I.

INTRODUCTION
Peptic ulcer disease (PUD) is a common disorder that affects
millions of individuals in the United States each year. PUD has a
major impact on our health care system by accounting for roughly
10% of medical costs for digestive diseases. In the last two decades,
major advances have been made in the understanding of the
pathophysiology of PUD, particularly regarding the role of
Helicobacter pylori infection and nonsteroidal anti-inflammatory
drugs (NSAIDs). This has led to important changes in diagnostic and
treatment strategies, with the potential for improving the clinical
outcome and for decreasing health care costs.

Peptic ulcers are defects in the gastric or duodenal mucosa

that extend through the muscularis mucosa. H pylori infection and
NSAID use are the most common etiologic factors. Other less
common causes are hypersecretory states, such as Zollinger-Ellison
syndrome, G-cell hyperplasia, mastocytosis, and basophilic
leukemias.

Under normal conditions, a physiologic balance exists between

peptic acid secretion and gastroduodenal mucosal defense. Mucosal
injury and, thus, peptic ulcer occur when the balance between the
aggressive factors and the defensive mechanisms is disrupted.
Aggressive factors, such as NSAIDs, H pylori, alcohol, bile salts,
acid, and pepsin, can alter the mucosal defense by allowing back
diffusion of hydrogen ions and subsequent epithelial cell injury. The
defensive mechanisms include tight intercellular junctions, mucus,
mucosal blood flow, cellular restitution, and epithelial renewal.

II. BIOGRAPHICAL DATA

Name : Angelita Franko

Bed Number : FCW # 01

Hospital Number : 010101

Sex : Female

Age : 46 years old

Date of Birth : September 01, 1964

Birthplace : Danglas, La Paz Abra

Address : Danglas, La Paz Abra

Citizenship : Filipino

Religion : Christian

Status : Married

Occupation : none

III. MEDICAL HISTORY

HISTORY OF PRESENT ILLNESS

Patient has been having on and off epigastric pain for about a year

which was not associated with food intake.

One and a half month prior to admission, patient had recurrence of

epigastric pain, 6-7/10 in severity. She experienced loss of appetite, diarrhea

and a feeling of fullness in upper abdomen after eating. She then sought

consult with a medical doctor.

PAST HEALTH HISTORY

On her early childhood, she had chickenpox and measles. When she

had a fever, her mother wiped her whole body to relieve the heat. She

sometimes had headache and diarrhea but she will just take a medicine for

it. At the age of 18, she had felt pain at her epigastric area and her parents

brought her to the hospital for a checkup. She had a diagnosis of an acute
gastritis. She remembers that, she felt so tired at that time. She does not

have any allergies to foods or drugs.

VI. REVIEW OF SYSTEMS

HEENT:

• No complaints of headache change in vision, nose or ear Separate

each ROS section for easy identification
• problems, or sore throat.

Cadiovascular:

• No complaints of cardiovascular disease.

Gastrointestinal:

• No complaints of dysphagia, nausea, vomiting, or change in stool

pattern, consistency, or color. She complains of phrases or sentences
• epigastric pain, burning in quality, approximately twice a month, which
she notices primarily at night.

Genitourinary:

• No complaints of dysuria, nocturia, polyuria, hematuria, or vaginal

bleeding.

Musculoskeletal:

• She complains of lower back pain, aching in quality approximately

once every week after working in her garden.
• This pain is usually relieved with Tylenol. She complains of no other
arthralgias, muscle aches, or pains.

Neurological:

• She complains of no weakness, numbness, or incoordination.

