TABLE OF CONTENTS

 Dedication i

 Acknowledgement ii

 Introduction 5-6

 Review of Related Literature 7-18

 Nursing Health History 19-20

 Client Health History 21

 Treatments/ Medications 21

 Past Illness/Hospitalization 21

 Allergies 21

 Developmental History 22

 Nutritional Metabolic Pattern 23

 Elimination Pattern 23

 Activity Exercise Pattern 23

 Sexuality Reproduction Pattern 23

 Sleep-Rest Pattern 23

 Ellimination Pattern 23

 Recreation/Hobbies 23

 Family Relationship 23

 Ethnic Affiliation 24

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  Educational History 24

 Occupational History 24

 Health History 24

 History of Present Illness 24

 Past History 24

 Physical Examination 25

 General Physical Survey 25

 Mental Status Examination 25

 Skin 25

 Head and Face 25

 Eyes 25

 Ears and Nose 26

 Mouth and Throat 26

 Neck 26

 Arms, Hands and Fingers 26

 Thorax & Lungs 27

 Anterior Chest 27

 Breasts (Female) 27

 Heart 27

 Abdomen 27

 Legs, Feet and Toes 28

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  Genitalia (Male) 28

 Musculoskeletal and Neurologic Examination 28

 Cranial Nerve Assessment 29

 Review of System 30

 General Survey 30

 Integumentary System 30

 EENT 30

 Gastrointestinal System 30

 Musculoskeletal System 30

 Neurologic System 30

 Urinary System 30

 Reproductive System 30

 Hematologic 31

 Endocrine 31

 Psychiatric 31

 Laboratory Results 32

 Hematology 32

 Urinalysis 33

 Anatomy and Physiology 34-44

 Pathophysiology 45-47

 Drug Study 48-57

 Nursing Care Plan 58-73

 Discharge Plan 74-76

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 Appendices 77

 IVF Chart 77

 Vital Signs 78

 I and O Sheet 79-80

 CFAC 81

 Genogram 82-83

 References 84

INTRODUCTION

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 Peptic Ulcer

A peptic ulcer may be referred to as a gastric, duodenal, or esophageal ulcer, depending

on its location. A person who has a peptic ulcer has peptic ulcer disease. A peptic ulcer is an excavation
(hollowed-out area) that forms in the mucosal wall of the stomach, in the pylorus (the opening between
the stomach and duodenum), or in the esophagus. Erosion of a circumscribed area of mucous membrane
is the cause. This erosion may extend as deeply as the muscle layers or through the muscle to the
peritoneum.
Peptic ulcers are more likely to be in the duodenum than in the stomach. As a rule they
occur alone, but they may occur in multiples. Chronic gastric ulcers tend to occur in the lesser curvature
of the stomach, near the pylorus. Esophageal ulcers occur as a result of the backward flow of HCl from
the stomach into the esophagus ( gastroesophageal reflux disease [GERD] ).

Peptic ulcer disease occurs with the greatest frequency in people between 40 and 60 years of
age. It is relatively uncommon in women of childbearing age, but it has been observed in children and
even in infants. After menopause, the incidence of peptic ulcers in women is almost equal to that in men.
Peptic ulcers in the body of the stomach can occur without excessive acid secretion.

In the past, stress and anxiety were thought to be causes of ulcers, but research has
documented that peptic ulcers result from infection with the gram-negative bacteria H. pylori, which may
be acquired through ingestion of food and water. Person-to-person transmission of the bacteria also
occurs through close contact and exposure to emesis. It is not known why H. pylori infection does not

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cause ulcers in all people, but most likely the predisposition to ulcer formation depends on certain factors,
such as the type of H. pylori and other as yet unknown factors (Moss & Sood, 2003).
In addition, excessive secretion of HCl in the stomach may contribute to the formation of
peptic ulcers, and stress may be associated with its increased secretion. The ingestion of milk and
caffeinated beverages, smoking, and alcohol also may increase HCl secretion. Stress and eating spicy
foods may make peptic ulcers worse.
Familial tendency also may be a significant predisposing factor. People with blood type
O are more susceptible to peptic ulcers than are those with blood type A,B, or AB; this is another genetic
link. There also is an association between peptic ulcers and chronic pulmonary disease or chronic renal
disease. Other predisposing factors associated with peptic ulcer include chronic use of NSAIDs, alcohol
ingestion, and excessive smoking.

Peptic ulcers are found in rare cases in patients with tumors that cause secretion of excessive
amounts of the hormone gastrin. The Zollinger-Ellison syndrome (ZES) consists of severe peptic ulcers,
extreme gastric hyperacidity, and gastrin-secreting benign or malignant tumors of the pancreas.

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 REVIEW OF RELATED LITERATURE

Too much stress, too much spicy food, and you may be headed for an ulcer or so the
thinking used to go.

A peptic ulcer is an ulcer of one of those areas of the gastrointestinal tract that are usually
acidic. A more general term, peptic ulcer disease (PUD), is also in use. Most ulcers are
associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic
environment of the stomach. Ulcers can also be caused or worsened by drugs such as Aspirin and
other NSAIDs. Contrary to general belief, more peptic ulcers arise in the duodenum (first part of
the small intestine, just after the stomach) than in the stomach. About 4 % of stomach ulcers are
caused by a malignant tumour, so multiple biopsies are needed to make sure. Duodenal ulcers are
generally benign.

The common belief was that peptic ulcers were a result of lifestyle. Doctors now know
that a bacterial infection or medications — not stress or diet — cause most ulcers of the stomach
and upper part of the small intestine (duodenum). Esophageal ulcers may also occur and are
typically associated with the reflux of stomach acid.

Although stress and spicy foods were once thought to be the main causes of peptic ulcers,
doctors now know that many ulcers are caused by the corkscrew-shaped bacterium Helicobacter
pylori (H. pylori).

