Peptic Ulcer Disease

Alex john

Anatomy and Physiology

of GI Tract

Peptic Ulcer Disease (PUD)

Definition
Peptic ulcer
refers to erosion of the mucosa lining any portion of the
G.I. tract.
It is

defined

as

circumscribed

ulceration

of

the

gastrointestinal mucosa occurring in areas exposed to acid and

pepsin and most often caused by Helicobacter pylori infection.
(Uphold & Graham, 2003)

gastric ulcer : the ulcer that occurs in the stomach

lining ,some of them may be malignant

Peptic Ulcer Disease

Stomach Defense Systems

Mucous layer

Bicarbonate

Coats and lines the stomach

First line of defense
Neutralizes acid

Prostaglandins

Hormone-like substances that keep blood

vessels dilated for good blood flow
Thought to stimulate mucus and bicarbonate
production

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

Genetic factors

Duodenal: are
increasing in older
women
More likely if family
member has Hx

Other factors: stress

can worsen but not
the cause

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

Gastric and Duodenal

Ulcers

Duodenal Ulcers

Pain occurs 2-4 hours after

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

Duodenal Ulcer Vs. Gastric Ulce

duodenal

sites

are

common as gastric sites

4x

as common in late middle age.

incidence increases with age.

most common in middle age with Male to female ratio2:1

peak 30-50 years
Male to female ratio4:1

More common with bl. group

A

Genetic link: 3x more common in Use of NSAIDs: associated

1st degree relatives

with

three-

to

four-fold

more common with blood group increase in risk of gastric ulcer

O

Less related to H. pylori than

associated with increased serum duodenal ulcers : about 80%

pepsinogen

10 - 20% of patients with a

H. pylori infection common,up to gastric

95%

ulcer

have

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

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

Complications of Peptic
Ulcers

Hemorrhage

Perforation

Blood vessels damaged as ulcer erodes into the

muscles of stomach or duodenal wall
Coffee ground vomitus or occult blood in tarry stools
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

Diagnostic Tests

Esophagogastrodeuodenoscopy (EGD)

Endoscopic procedure

Upper gastrointestinal series (UGI)

Visualizes ulcer crater

Ability to take tissue biopsy to R/O cancer and
diagnose H. pylori
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

Drug Therapy/Primary
Goals

Provide pain relief

Eradicate H. pylori infection

Two antibiotics and one acid suppressor

Heal ulcer

Antacids and mucosa protectors

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

Hyposecretory Drugs

Proton Pump Inhibitors

Suppress acid production

Prilosec, Prevacid

Prostaglandin
Analogs

H2-Receptor Antagonists

Block histaminestimulated gastric

secretions
Zantac, Pepcid, Axid

Antacids

Neutralizes acid and

prevents formation of
pepsin (Maalox, Mylanta)
Give 2 hours after meals
and at bedtime

Reduce gastric acid

and enhances
mucosal resistance to
injury
Cytotec

Mucosal barrier
fortifiers

Forms a protective
coat

Carafate/Sucralfate

cytoprotective

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

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

Types of Surgical
Procedures

Vagotomy

Cuts vagus nerve

Eliminates acidsecretion stimulus

Surgical
Procedure/Pyloroplasty

Pyloroplasty

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

Types of Surgical
Procedures

Antrectomy/ Subtotal Gastrectomy

Subtotal gastrectomy

Lower half of stomach (antrum) makes most

of the acid
Removing this portion (antrectomy)
decreases acid production
Removes to 2/3 of stomach

Remainder must be reattached to the

rest of the bowel

Billroth I
Billroth II

Billroth I

Distal portion of
the stomach is
removed
The remainder is
anastomosed to
the duodenum

Billroth II

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

Postoperative Care

NG tube care and management

Monitor for post-operative
complications

Post-op Complications

Bleeding

Occurs at the anastomosed

site
First 24 hours and post-op
days 4-7

Billroth II
Severe abdominal pain
Bile stained drainage on
dressing

Gastric retention

WILL NEED TO PUT NG

TUBE BACK IN

Dumping Syndrome (page

1303)

Duodenal stump leak

Anemia

Prevalent with sub total

gastrectomies
Early-30 minutes after meals
Vertigo, tachycardia,
syncope, sweating, pallor,
palpatations
Late 90 min-3 hours after
meals
Rapid gastric empyting
decreases absorption of iron

Malabsorption of fat

Decreased acid secretions,

decreased pancreatic
secretions, increased upper
GI mobility

Dumping Syndrome

Rapid emptying of food and fluids from

the stomach into the jejunum
Symptoms

Weakness
Faintness
Palpatations
Fullness
Discomfort
Nausea
diarrhea

Minimize Dumping
Syndrome

Decrease CHO intake

Eat slowly
Avoid fluids during meals
Increase fat
Eat small, frequent meals

Peptic Ulcer Disease

Nursing Management

Overall Goals (cont.)

Exhibits no signs of GI complications

Have complete healing
Lifestyle changes to prevent
recurrence

Peptic Ulcer Disease

Nursing Implementation

Health Promotion

Identify patients at risk

Early detection and morbidity
Encourage patients to take
ulcerogenic drugs with food or milk
Teach patients to report symptoms
related to gastric irritation to health
care provider

Peptic Ulcer Disease

Nursing Implementation

Acute Intervention

Patient generally complains of pain,

nausea, vomiting, and some bleeding
May be maintained on NPO status for
a few days, have NG tube inserted,
fluids replaced intravenously
Physical and emotional rest are
conducive to ulcer healing

Peptic Ulcer Disease

Nursing Implementation

Hemorrhage

Changes in vital signs, in amount

and redness of aspirate signal
massive upper GI bleeding
amount of blood in gastric contents
pain because blood helps neutralize
acidic gastric contents
Keep blood clots from obstructing NG
tube

Peptic Ulcer Disease

Nursing Implementation

Perforation

Sudden, severe abdominal pain

unrelated in intensity and location to
pain that brought patient to hospital

Peptic Ulcer Disease

Nursing Implementation

Perforation (cont.)

Indicated by a rigid, boardlike

abdomen
Severe generalized abdominal and
shoulder pain
Shallow, grunting respirations

Peptic Ulcer Disease

Nursing Implementation

Perforation (cont.)

Ensure any known allergies are

reported on chart

Antibiotic therapy is usually started

Surgical closure may be necessary if

perforation does not heal
spontaneously