VII. Pathophysiology and Schematic Diagram

The stomach's lining has a protective layer of cells that

produce mucus. The mucus prevents the stomach from being injured
by stomach acids and digestive juices. When this protective layer is
damaged, it cannot secrete enough mucus to act as a barrier
against HCl, thus an ulcer may occur. Peptic ulcers occur mainly in
the gastroduodenal mucosa because this tissue cannot withstand
the digestive action of gastric acid (HCl) and pepsin. Normally, when
the mucosa is damaged, the defensive forces will respond.
Stomach ulcers may develop from: the presence of bacteria called
Helicobacter pylori (H. pylori), the most common cause of stomach
ulcers; decreased resistance of the lining of the stomach to stomach
acid and increased production of stomach acid.
Stomach ulcers are more likely to occur in people who:
regularly take nonsteroidal anti-inflammatory drugs (NSAIDS), such
as aspirin, ibuprofen, and naproxen; smoke cigarettes and intake of
excessive alcohol. In addition, substances that increase the
production of stomach acids, such as caffeine, may increase the risk
of ulcers and are known to worsen the pain.
Usually, the ulceration is preceded by shock; this leads to decreased
gastric mucosal blood flow and to reflux of duodenal contents into
the stomach. In addition, large quantities of pepsin are released.
The combination of ischemia, acid, and pepsin creates an ideal
climate for ulceration.

IX. MEDICAL & SURGICAL MANAGEMENT

Medical Care
• Given the current understanding of the pathogenesis of PUD, most
patients with PUD are treated successfully with cure of H pylori
infection and/or avoidance of NSAIDs, along with the appropriate use of
antisecretory therapy.
• A number of treatment options exist for patients presenting with
symptoms suggestive of PUD or ulcerlike dyspepsia, including empiric
antisecretory therapy, empiric triple therapy for H pylori infection,
endoscopy followed by appropriate therapy based on findings, and H
pylori serology followed by triple therapy for patients who are infected.
Breath testing for active H pylori infection may be used.
• Computer models have suggested that obtaining H pylori serology
followed by triple therapy for patients who are infected is the most
cost-effective approach; however, no direct evidence from clinical trials
provides confirmation.
• Perform endoscopy early in patients older than 45-50 years and in
patients with associated so-called alarm symptoms, such as dysphagia,
recurrent vomiting, weight loss, or bleeding.
Surgical Care
With the success of medical therapy, surgery has a very limited role in the
management of PUD.
• Potential indications for surgery include refractory disease.
Complications of PUD include the following:
○ Refractory, symptomatic peptic ulcers, though rare with the cure
of H pylori infection and the appropriate use of antisecretory
therapy, are a potential complication of PUD.
○ Perforation usually is managed emergently with surgical repair.
However, this is not mandatory for all patients.
○ Obstruction can complicate PUD, particularly if PUD is refractory
to aggressive antisecretory therapy, H pylori eradication, or
avoidance of NSAIDs. Obstruction may persist or recur despite
endoscopic balloon dilation.
○ Penetration, particularly if not walled off or if a gastrocolic fistula
develops, is a potential complication of PUD.
○ Bleeding can complicate PUD, particularly in patients with
massive hemorrhage and hemodynamic instability, recurrent
 bleeding on medical therapy, and failure of therapeutic
endoscopy to control bleeding.
• The appropriate surgical procedure depends on the location and nature
of the ulcer.
○ Many authorities recommend simple oversewing of the ulcer with
treatment of the underlying H pylori infection or cessation of
NSAIDs for bleeding PUD.
○ Additional surgical options for refractory or complicated PUD
include vagotomy and pyloroplasty, vagotomy and antrectomy
with gastroduodenal reconstruction (Billroth I) or gastrojejunal
reconstruction (Billroth II), or a highly selective vagotomy.

X. LIST OF POSSIBLE NURSING DIAGNOSES

1. Increased risk of GI bleeding and perforation of stomach,
related to gastric or intestinal wall erosion.

2. Increased risk of pyloric obstruction related to complication of

the peptic ulcer.

3. Increased risk of anemia due to acute or chronic GI bleeding,

related to ulcer.

4. Pain and heartburn, related to diagnosis of peptic ulcer.

5. Appetite changes and weight changes due to symptoms of the

ulcer.

6. Increased risk of aspiration due to vomiting, related to ulcer.

7. Anxiety related to the symptoms of disease and fear of the

unknown.