H. pylori lives and multiplies within the mucous layer that covers and protects tissues that
line the stomach and small intestine. Often, H. pylori causes no problems. But sometimes it can
disrupt the mucous layer and inflame and erode digestive tissues, producing an ulcer. One reason
may be that people who develop peptic ulcers already have damage to the lining of the stomach
or small intestine, making it easier for bacteria to invade and inflame tissues.

The most common ulcer symptom is gnawing or burning pain in the abdomen between
the breastbone and the belly button. The pain often occurs when the stomach is empty, between
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meals and in the early morning hours, but it can occur at any other time. It may last from minutes

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to hours and may be relieved by eating food or taking antacids. Less common symptoms include
nausea, vomiting, or loss of appetite. Sometimes ulcers bleed. If bleeding continues for a long
time, it may lead to anemia with weakness and fatigue. If bleeding is heavy, blood may appear in
vomit or bowel movements, which may appear dark red or black.

SIGN AND SYMPTOMS

Most patients with peptic ulcer disease present with abdominal discomfort, pain or nausea. The
pain is located in the epigastrium and usually does not radiate. However, these symptoms are neither
sensitive nor specific. Pain radiating to the back may suggest that an ulcer has penetrated posteriorly, or
the pain may be pancreatic in origin. Pain radiating to the right upper quadrant may suggest disease of the
gallbladder or bile ducts. Patients may describe the pain of peptic ulcer as burning or gnawing, or as
hunger pains slowly building up for 1–2 hours, then gradually decreasing. Use of antacids may provide
temporary relief. Classically, gastric ulcer pain is aggravated by meals, whereas the pain of duodenal
ulcers is relieved by meals. Hence, patients with gastric ulcers tend to avoid food and present with weight
loss, while those with duodenal ulcers do not lose weight. It is important to remember that although these
patterns are typical, they are not pathognomonic. The nature of the presenting symptoms alone does not
permit a clear differentiation between benign ulcers and gastric neoplasm.

Peptic ulcers are open sores that develop on the inside lining of your stomach and the upper
portion of your small intestine. The most common symptom of a peptic ulcer is stomach pain. Peptic
ulcers include gastric ulcers that occur on the inside of the stomach, Duodenal ulcers that occur on the
inside of the upper portion of your small intestine (duodenum)

The most common peptic ulcer symptom is burning stomach pain. Stomach acid makes the pain
worse, as does having an empty stomach. The pain can often be relieved by eating certain foods that
buffer stomach acid or by taking an acid-reducing medication, but then it may come back. The pain may
be worse between meals and at night.

Nearly three-quarters of people with peptic ulcers don't have symptoms. Less often, ulcers may
cause severe signs or symptoms such as, Vomiting or vomiting blood — which may appear red or black,
dark blood in stools, or stools that are black or tarry, trouble breathing, feeling faint, nausea or vomiting,
unexplained weight loss, appetite changes.

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Causes

The most common causes of peptic ulcers are infection with the bacterium Helicobacter pylori
(H. pylori) and long-term use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) (Advil,
Aleve, others). Stress and spicy foods do not cause peptic ulcers. However, they can make your
symptoms worse.

Peptic ulcers occur when acid in the digestive tract eats away at the inner surface of the stomach
or small intestine. The acid can create a painful open sore that may bleed. Your digestive tract is coated
with a mucous layer that normally protects against acid. But if the amount of acid is increased or the
amount of mucus is decreased, you could develop an ulcer. Common causes include, A bacterium,
Helicobacter pylori bacteria commonly live in the mucous layer that covers and protects tissues that line
the stomach and small intestine. Often, the H. pylori bacterium causes no problems, but it can cause
inflammation of the stomach's inner layer, producing an ulcer. It's not clear how H. pylori infection
spreads. It may be transmitted from person to person by close contact, such as kissing. People may also
contract H. pylori through food and water.

Regular use of certain pain relievers. Taking aspirin, as well as certain over-the-counter and
prescription pain medications called nonsteroidal anti-inflammatory drugs (NSAIDs) can irritate or
inflame the lining of your stomach and small intestine. These medications include ibuprofen (Advil,
Motrin IB, others), naproxen sodium (Aleve, Anaprox, others), ketoprofen and others. They do not
include acetaminophen (Tylenol). Peptic ulcers are more common in older adults who take these pain
medications frequently or in people who take these medications for osteoarthritis. Other medications.
Taking certain other medications along with NSAIDs, such as steroids, anticoagulants, low-dose aspirin,
selective serotonin reuptake inhibitors (SSRIs), alendronate (Fosamax) and risedronate (Actonel), can
greatly increase the chance of developing ulcers.

“No gastric acid, no peptic ulcer” is a misconception. Excessive gastric acid secretion is only one
factor in the pathogenesis of peptic ulcer disease. Decreased mucosal defense against gastric acid is
another cause. The integrity of the upper gastrointestinal tract is dependent upon the balance between
“hostile” factors such as gastric acid, H. pylori, NSAIDs and pepsin, and “protective” factors such as
prostaglandins, mucus, bicarbonate, and blood flow to mucosa affecting gastrointestinal mucosa. Injury to
gastric and duodenal mucosa develops when deleterious effects of gastric acid overwhelm the defensive
properties of the mucosa. Inhibition of endogenous prostaglandin synthesis leads to a decrease in
epithelial mucus, bicarbonate secretion, mucosal blood flow, epithelial proliferation, and mucosal
resistance to injury. Lower mucosal resistance increases the incidence of injury by endogenous factors

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such as acid, pepsin, and bile salts as well as exogenous factors such as NSAIDs, ethanol and other
noxious agents.

