PEPTIC ULCER DISEASE

Michele Czerwinski BSN, RN

Nur 652 Primary Care

Definition Sores or erosion that form the lining of the

gastrointestinal tract (GI) system that break down the mucosa of the stomach or duodenum

Gastric Ulcer Duodenal Ulcer most common Esophageal & Ectopic gastric mucosal

irritation Penetrates the muscularis mucosa larger

then 5mm in diameter Primary cause Helicobacter pylori and

NSAIDS

Dunphy, Winland-Brown, Porter & Thomas (2011)

UPTODate (2013)

Pathophysiology

Most patients with ulcers have normal or subnormal amounts gastric secretion. The mucosal defense is supported by surface mucus and bicarbonate that forms a thin alkaline gel coating the mucosal cells and Dunphy et al.(2011)

Imbalance between aggressive and defensive factors (A) gastric, pepsin, bile salts, pancreatic enzymes ( D) mucus,bicarbonate,blood flow, prostaglandins, growth factors, cell

turnover O’Callahan (2014) Breakdown the mucosal defenses by inhibiting prostaglandin synthesis leaving

the mucosa vulnerable to the effects of gastric acid

Etiology

Helicobacter pylori: attaches to the gastric epithelial cells and secretes enzymes that break down the mucosal layer. (70-90% of gastric ulcers and 90% of duodenal ulcers)

NSAIDS: inhibits prostaglandin synthesis Zollinger –Ellison syndrome: tumors in the wall of the pancreas or intestine

secrete high levels of gastrin

Incidence

Can affect more than 4 million people each year in the United States Effects both genders equally Occurs within 70% of patients between 25-64 years and increase with age Annual rate for hospital admission is over 160 per 100,000 cost of care totals

more than two billion in the United States Global incidence rate ranges between 0.1-0.19%

Screening/Risk factors

No current screening guidelines for PUD O’Callahan (2014) suggest testing for H. pylori before starting therapy with NSAIDS to reduce the risk of ulcers

Risk factors Age H. pylori and Gastrinoma History of PUD Family History Use of multiple NSAIDS and systemic corticosteroids Smoking and alcohol use Stress Mechanical ventilation

Clinical Findings

Gastric ulcers- nausea, vomiting, and pain exacerbated by eating Duodenal Ulcers – (Dyspepsia) Epigastric pain during the fasting state or during

the night relived by food intake or acid-neutralizing agent Manlertheiner,Chan& McColl (2009). Also may have heartburn

Epigastric tenderness and bloating Acute hemorrhage- coffee ground emesis, bloody or tarry stools ,Iron deficiency

anemia ,board like abdomen with rebound tenderness ( perforation) Positive guaiac Positive for H.pylori Burning or a gnawing hunger Clustering pain lasting for minutes Anorexia

normal gastric antrum and pylorus

Large gastric ulcers in the gastric antrumGASTROLAB (2013)

Normal descending duodenum

A huge duodenal ulcer with black spots in the necrotic area indicating recent bleeding

GASTROLAB (2013)

Differential Diagnosis

Gastroesophageal reflux disease Gastric carcinoma Drug induced dyspepsia ( coffee, theophylline, digitalis) Myocardial infraction, cardiac disease Esophageal spasm Lower respiratory infection Cholelithiasis Chron’s disease Pancreatitis Gastritis Gastroenteritis Biliary colic Intestinal ischemia

Social/Environmental Considerations

Smoking Excessive consumption of alcohol Medications (NSAIDS),multiple Stress Seasonal patterns

Laboratory Tests

Standard upper GI endoscopy* accurate GI radiographic * concern for pregnant women CBC, metabolic panel (anemia, elevated liver enzymes) Fecal occult blood Stool antigen

H. pylori Serologic antibody test(ELISA) can not distinguish between active or past

disease. Direct bacteriologic analysis through esophagogastrodenoscopy (EGD)

expensive Urea breath test –based on the production of ammonia from the metabolism of

urea test for active infection. Serum gastrin level fasting 200/pg/ml repeat test then followed by basal and

peak acid-output measurements. If higher than 600pg/ml and basal acid output of more then 15mmol/h suspect Zollinger-Ellison syndrome

Management/Treatment

Smoking cessation Avoid caffeine Foods that exacerbate symptoms Lifestyle changes Surgery if resistant to medical treatment

Hollier, A., Hensley,R. (2011)

NON-PHARMACOLOGICAL

Pharmacological Management

Proton pump inhibitors(PPIs) and agents that in enhance the mucosal defenses and heal duodenal ulcers in four weeks and gastric ulcers in eight weeks

Antacids PRN 1-3 hours Carafate, Pepto-Bismol Mylanta II

H2 receptors blockers-inhibit only 65% of acid secretion >24hrs mild symptoms x two weeks

Cimetidine inhibits hepatic cytochrome P-450 may increase levels of warfarin, theophylline and dilantin

Ranitidine Famotidine Nizatidine

Pharmacologic Management

Prostaglandins –antisecretory and mucosal protective properties Misoprostol ( Cytotec) *PPIs suppress gastric secretion inhibits the hydrogen /potassium pump in gastric

cells (daily / >24hrs) long-term use decreases B12 and iron absorption. Dexlansoprazole (Dexilant) Esomeprazole (Nexium) Omeprazole (Prilosec) Pantoprazole (Protonix) Lansoprazole

