acidic digestive juices which are secreted by the stomach cells.

Normal stomach Gastric Ulcer

Sites

Incidence & Epidemiology

Frequency: In the US: One-year point prevalence is 1.8%. Lifetime prevalence is approximately 10%. PUD affects approximately 4.5 million people annually.

Internationally: Frequency of PUD is decreasing in the developed world but increasing in developing countries.

H. pylori is found in 50% of people worldwide; 70% of KSA population

Sex: Male-to-female ratio of PUD is approximately 2:1

Age: Duodenal ulcers usually occur in those aged 25-75 years.Gastric ulcer prevalence peaks in those aged 55-65 years.

Mortality/Morbidity: The mortality rate has decreased in the last few decades and is approximately 1 death per 100,000 cases.

The hospitalization rate is approximately 30 patients per 100,000 cases.

What Causes Peptic Ulcers? H pylori (most common cause of ulceration)NSAIDs, aspirinGastrinoma (Zollinger-Ellison syndrome)Heredity (large parietal cell mass, blood group O & blood group antigen)SmokingSevere stress (eg, trauma, burns)AlcoholBile refluxPancreatic enzyme refluxRadiation

H. pylori

gram –ve spirochetal bacteriumfound in the antral and duodenal mucosa.

Mechanism: it is urease +ve split urea and lead to

formation of ammonia alkaline media around the bacteria 2ry high acid ULCER

also it affect the cells through cytotoxin

NSAIDs

Nonsteroidal anti-inflammatory drugs Second most common cause of PUD Addition of steroids potentiates risk Accounts for many H pylori–negative

ulcers

Normal Physiology

Mucosal Defense FactorsTight junctions between epithelial cells which form a physical barrier to diffusing hydrogen ions.

Mucus layer on epithelial cells.

Bicarbonate secreted by epithelial cells.

Adequate blood supply of gastric mucosa, which prevents accumulation of hydrogen ion within mucosal cells.

Competent sphincters(pyloric & lower esophageal) block reflux of bile salts into the stomach & esophagus.

Pathogenesis

Ulcers occur only in the presence of acid & pepsin. Therefore we can say that aggressive factors break the defensive mucosal barrier & then acid, pepsin cause destruction & ulceration.

NSAIDs are non-selective inhibitors of prostaglandins by inhibiting both enzymes cyclooxygenase (COX)1 & 2, so it inflammation & reduce pain along with decreasing the defensive mechanism of gastric mucosa & leave it susceptible to ulcerogenic effect of acid & pepsin

Etiology of PUD

Normal

Increased Attack Hyperacidity

Weak defense Helicobacter pylori* Stress, drugs, smoking

Duodenal Ulcer Gastric UlcerIt usually occurs in the first part of duodenum.It is virtually never malignant.More common 4 times than gastric ulcer.More common in male at age 33-55 years.Risk factors: H pylori, smoking, NSAIDs, COPD,cirrhosis,CRF.

More than 90% of gastric ulcers occur in lesser curvature.It is may be malignant.Less common than duodenal ulcer. More common at age 50-60 years.Most common cause NSAID use, bile reflux &H pylori.

Duodenal Ulcer Gastric Ulcer

Clinical presentaion

Alternating symp. & symp. Free periods

Gnawing,burning epigastric pain

Nocturnal pain➔ early awakening

Duodenal relieved by foods , antacids ,

-if gastric by foods & by vomitting

Clinical presentation ,, cont.