Helicobacter pylori H. pylori is the etiologic factor in most patients with peptic ulcer disease and
may predispose individuals to the development of gastric carcinoma. H. pylori colonizes in the human
stomach (Figure 5). The method of H. pylori transmission is unclear, but seems to be person-to-person
spread via a fecal-oral route. The prevalence of H. pylori in adults appears to be inversely related to the
socioeconomic status. It is also thought that water is a reservoir for transmission of H. pylori.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDS) A small but important percentage of patients

have adverse gastrointestinal events associated with NSAID use that results in substantial morbidity and
mortality. Risk factors for the development of NSAID-associated gastric and duodenal ulcers include
advanced age, history of previous ulcer disease, concomitant use of corticosteroids and anticoagulants,
higher doses of NSAIDs, and serious systemic disorders. The concept of gastroduodenal mucosal injury
has evolved from the notion of topical injury to concepts that involve multiple mechanisms. NSAIDs
initiate mucosal injury topically by their acidic properties. By diminishing the hydrophobicity of gastric
mucus, endogenous gastric acid and pepsin may injure surface epithelium. Systemic effects of NSAIDs
appear to play a predominant role through the decreased synthesis of mucosal prostaglandins. The
precursor of prostaglandins, arachidonic acid, is catalyzed by the two cyclo-oxygenase isoenzymes,
cyclo-oxygenase-1 and cyclo-oxygenase-2. The gene for cyclo-oxygenase-1, the housekeeping enzyme,
maintains the homeostasis of organs. Cyclo-oxygenase-2, the inflammatory enzyme, is inducible.
Although NSAIDs can inhibit both pathways, only the gene for cyclo-oxygenase-2 contains a
corticosteroid-responsive repressor element. Literature suggests that the anti-inflammatory properties of
NSAIDs are mediated through inhibition of cyclo-oxgenase-2, and adverse effects, such as gastric and
duodenal ulceration, occur as a result of effects on the constitutively expressed cyclo-oxygenase.

Hypercalcemia has a direct bearing on the gastric acid hypersecretory state found in patients with
Zollinger-Ellison syndrome and MEN I. Intravenous calcium infusion in normal volunteers induces
gastric acid hypersecretion. Additionally, calcium has been demonstrated in vivo and in vitro to stimulate
gastrin release directly from gastrinomas. Resolution of hypercalcemia (by parathyroidectomy) reduces
the basal acid output and serum gastrin concentration in fasting gastrinoma patients and those with MEN
I, suggesting that resolution of hypercalcemia plays an important role in the therapy of this subgroup of
patients.

Genetic factors play a role in the pathogenesis of ulcer disease. The lifetime prevalence of
developing ulcer disease in first-degree relatives of ulcer patients is about three times greater than the

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general population. Approximately 20–50% of duodenal ulcer patients report a positive family history;
gastric ulcer patients also report clusters of family members who are likewise affected.

The literature reveals a strong positive correlation between cigarette smoking and the incidence of
ulcer disease, mortality, complications, recurrences and delay in healing rates. Smokers are about two
times more likely to develop ulcer disease than nonsmokers. Cigarette smoking and H. pylori are co-
factors for the formation of peptic ulcer disease. There is a strong association between H. pylori infection
and cigarette smoking in patients with and without peptic ulcers. Cigarette smoking may increase
susceptibility, diminish the gastric mucosal defensive factors, or may provide a more favorable milieu for
H. pylori infection

Stress Numerous studies have revealed conflicting conclusions regarding the role of
psychological factors in the pathogenesis and natural history of peptic ulcer disease. The role of
psychological factors is far from established. Acute stress results in increases in pulse rate, blood pressure
and anxiety, but only in those patients with duodenal ulcers did acute stress actually result in significant
increases in basal acid secretion. There is no clearly established “ulcer-type” personality. Ulcer patients
typically exhibit the same psychological makeup as the general population, but they appear to perceive
greater degrees of stress. In addition, there is no evidence that distinct occupational factors influence the
incidence of ulcer disease.

Although alcohol has been shown to induce damage to the gastric mucosa in animals, it seems to
be related to the absolute ethanol administered (200 proof). Pure ethanol is lipid soluble and results in
frank, acute mucosal damage. Because most humans do not drink absolute ethanol, it is unlikely there is
mucosal injury at ethanol concentrations of less than 10% (20 proof). Ethanol at low concentrations (5%)
may modestly stimulate gastric acid secretions; higher concentrations diminish acid secretion. Though
physiologically interesting, this has no direct link to ulcerogenesis or therapy. Some types of food and
beverages are reported to cause dyspepsia. There is no convincing evidence that indicates any specific
diet causes ulcer disease. Epidemiologic studies have failed to reveal a correlation between caffeinated,
decaffeinated, or cola-type beverages, beer, or milk with an increased risk of ulcer disease. Dietary
alteration, other than avoidance of pain-causing foods, is unnecessary in ulcer patients.

Etiology

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 Peptic ulcer disease (PUD) has various causes however Helicobacter pyloriassociated PUD and
NSAIDassociated PUD account for the majority of the disease etiology.

Causes of Peptic Ulcer Disease Common

H. pylori infection, NSAIDs, Medications. Rare, ZollingerEllison syndrome,

Malignancy (gastric/lung cancer, lymphomas) Stress (Acute illness, burns, head injury) Viral infection,
Vascular insufficiency, Radiation therapy Crohn disease, Chemotherapy

Helicobacter PyloriAssociated PUD

H. pylorus is a gramnegative bacillus that is found within the gastric epithelial cells. This
bacterium is responsible for 90% of duodenal ulcers and 70% to 90% of gastric ulcers. H. pylori
infection is more prevalent among those with a lower socioeconomic status and is commonly
acquired during childhood. The organism has a wide spectrum of virulence factors allowing it to
adhere to and inflame the gastric mucosa. This results in hypochlorhydria or achlorhydria leading
to gastric ulceration. For many years, excess acid was believed to be the major cause of ulcer disease.
Accordingly, the emphasis of treatment was on neutralizing and inhibiting the secretion of stomach acid.
While acid is still considered necessary for the formation of ulcers and its suppression is still the primary
treatment, the two most important initiating causes of ulcers are infection of the stomach by a bacterium
named "Helicobacter pylori" (H. pylori) and chronic use of nonsteroidal anti-inflammatory medications or
NSAIDs, including aspirin. Cigarette smoking also is an important cause of ulcers as well as failure of
ulcer healing.