8. Deficient fluid volume, related to acute bleeding duodenal

ulcer

9. Risk for injury, related to acute blood loss

10. Fear, related to threat to well-being

XII. DISCHARGE PLAN

The discharge plan for this case were directed toward

resulting the patient’s individual needs for knowledge of self-care

and health maintenance activities. I, as a student nurse, shared

necessary health teachings to my patient. I discussed to him the

importance of having adequate rest, avoiding stress and having

lifestyle modification like cessation of drinking alcoholic

beverages. I stressed out to him the benefits he could get out

from quitting smoking and the reasons why he needs to do it. I

encouraged him not to forget the medications prescribed by the

physician. I also taught him on what kind of food that he needs to

be avoided, which includes the salty, spicy and acidic food,

because these can stimulate acid secretion.

XIII. RECENT UPDATES

Hospitalization for Upper GI Bleeding

Declines
By Charles Bankhead, Staff Writer, MedPage Today
Published: December 19, 2009
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine.

ROCKVILLE, Md., Dec. 19 -- Hospitalizations for upper gastrointestinal

bleeding declined by 14% from 1998 to 2006, according to a government
report.

Hospital mortality associated with any type of GI bleeding declined by 23%.

The declines probably reflect advances in the treatment of gastroesophageal

reflux disease and other common causes of upper GI bleeding, suggested the
Agency for Healthcare Research and Quality in a Statistical Brief.

Admissions for lower GI bleeding increased slightly during the same period,
said Yafu Zhao, M.S., and William Encinosa, Ph.D., the authors of the report.
The findings came from an analysis of data from the 1998 and 2006
Nationwide Inpatient Sample. The analysis showed that hospitalization
associated with a principal diagnosis of GI bleeding decreased from 189 per
100,000 in 1998 to 182 per 100,000 in 2006, a difference of 3.8%.
Hospitalizations for any diagnosis of GI bleeding decreased from 390 per
100,000 to 375 per 100,000, representing a difference of 3.7%.
Analysis of discharges by site of bleeding showed that the rate for upper GI
bleeding decreased from 96 per 100,000 in 1998 to 82 per 100,000 in 2006.
The difference was attributed in part to a 25% decline in hospitalization for
bleeding related to upper GI ulcers and a 31% decline in hospitalization for
bleeding associated with gastritis/duodenitis.
Upper GI bleeding accounted for the largest proportion of admissions for GI
bleeding, but the share declined from 51% in 1998 to 45% in 2006.
Hospitalizations for lower GI bleeding increased by 2%, from 43/100,000 to
44/100,000. The rate for bleeding by unspecified site increased 11%, from 50
per 100,000 to 56 per 100,000.
GI bleeding-associated hospitalization rates declined across all age groups
except the youngest: the rate increased by 8.6% in patients ages 20 and
younger. The largest decrease (18.4%) occurred in patients 85 and older,
followed by a 7.8% decline among patients ages 65 to 84.
In 2006, those 65 and older accounted for 65% of the hospitalizations for GI
bleeding, those 45 to 64 accounted for 25%, and those younger than 45
accounted for 10%.
The number of hospital deaths attributed to all forms of GI bleeding
decreased from 20,013 in 1998 to 16,344 in 2006. The death rate declined
from 3.9% in 1998 to 3.0% in 2006, a 23% difference.
The inpatient death rate declined for all three groups of the GI bleeding sites.
The death rate in unspecified GI bleeding hospitalizations decreased 28%,
while upper and lower GI bleeding hospitalizations decreased 23% and 17%,
respectively.
The authors cited two countervailing trends as having the greatest impact on
their findings:
• An increased prevalence of obesity, which has a strong association
with GERD. They noted that a previous AHRQ study showed that
hospitalizations for GERD increased by 216% from 1998 to 2005.
• Therapeutic advances that benefited upper GI bleeding the most, such
as eradication of Helicobacter pylori infection, development of more
effective medications for GERD, and increased use of more GI-friendly
medications, such as such as the COX-2 inhibitor class of nonsteroidal
anti-inflammatory drugs.
 Divine Word College of Bangued
Bangued, Abra

NURSING DEPARTMENT

A Case Study on

COMMUNITY-ACQUIRED PNEUMONIA

In Partial Fulfillment to the requirement in NCM

101
(Related Learning Experience)

ABRA PROVINCIAL HOSPITAL

(MEDICAL WARD)

Presented to:
Mr. Roel M. Beljamin, RN,RM,MAN

Presented by:
Demie Caine Q. Dela Vega
SN-II
February 2010