Dyspeptic complaints (belching,bloating,abd.distension)

Weight loss

Epigastric tenderness

Remember .. Heart burn is NOT a sign of PU but of GERD

Clinical presentation in complicated ulcerGI bleeding ➔heme +ve stool , melena ,

hematemesis , anemia

Obstruction ➔ N&V,abd.distension, succussion splash on auscultation

Penetration or perforation ➔ severe abd. Pain , & signs of peritonitis

CA➔ wt loss & anorexia

Non ulcer dyspepsia

CA (gastric , pancreatic , lymphoma)

H.pylori assosciated gastritis

GERD

Chron’s dis

Pancreatitis

Dissecting aneurysm

Billiary colic & acute cholecystitis

Differentials

Investigations A .Routine lab. Tests :

CBC & iron studies➔ can detect anemia (anemia & wt. loss are alarm signs that mandate

endoscopy to know the source of chronic GI bleeding)Serum amylase➔to exclude pancreatitisSerum gastrin➔to exclude zollinger ellisonElectrolytes, BUN, and creatinine ➔in critical-appearing patients who require fluid resuscitation.Type, crossmatch, and screen are indicated if transfusion in unstable or potentially critical patients is needed.

Investigations

B .H.pylori testing:

Urea breath test: very sensitive & specific, if +ve ➔ H.pyloriH.pylori stool antigen test

Blood antibody test for H.pylori (ELIZA)

Investigations ,,, cont.C . Imaging :

Upper GI x-ray with double barium contrast:Helps to confirm or rule out malignancy70-90% accurte in PU Dx.

Chest x-ray ➔ to detect free abdominal air if perforation is suspected

Investigations ,,,imaging .. cont.

Diagnostic endoscopy (Esophagogastrodudenoscopy)Endoscopy ➔the gold standard for accurate diagnosis of peptic ulcer(>95%) & malignancy (>99%), also help in prognosis & sometimes in tttAllows taking biopsies➔culture➔+urease,

+H.pylori

Treatment

Stop orreduce

NSAIDs

Prevent Further flare

ups

Ttt of complications

EliminateOr reducesymptoms

EradicateH.pylori

Goals

Medical Treatment ,,

For eradication of H.pylori :Quadrable therapy(for at least 2 wks) = 2 antibiotics +PPI+bismuth

(clarithromycin , amoxycillin , omeprazole , bismuth subsalicylate )For –ve H.pylori ulcers :PPI , H2 antagonists as cemitidine or ranitidine (zantac)

Medical Treatment ,, cont.

In NSAIDs ulcers :

The same(H2antagonists , cemitidine) + stop NSAIDs

If discontinuing is not possible:

Either give omeprazole concurrently OR specific COX-II anti inflammatory drugs as

celecoxib

Medical Treatment ,,, cont.

Endoscopic therapy :

Indicated in bleeding ulcers with high risk signs(active bleeding, visible vessels, and adherent

clots)

Help determining & evaluating the bleeding & the risk for rebleeding

Several modalities ( injection , coagulation , thermal , hemostatic clips )

Surgical Treatment

Indications for surgery :

1. ulcer perforation,

2. gastric outlet obstruction,

3. giant gastric ulcer, and

4. Failure of medical ttt

Surgical Treatment ,,, cont.

A. Gastric ulcer :

Gastroduodenostomy –billroth I-

Gastrogegunestomy –billroth II-

Both include removal of both the ulcer & the diseased antrum

Surgical treatment ,, cont.

B . Duodenal ulcer :Vagotomy 4 types: Truncal vagotomy➔total abdominal vagal denervation and requires a drainage procedure-pyloroplasty- to prevent gastric stasis. Selective vagotomy➔spares the vagal branches to the liver and small intestine (celiac & hepatic), but produces a total gastric vagotomy. A pyloroplasty is required. Highly selective vagotomy➔diverting innervation of the body only(selective denervation of the parietal cell mass), no pyloroplasty Posterior truncal vagotomy with anterior seromyotomy (Taylor procedure) divides one vagal trunk while preserving the other. This procedure does not require a pyloroplasty.

Prevention

1ry• Stop smoking & Alcohol• Avoid NSAIDs• Low fat diet with Emphasis On 3meals/day• education

2ry• Life style changes will not cure the ulcer but decrease the recurrence &complications incidence

Thank u