peptic ulcer disease

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Peptic Ulcer Disease Carol Lynn Pence RN, MSN

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Page 1: Peptic ulcer disease

Peptic Ulcer Disease

Carol Lynn Pence RN, MSN

Page 2: Peptic ulcer disease

Anatomy and Physiology of GI Tract

Page 3: Peptic ulcer disease

Peptic Ulcers

Defined Ulcerated lesion in the mucosa of the

stomach or duodenum Types

Gastric Duodenal

Page 4: Peptic ulcer disease

Peptic Ulcer Disease

Page 5: Peptic ulcer disease

Stomach Defense Systems Mucous layer

Coats and lines the stomach First line of defense

Bicarbonate Neutralizes acid

Prostaglandins Hormone-like substances that keep blood

vessels dilated for good blood flow Thought to stimulate mucus and

bicarbonate production

Page 6: Peptic ulcer disease

Risk Factors Lifestyle

Smoking Acidic drinks Medications

H. Pylori infection 90% have this

bacterium Passed from person to

person (fecal-oral route or oral-oral route)

Age Duodenal 30-50 Gastric over 60

Gender Duodenal: are

increasing in older women

Genetic factors More likely if family

member has Hx Other factors: stress

can worsen but not the cause

Page 7: Peptic ulcer disease

Gastric Ulcers

Pain occurs 1-2 hours after meals Pain usually does not wake patient Accentuated by ingestion of food Risk for malignancy Deep and penetrating and usually

occur on the lesser curvature of the stomach

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Gastric and Duodenal Ulcers

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Duodenal Ulcers

Pain occurs 2-4 hours after meals

Pain wakes up patient Pain relieved by food Very little risk for malignancy

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General Peptic Ulcer Symptoms

Epigastric tenderness Gastric: epigastrium; left of midline Duodenal: mid to right of

epigastrium Sharp, burning, aching, gnawing pain Dyspepsia (indigestion) Nausea/vomiting Belching

Page 11: Peptic ulcer disease

Complications of Peptic Ulcers Hemorrhage

Blood vessels damaged as ulcer erodes into the muscles of stomach or duodenal wall

Coffee ground vomitus or occult blood in tarry stools Perforation

An ulcer can erode through the entire wall Bacteria and partially digested fool spill into

peritoneum=peritonitis Narrowing and obstruction (pyloric)

Swelling and scarring can cause obstruction of food leaving stomach=repeated vomiting

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Diagnostic Tests Esophagogastrodeuodenoscopy (EGD)

Endoscopic procedure Visualizes ulcer crater Ability to take tissue biopsy to R/O cancer and

diagnose H. pylori Upper gastrointestinal series (UGI)

Barium swallow X-ray that visualizes structures of the upper GI

tract Urea Breath Testing

Used to detect H.pylori Client drinks a carbon-enriched urea solution Excreted carbon dioxide is then measured

Page 13: Peptic ulcer disease

Etiology and Genetic Risk PUD primarily associated with NSAID

use and infection with H. Pylori Certain drugs may contribute to cause:

Theo-Dur Caffeine – stimulates hydrochloric acid

production Corticosterioids – associated with an

increased incidence of PUD Genetic factors

Page 14: Peptic ulcer disease

Drug Therapy/Primary Goals Provide pain relief

Antacids and mucosa protectors Eradicate H. pylori infection

Two antibiotics and one acid suppressor Heal ulcer

Eradicate infection Protect until ulcer heals

Prevent recurrence Decrease high acid stimulating foods in susceptible

people Avoid use of potential ulcer causing drugs Stop smoking

Page 15: Peptic ulcer disease

Hyposecretory Drugs Proton Pump Inhibitors

Suppress acid production Prilosec, Prevacid

H2-Receptor Antagonists Block histamine-

stimulated gastric secretions

Zantac, Pepcid, Axid Antacids

Neutralizes acid and prevents formation of pepsin (Maalox, Mylanta)

Give 2 hours after meals and at bedtime

Prostaglandin Analogs

Reduce gastric acid and enhances mucosal resistance to injury

Cytotec Mucosal barrier

fortifiers Forms a protective

coat Carafate/Sucralfate

cytoprotective

Page 16: Peptic ulcer disease

Surgery Greatly decreased in the last 20-30 years

secondary to the discovery of H. pylori Required if ulcer in one of these states

Perforated and overflowed into the abdomen Scarred or swelled so that there is obstruction Acute bleeding Non-responsive to medications

Page 17: Peptic ulcer disease

Types of Surgical Procedures Gastroenterostomy

allows regurgitation of alkaline duodenal contents into the stomach

Creates a passage between the body of stomach to small intestines

Keeps acid away from ulcerated area

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Types of Surgical Procedures Vagotomy

Cuts vagus nerve Eliminates acid-

secretion stimulus

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Surgical Procedure/Pyloroplasty Pyloroplasty

Widens the pylorus to guarantee stomach emptying even without vagus nerve stimulation

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Types of Surgical Procedures Antrectomy/ Subtotal Gastrectomy

Lower half of stomach (antrum) makes most of the acid

Removing this portion (antrectomy) decreases acid production

Subtotal gastrectomy Removes ½ to 2/3 of stomach

Remainder must be reattached to the rest of the bowel Billroth I Billroth II

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Billroth I Distal portion of

the stomach is removed

The remainder is anastomosed to the duodenum

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Billroth II The lower

portion of the stomach is removed and the remainder is anastomosed to the jejunum

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Postoperative Care

NG tube – care and management Monitor for post-operative

complications

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Post-op Complications Bleeding

Occurs at the anastomosed site

First 24 hours and post-op days 4-7

Duodenal stump leak Billroth II Severe abdominal pain Bile stained drainage on

dressing Gastric retention

WILL NEED TO PUT NG TUBE BACK IN

Dumping Syndrome (page 1303)

Prevalent with sub total gastrectomies

Early-30 minutes after meals

Vertigo, tachycardia, syncope, sweating, pallor, palpatations

Late – 90 min-3 hours after meals

Anemia Rapid gastric empyting

decreases absorption of iron Malabsorption of fat

Decreased acid secretions, decreased pancreatic secretions, increased upper GI mobility

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Dumping Syndrome Rapid emptying of food and fluids from

the stomach into the jejunum Symptoms

Weakness Faintness Palpatations Fullness Discomfort Nausea diarrhea

Page 26: Peptic ulcer disease

Minimize Dumping Syndrome

Decrease CHO intake Eat slowly Avoid fluids during meals Increase fat Eat small, frequent meals