Infection with H. pylori is very common, affecting more than a billion people worldwide. It is
estimated that half of the United States population older than age 60 has been infected with H. pylori.
Infection usually persists for many years, leading to ulcer disease in 10% to 15% of those infected. In the
past, H. pylori was found in more than 80% of patients with gastric and duodenal ulcers. With increasing
appreciation, diagnosis and treatment of this infection, the prevalence of infection with H. pylori as well
as the proportion of ulcers caused by the bacterium has decreased. It is estimated that currently only 20%
of ulcers are associated with the bacterium. While the mechanism by which H. pylori causes ulcers is
complex, elimination of the bacterium by antibiotics has clearly been shown to heal ulcers and prevent
their recurrence.

Along with these causes there are 2 other major risk factors for Peptic ulcers. These factors are
H. pylori and the use of non-steroidal anti-inflammatory drugs (NSAIDs).

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 H. pylori is a gram-negative bacteria attached to gastric epithelial cells living within the gastric
mucous layer. Transmission of the organism is most likely from person to person, either through oral or
fecal contamination. Although the mechanism by which H. pylori leads to ulcers is not fully understood,
scientists believe an infection may cause malfunction of acid secretion. They also believe the bacteria
may cause chronic inflammation of the GI tract, resulting in weakening mucosa and allowing acid to form
an ulcer in the mucosal lining. It is estimated that 92% of duodenal ulcers and 70% of gastric ulcers are
caused by H. pylori. Even though H. pylori is a factor in a considerable number of cases, only 15% to
20% of individuals infected with H. pylori develop PUD in their lifetime.9 A study done from 1998 to
2005 showed a significant decline of the overall rate for H. pylori diagnosis. This suggests that a decrease
in H. pylori infections may be partially responsible for the decrease in PUD hospitalizations.

NSAIDs, short for non-steroidal anti-inflammatory drugs, are medicines that reduce pain, fever,
and inflammation. NSAIDs offer many benefits, however, people who regularly take these medicines are
5 times more likely to develop PUD than people who do not take them. Cyclooxygenase-1 (COX-1) and
cyclooxygenase-2 (COX-2) are enzymes that produce prostaglandins, which promote pain, inflammation,
and fever. NSAIDs work by inhibiting these two enzymes. These medications often cause ulcers because
COX-1 produces an additional type of prostaglandin that protects the stomach lining from stomach acid.
By inhibiting COX-1, NSAIDs increase the risk of ulcers and GI bleeding by making the mucosal cells
more vulnerable to hydrochloric acid and pepsin damage. The elderly population often suffers from
musculoskeletal and joint disorders, which are commonly treated with NSAIDs. This explains why
peptic ulcer bleeding is most common in adults > 65 years of age. Low-dose aspirin is also a cause of
drug-induced peptic ulcer bleeding. Aspirin is used for the prevention of cardiovascular incidents. With
the continuing rise of coronary and cerebrovascular diseases, the number of low-dose aspirin users may
also increase, leading to more cases of PUD. Lifestyle factors such as consumption of tobacco, alcohol,
tea, coffee, and spicy foods are believed to stimulate gastric acid secretion, however, findings of
epidemiological studies have been inconsistent.

A Japanese study revealed that smokers were at higher risk of gastric and duodenal ulcers,
compared to non-smokers. Yet, another study failed to confirm the association between PUD and use of
tobacco. The inconsistent results from studies performed on the effect of lifestyle factors with PUD
leads the evidence to be inconclusive. Although emotional stress is no longer though to be a cause of
PUD, Physical stress may increase the risk of developing complications. People with injuries such as
severe burns, spinal injuries, brain damage and people undergoing major surgery often require rigorous
treatment to prevent ulcers from developing as a secondary condition.

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 When assessing a patient, typical symptoms of PUD to watch for include gnawing or burning
gastric pain, pain occurring 2-5 hours after meals or on an empty stomach, and nocturnal pain. Food
intake or antacids may relieve these symptoms. Less common features include indigestion, vomiting, loss
of appetite, intolerance of fatty foods, and heartburn. Emergency Symptoms consist of severe stomach
pain, bloody or black stools and bloody vomit. These deadly symptoms could be signs of bleeding,
hemorrhaging, perforation or obstruction. Anyone younger than 55 years old, diagnosed with PUD,
should be tested for H. pylori. They should also be advised to discontinue the use of NSAIDs, tobacco,
and alcohol. A food recall assessment should focus on the patient’s consumption of food that could
potentially increase gastric acidity or foods that the patient cannot tolerate due to pain or gastric
aggravation. Although routine laboratory tests usually are not helpful in patients with PUD, lab values to
be cognizant of when assessing a patient are CBC (complete blood count), amylase, hemoglobin and
lipase. CBC and hemoglobin can help detect anemia, which mandates early endoscopy to prevent GI
blood loss.

According to the Academy of Nutrition and Dietetics’ Nutrition Care Manual, common
nutritional diagnoses are Food-and nutrition-related knowledge deficit. Inadequate oral intake, Excessive
oral intake, and Undesirable food choices. Other diagnoses frequently accompanied with PUD are
hypertension, acute anemia, iron deficiency, diaphragmatic hernia, and H. pylori infection. ( Elsevier.
Peptic Ulcer Disease. Clinical Key. 2012)

Diagnostic tests

Diagnostic tests typically performed by a gastroenterologist to test for peptic ulcer include upper
gastrointestinal barium x-ray, and endoscopy. Tests to confirm H. pylori infection include gastric biopsy,
urea breath test, H. pylori culture, stool antigen test and a simple blood test.