Hollier, A., Hensley,R. (2011)

PharmacologicalManagement

H.pylori PPI treatment triple therapy ( Nexium)Esomeprazole 40 mg daily, amoxicillian 1000mg BID and

clarithromycin 500 mg BID x 10 days (Prevacid) lansprazole 30 mg BID, amoxicillin 1000mg BID, and

clarithromycin 500 mg daily x10-14 days (Prilosec) omeprazole 20 mg BID, amoxicillin 1000mg BID and

clarithromycin 500 mg daily x 10 days

H.Pylori H2 receptor based treatment triple therapy (Axid)nizatidine 300mg at bedtime with any antibiotic combination x 14 days (Pepcid) famotidine 40 mg at bedtime with any antibiotic combination x 14

days (Tagamet)cimetidine 800mg at bedtime with any antibiotic combination x 14

days

Hollier, A., Hensley,R. (2011)

Complications

Hemorrhage Perforation Obstruction Gastric adenocarcinoma

Follow- Up

Monitor clinical response of duodenal ulcer Confirm eradication of H.pylori Endoscopy with cytology and biopsy to confirm

healing in 6-12 weeks

Counseling/Education/Referral

Smoking cessation Nutrition ( alcohol intake and caffeine) Medication adherence NSAIDS Refer to Gastroenterologist if treatment fails and if Zollinger –Ellison syndrome

is present

Questions

1)Which ulcer is the most common?

a)Ectopic

b)Gastric

c)Esophageal

d)Duodenal

2)What is the primary cause of PUD?

a) H.pylori and NSAIDS

b)Anemia

c)steroids

4)antacids

3)What is one pathological reason an ulcer occurs?a) Balance between aggressive and defensive factorsb) Imbalance between aggressive and defensive factorsc) Stressd) smoking

4) NSAIDS inhibit prostaglandin synthesis.a) trueb) false

5) Does PUD effect only female younger adults?a) Nob) Yes

6)Which is not a risk factor for PUD?a) Ageb) Stressc) Smokingd) Asthma

7) Gastric ulcers cause pain during the fasting .a) Trueb) False

8) Which diagnostic test is the most accurate in diagnosing PUD? a)GI endoscopy

b) CBCc) GI radiographicd) Serologic antibody test

9) H2 RBS are the drug of choice for treating PUD?a) Trueb) False

10) H. pylori can be eradicated with single drug therapy?a) trueb) false

1) D- duodenal can have multiple ulcers distal to the second portion of the duodenum

2) A- multiple use of NSAIDS cause 90% of duodenal ulcers are caused by H.pylori

3) B -the imbalance causes the breakdown the mucosal defenses by inhibiting prostaglandin synthesis leaving the mucosa vulnerable to the effects of gastric acid

4) A -breakdown the wall and the mucosal wall will become vulnerable5) A -effects gender equally

6) D -not a risk factor for PUD

7) B- duodenal ulcer patients during the fasting state in the morning

8) A -most accurate in the diagnosis and does not harm the patient

9) B- PPIs are given daily and H2RBS are BID and only inhibit 65% of acid secretion

10) B triple therapy is the drug regimen to eradicate H. pylori

References

Alhazzani, W. J.,Mohammed,A., Moayyedi,P.,Jaeschkle,R. (2013, September 22). Stress ulcer prophylaxis in critically ill patients: Retrieved from CINAHL Plus.

Crowe, S. (2013, September 22). Patient information: Peptic ulcer disease (Beyond the Basics). Retrieved from UpTODate: http://www.uptodate.com/contents/peptic-ulcer-disease-beyond-the-basics

Dunphy, L.,Winland-Brown,J.,Porter,B.&Thomas,D. (2011). Primary Care: The Art and Science of Advanced Practice Nursing (3rd ed.). Philadelphia, PA: F.A.Davis.

Gralnek, M.,Barkun,A.,Bardou,M. (2013, September 22). Management of acute bleeding ulcer. Retrieved from CINHAL Plus.

Hollier, A., Hensley,R. (2011). Peptic Ulcer Disease (PUD). In Clinical Guidelines in Primary Care: A Reference and Review Book (pp. 263-266). Advanced Practice Education Associates, Inc.

Malfertheiner, P., Francis.C.,McColl,K. (2013, September 22). Peptic ulcer diease.Retrieved from CINAHL Plus. Retrieved from http://jvsmedicscorner.com/Medicine_files/Peptic%20ulcer%20disease%20review.pdf Manfredini, R., De -Giorgio,R.,Smolensky,Benedetta,B.,Salmi,R.,Fabbri,D.,Edgardo,C.,Serra,M.,Barbara,G.,Stanghellini,V.,Corinaldesi,R.& Massimo.(2013, September 22). Seasonal pattern of peptic ulcer hospitalizations: analysis of the hospital discharge data of the E-milia Romagna region of Italy. Retrieved from CINHAL Plus.

O'Callahan, K. (2014). Peptic Ulcer Disease. In 5-Minute Clinical Consult) In Domino,F.Editor,Baldor,R.Golding,J. Editor& Grimes,J. Editor (22nd ed. (pp. 912-913). Lippinincott Williams & Wilkins.