( Johns Hopkins Medicine. Peptic Ulcer: U.S. News Health. 2009)

Medical Treatment

PUD is primarily treated using medication intervention. Medical treatment for an H. pylori
infection includes 1-2 weeks of antibiotics with an antacid. Other medications such as Proton Pump
Inhibitors, H2 blockers and mucosal protectants are used to treat PUD. A Swedish study conducted from
1974 to 2002 reported that the increase of proton pump inhibitors (PPI) has reduced the incidence of
peptic ulcer complications. Administration of a H2 blocker or PPI for 4 weeks induces healing in most
ulcers. PPIs are recommended as initial therapy for most PUD patients because they suppress acid,

14
increase healing rates and relieve most symptoms. A research trial comparing PPIs with H2 blockers
revealed that after 4 weeks PPIs provided earlier pain control and better healing rates.18 Another study
revealed that PPIs healed duodenal ulcers in more than 95% of patients in 4 weeks and gastric ulcers in
80- 90% of patients in 8 weeks. Based on these results, there is little reason to prescribe PPIs for longer
than 4 weeks for duodenal ulcers or longer than 8 weeks for gastric ulcers, unless ulcers are unresponsive
to initial treatment. Maintenance therapy with H2 blockers or PPIs prevents PUD recurrence in high-risk
patients but is not generally recommended for patients in which H. pylori has been eliminated or who are
taking short-term NSAIDs.

Surgery is rarely performed to treat PUD, due to the effectiveness of anti-ulcer medications like
PPIs, H2 blockers and mucosal protectants. However, some patients do not respond to medication and
may require surgery to treat serious complications such as GI hemorrhage, perforation, or gastric
obstruction. When patients with duodenal ulcers require surgery, it is usually a vagotomy, vagotomy with
antrectomy, or subtotal gastrectomy. Even though the evidence of lifestyle factors on PUD remains
inconclusive, it is recommended to avoid certain habits such as smoking, alcohol use, and the
consumption of high caffeine and spicy foods, in order to achieve optimal health. People who need the

benefits of NSAIDs, and continue taking them may take steps to reduce the risk of ulcer occurrence.
They can do this by taking the NSAID with a meal, using the lowest effective dose possible, and avoid
smoking and alcohol. Patients suffering from painful PUD symptoms may consider eating smaller, more
frequent meals and avoid eating before bedtime. A study of Traditional Iranian Medicine claims there are
several edible fruits and spices used for the management of PUD. They found these remedies were
effective in reducing inflammation, discouraging H. pylori growth and healing wounds.

Nevertheless, this holistic approach of managing PUD needs pharmaceutical and clinical
verification of conclusive results. Goals for patients with PUD are to optimize nutritional intake to meet
nutrient needs and implement dietary and lifestyle factors that will reduce symptoms, decrease pain, and
promote healing.

Identification of H. pylori as the causative agent in the majority of PUD cases has revolutionized
the understanding and management of the GI disease. The overall incidence of peptic ulcers is declining,
perhaps as a result of the increasing use of PPIs and decreasing rates of H. pylori infection. This disease
causing bacteria was identified as a major culprit only 20 years ago, which leads much to be discovered
about the development of PUD. The use of surgery to treat PUD has also declined thanks to the
widespread use of H2 blockers and PPIs. These highly effective anti-ulcer medications have been some of
the most significant advances in the field of gastroenterology in the past 15 years.

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 Researchers are searching for ways to give people the benefits of NSAIDs without the risk of
gastrointestinal bleeding. Current research includes studies that; Compare the effectiveness of current
medicines used to treat PUD and its complications, Develop new drugs to prevent ulcer development and
complications, Identify GI-friendly alternatives to NSAIDs, and Improve understanding of how the
mucosal lining can protect itself from stomach-acid erosion. Although PUD is primarily treated using
medication intervention, it is important to assess patients thoroughly and treat using proper medical
nutrition therapy. Goals for patients with PUD are to optimize nutritional intake to meet nutrient needs
and implement dietary and lifestyle factors that will reduce symptoms, decrease pain, and promote
healing. ( Academy of Nutrition and Dietetics (AND). Peptic Ulcers: Nutrition Care Manual. 2013.)

COMPLICATION
Complications of peptic ulcer disease (PUD) include bleeding, perforation, penetration, and
gastric outlet obstruction. With time, there have been major shifts in the etiologies of complicated peptic
ulcers and in the affected patient populations. In addition, management has undergone dramatic changes.
Management now includes the early use of high-dose intravenous proton pump inhibitors (PPIs),
treatment to eradicate Helicobacter pylori (H. pylori), improved endoscopic methods for control of
hemorrhage, and changes in surgical indications and procedures.

 DIAGNOSIS

Peptic ulcer disease is suspect in patients with epigastric distress and pain; however, these
symptoms are not specific. Lack of response to conventional treatment for peptic ulcer disease should
suggest conditions other than benign peptic ulcers, and should warrant endoscopy or abdominal imaging.

Radiological Diagnosis

Barium x-ray or upper GI series is a widely available and accepted method to establish a
diagnosis of peptic ulcer in the stomach. Though less invasive than endoscopy, the barium x-ray is limited
by being less sensitive and accurate at defining mucosal disease, or distinguishing benign from malignant
ulcer disease . In patients who have anatomic deformities from previous gastric surgery or scarring from
chronic inflammation, barium x-rays may be difficult to interpret. Generally, these x-rays have up to a
30% false negative and a 10% false positive rate. Until 1970, peptic ulcers were diagnosed almost
exclusively by radiological methods. The most common inaccuracies of radiological diagnosis include the

16
failure to recognize true ulcers, or the misdiagnosis of a scar or a deformed duodenal bulb as a true ulcer.
Since the 1970s, increasing numbers of peptic ulcers are diagnosed by endoscopy.  

Risk factors

Peptic ulcers can be caused by nonsteroidal anti-inflammatory drugs(NSAIDs). The Department

of Gastroenterology & Hepatology at Singapore General Hospital shares its symptoms and ways to
prevent peptic ulcers.

Prevalence

While more than 90 per cent of patients with peptic ulcers used to be infected by H. pylori, the
prevalence now ranges from 50 to 75 per cent. It is continuing to decrease in developed countries due in
part to widespread anti- H. pylori therapy in both primary practice and the hospital setting, and the
improvement of socio-economic and living conditions, says Dr Chuah Sai Wei, Consultant, Department
of Gastroenterology & Hepatology, Singapore General Hospital (SGH), a member of the SingHealth
group. However, the prevalence of H. pylori infection remains high in the elderly and in less developed
countries. “No one knows for sure how H. pylori is transmitted, although researchers believe that it may
be spread through contaminated food or water; or through contact with the stool or vomit of an infected
person. H. pylori has also been found in the saliva of some infected people, which means infection could
be spread through direct contact with saliva,” adds Dr Chuah. In the absence of definitive evidence on
how H. pylori spreads, prevention is difficult. The usual advice, says Dr Chuah, is to wash your hands
with soap and water after using the bathroom and before eating, to eat food that has been washed well and
cooked properly, and to only drink water from clean, safe sources.

NSAIDs use and peptic ulcers

Studies have shown that the use of NSAIDs is a major risk factor for non-H. pylori-associated
peptic ulcers, especially gastric ulcers. Moreover, NSAIDs increase the risk of peptic ulcer complications
three- to five-fold, and are responsible for 15 to 35 per cent of all peptic ulcer complications. NSAIDs are
frequently used for various indications. Many people take them on a regular basis to relieve a throbbing
headache, muscle ache or arthritis pain. “Occasional use of NSAIDs for pain relief only poses a low risk
but as many as 15 to 25 per cent of chronic NSAID users will develop peptic ulcers. The annual risk of
serious complications is 1 to 4 per cent with chronic NSAIDs use,” says Dr Chuah. NSAIDs use increases
with age. The elderly are more likely to develop complications from NSAIDs-induced ulcers and to suffer
increased morbidity and mortality from these complications, adds Dr Chuah. According to the US Food
and Drug Administration (FDA), a daily dose of 75 to 300 mg of aspirin can double or triple the risk of

17
bleeding ulcers in the stomach and intestine (gastro-intestinal bleeding).(Teresa Cheong Copyright ©
SingHealth 2016)

 PREVENTION  
If you smoke, quit. People who smoke are twice as likely to develop ulcers. Ulcers also heal
more slowly in people who smoke. Don’t drink too much alcohol. If you have symptoms of an ulcer,
contact your doctor. Don't overuse NSAIDs. (
Maricano E. Peptic Ulcer Disease and Helicobacter pylori infection. Mo Med. 2018 MayJun;11)

EPIDEMIOLOGY

PUD is a global problem with a lifetime risk of development ranging from 5% to 10%.[4]
[5] Overall, there is a decrease in incidence of PUD worldwide due to improved hygienic and
sanitary conditions combined with effective treatment and judicious use of NSAIDs.
[5] Duodenal ulcers are four times more common than gastric ulcers. Also, duodenal ulcers are
more common in men than in the woman. ( Maricano E. Peptic Ulcer Disease and Helicobacter pylori
infection. Mo Med. 2018 MayJun;11)

Incidence and prevalence

In a systematic review of 31 published studies, the pooled incidence of uncomplicated peptic

ulcer disease (PUD) was approximately one case per 1000 person-years in the general population, and the
incidence of ulcer complications was approximately 0.7 cases per 1000 person-years .

The incidence and prevalence of PUD varies based upon the presence of Helicobacter pylori (H.
pylori). Higher rates are found in countries where H. pylori infection is higher [3-6]. The incidence of
PUD in H. pylori-infected individuals is approximately 1 percent per year, a rate that is 6- to 10-fold
higher than for uninfected individuals [7,8]. A systematic review of seven studies from developed
countries indicated a population-based one-year prevalence of PUD of 0.1 to 1.5 percent based on
physician diagnosis and 0.1 to 0.19 percent based on hospitalization data [9]. A study in the United States
reported an endoscopic point prevalence for peptic ulcers in asymptomatic, H. pylori-positive adults of 2
percent [10]. Other studies, in presumably asymptomatic subjects in whom H. pylori status was unknown,
have reported an endoscopic point prevalence ranging from 1 and 6 percent [5,11-13].

18
 Ulcer incidence increases with age for both duodenal ulcers (DUs) and gastric ulcers (GUs), but
the incidence of uncomplicated PUD reached a plateau with age, whereas for complicated PUD, the
incidence increases with age [14]. DUs occur two decades earlier than GUs, particularly in males

PROGNOSIS

The prognosis of PUD is excellent after the underlying cause is successfully treated. Recurrence
of the ulcer may be prevented by maintaining good hygiene and avoiding alcohol, smoking, and NSAIDs.
(Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017)
 
  
NURSING HEALTH HISTORY

BIOGRAPHIC DATA

Hospital : Surigao Medical Center

Case Number : 178832

Room : Private Room 2

Name : Patient A

Age : 81 years old

Sex : Female

Address : BRGY LUNA SURIGAO CITY

Civil Status : Married

Date of Birth : April 29, 1939

Birthplace : Surigao City

Nationality : Filipino

Religion : Catholic

Height : 5’4”

Weight : 55 kg

19
Health Financing and

Source of Medical Care : Phil health

Source and Reliability

of data gathered : Patient and patient’s chart

Admission data

Hospital : Surigao Medical Center

Admission Date : September 19, 2019

Time : 07:00 pm

Mode of Transmission : Wheelchair

Admitting Vital Signs : Temperature – 36 degree celcius

Respiratory Rate – 18cpm

Pulse Rate - 72

Admitting Physician : Dr. MIRABELEE, MARILYN, MD

Attending Physician : Dr. HOWELL G. HIPE, MD

Impression : PUD

Final Diagnosis : PEPTIC ULCER

Chief Complaint : Abdominal Pain

20
 Client Health History

Patients Profile

Patient B a 74 years old; a Roman Catholic; and a Filipino citizen born on April 29, 1939. A
widowed woman living with her three children and presently residing at Brgy, Luna Surigao City. Major
reasons for seeking health care is due to peptic ulcer disease on the morning of September 21, 2019.

Treatment/Medications:

Prescribed: No prescribed medications

OTC: Maalox Plus Suspension

Allergies

Patient has no known food allergies and drug allergies.

HISTORY OF HOSPITALIZATION

Patient was hospitalized on 1965 due to Caesarian Section and on 1976 due to thyroidectomy
and also in the year of 1970 due to sub. total hysterectomy. She was also diagnosed with Peptic
Ulcer.

SURGICAL HISTORY

In the year of 1965 patient has a surgical history of Caesarian Section at the age of 24, in the year
of 1976 patient has a surgical history of thyroidectomy, in the year of 1970 patient has a surgical history
of sub. total hysterectomy at the age of 33.

Accidents and Injuries

Patient had a history of Femor fracture last April 14, 2019

Family Health History

Patient’s father died of a hereditary illness of liver cirrhosis at the age of 56 her mother
died with no known cause illness. The patient has three children and still alive and well. She is
the only daughter of the family and had been diagnosed with peptic ulcer disease.

21
DEVELOPMENTAL HISTORY

The stage of older adulthood is considered to begin at 65 years of age.  Many physical,
psychological, and social changes occur during later adulthood.  The critical transition comes at the time
of retirement for both the husband and the wife.  In old age persons are moving toward completion of
their life cycles.    Old age can be a time when a person can enjoy his/her  time with his/her grandchildren
and leisure time activities, and forget about things caused him/her a great deal of stress and anxiety in the
past three or four decades . During this stage a person must adapt to changing physical abilities. This
stage is characterized by increased wisdom although many other things are lost such as health, friends,
family and independence. The aging process of people in this stage of development varies greatly.  Ego
integrity Vs despair represents this stage in the psychosocial theory. The developmental tasks of the older
adult are: adjusting to decreases physical strength and loss of health, adjusting to retirement and reduced
income, coping with death of a husband or wife and preparing for one's own deatheating periods.

According to Erik Erickson’s Psychosocial Development Theory lies on the stage 8 (integrity
vs. Despair), wherein, ego integrity is the ego's accumulated assurance of its capacity for order and
meaning. And despair is signified by a fear of one's own death, as well as the loss of self-sufficiency, and
of loved partners and friends.

This stage is focused on reflecting back on the person’s life, that is, those who are unsuccessful
during this phase will feel that their life has been wasted and will experience many regrets. The individual
will be left with feelings of bitterness and despair.

Those who feel proud of their accomplishments will feel a sense of integrity. Successfully
completing this phase means looking back with few regrets and a general feeling of satisfaction. These
individuals will attain wisdom, even when confronting death.

In general, this is the patients time for reflecting on and reviewing how he met previous
challenges and lived his life. Adjusting to decreasing physical strength and health; Adjusting to retirement
and reduced income; Establishing an explicit affiliation with one's age group; and Meeting social and civil
obligations are the right ways on how to establish a satisfactory physical living arrangements on his kind
of stage.

22
Nutritional Metabolic Pattern
Before hospitalization: The patient eats spicy foods such as bicol express, sour foods and at her
young age she always drinks alcohol, soft drinks and coffee. She also takes NSAIDs whenever
she felt abdominal pain.

During hospitalization: The patient eats what meals the hospital gives her and does not fully
consume it. She eats at 6 am, have lunch at 11 am and eats dinner at 7 pm.

Sleep/Rest Pattern
She sleeps normally at 7:00 pm and wakes up at 5. She has no difficulty in sleeping.

At the hospital, her sleeping pattern was interrupted due to constant monitoring of vital
signs, giving prescribed medications and abdominal pain.

Elimination Pattern
Patient defecates once a day with soft and form stool and urinates at least 4-6 times a day
with clear yellow urine.
At the hospital she defecates with black bloody, mucoid stool.
Activity of Daily Living

Patient arises at 5 in the morning. Her daughter assists her in some of her activities such
as getting up and walking since she has femor fracture. Eats breakfast at 6am and television as
her past time. Doesn’t have chest pain, fatigue, wheezing, stiffness, with an activity. During
evening she would have dinner with her family at 6pm and she sleeps at 7pm.

Recreation/Hobbies

Patient watches television as her past time activity and get along with her grand daughter
and grand son.

SOCIAL DATA

Family Relationship

Her relationship with her children are close and when there are any problems, they talk
about it as a way to fix it.

23
Ethnic Affiliation
Patient was born and raised in Surigao city and she is a pure Surigaonon.

Educational History
Patient is a college graduate.
Occupational History
Patient is a retired Nurse.
Economic Status
Patient is currently receiving her pension monthly at SSS and has a Phil health that
support his hospital bills.

HEALTH HISTORY

A. History of Present Illness

2 days prior to admission, patient was experiencing severe pain on his abdominal area when
she does not eat his meals. Since the cause of discomforts felt by the patient on his abdomen, as well
as the bloody stools during defecation, and with laboratory examination taken by ( e.g. CBC), the
patient is then positive with a peptic ulcer disease. After a day her daughter decided to seek
medical attention at Surigao Medical Center on September 21, 2019 at 7:00 am which was
where she was admitted.

B. PAST HEALTH HISTORY

Patient has a history of chickenpox, mumps and measles when she was still in grade
school. Patient did not receive any immunizations when she was a child. The patient had a
history of Femor fracture last April 14, 2019. In the year of 1965 patient has a surgical history of
Caesarian Section at the age of 24, in the year of 1976 patient has a surgical history of thyroidectomy, in
the year of 1970 patient has a surgical history of sub. total hysterectomy at the age of 33.

24
 PHYSICAL EXAMINATION

General Survey

Properly groomed alert, awake with eyes open and looking at the examiner; client
responds appropriately. Sitting comfortably on bed with back slightly bended down, and
appears fatigue. Hooked with an IVF of NSS 1000 ml at 10gtt/min at right cephalic vein.
Oriented to time and place and also oriented to people around. Able to recall when and
who visits a while ago for immediate memory. Has short term memory. Ht: 5’4” Wt: 55
kg, Apical pulse: 72 Resp: 18 Temp: 36 C Blood Pressure: 130/80 O2 Saturation: 98%

Skin
Inspection
Skin is white and wrinkled. Seborrheic warts are visible on the lateral side of the
neck. No scalp lesions and edema.
Palpation
Skin is warm to touch indicated elevated temperature. No edema noted. Has a
poor skin turgor.
Head and Face
Inspection
No scalp lesions or flaking. Central facial palsy noted. Smiles, frowns, shows
teeth, blows cheeks, and raises eyebrows as instructed.

Palpation
Patient identifies light touch and sharp touch to forehead, cheek and chin. Head
symmetrically rounded upon palpation.
Eyes

Inspection

Eyebrows sparse with equal distribution. No scaliness noted. Lids brown without
lesions. Sclera without increased vascularity or lesions noted. Palpebral and bulbar
conjunctiva pale without lesions noted. Irises uniformly black. Pupils are round and react
to light and accommodation.

Palpation

25
 No edema noted. No masses noted
Ears and Nose
Inspection

Auricle without deformity, lumps or lesions. Auricle aligned with outer canthus
of eye about 10 degrees from vertical. Nares patent. No redness, swelling, and abnormal
discharge on the nasal mucosa. Whisper test: Patient is unable to hear whispered words or
watch tick.

Palpation
Auricles and mastoid processes are non-tender. Pinna recoils after it is folded.
Nose is symmetrical and straight upon palpation.

Mouth and Throat

Inspection

Lips are moist pink, smooth and with no lesions. Central facial palsy noted.
Second and third molar removed. Tonsils appear to be normal.

Palpation
No palpable nodules noted.
Neck

Inspection

Neck is symmetrical with seborrheic warts visible on the lateral side. Trachea is in
center placement in midline of neck.

Palpation

Lymph nodes are non-palpable.

Arms, Hands, and Fingers

Inspection

26
 Arms are equal in size and symmetry bilaterally. Brown in color. Three flexion
creases present in palm. Fingernails are finely cut, clean and clear. No clubbing. Hands
are wrinkled.

Palpation

Poor skin turgor and elasticity. Warm and dry to touch. No edema

Thorax and Lungs

Inspection

Posterior lateral diameter is 1:2 ratio. Anterior lateral diameter is 1:2 ratio.
Symmetrical expansion on posterior thorax. Chest symmetry is equal. Shape and position
of sternum is level with ribs. Position of trachea is in midline.

Palpations

No pain or tenderness in the anterior and posterior thorax. No masses noted.

Auscultation

No rales, rhonchi, friction rubs noted.

Breasts (Female)
Inspection
Skin is the same color as the abdomen/back. No swelling, ulcerations. Skin
uniform in color. Nipples are round and equal in size. Areola is round and bilaterally the same

Palpation
No masses. Nodules noted

Abdomen
Inspection
Abdomen is uniform in color. No rashes or lesions. No evidence of enlargement
of liver and spleen.

Palpation

Abdomen is soft. No evidence of enlargement of liver and spleen upon palpation

27
Auscultation

Bowel sounds are normal.

Legs, Feet and Toes

Inspection
Gangrene scars visible on both anterior and posterior tibia. Toenails are finely cut,
clean, and clear. No clubbing.
Palpation

No edema noted.

Genitalia ( Female)

Inspection

Decreased in size and firmness of testicles. Small amount of hair abundant in pubic area.
Erections are slowed and there are less ejaculations

Muskoloskeletal and Neurologic examination

Inspection

Muscle strength 3/5.No edema noted at both lower extremities. Passive range of
motion. No deviations, inflammations, or bony deformities. Pt. is alert and awake with
eyes open and looking at the examiner; client responds appropriately. Oriented to time
and place and also oriented to people around. Able to recall when and who visits a while
ago for immediate memory. Can recall her name. She has trouble regaining her memory
on what she was doing from the past days. Takes incoming information appropriately.
Right and Left hand: Alternates finger to nose with eyes closed; occasionally tends to hit
opposite side of nose. Rapidly opposes fingers to thumb bilaterally without difficulty.
Alternates pronation and supination of hands rapidly without difficulty. Heel to chin
intact bilaterally.

Palpation

28
Can feel sense of touch on the left and right side of her body.

29
 Cranial Nerve Assessment
Cranial Nerve Name Result
I Olfactory Can smell and can identify what it
is.
II Optic No difficulty of reading either
near or far.
III Occulomotor Pupils are round and react to light
and accommodation.

IV Trochlear Both eyes are well coordinated

and moves in unison without
tenderness felt when left and right
eyes moves. Patient lids close
symmetrically.
V Trigeminal Eyelids blink bilaterally
VI Abducens Can move left and right eyeballs
in a moderate manner.
VII Facial Raises his left and right eyebrows
whenever you say something to
him. Can close his both eyes.

VIII Acoustic Cannot clearly hear normal voice

tone.
IX Glossopharyngeal Positive gag reflex
X Vagus Positive swallowing reflex
XI Spinal Accessory Patient can move his neck
XII Hypoglossal Can protrude tongue

REVIEW OF SYSTEMS

General Survey

30
 The usual weight of the client is 55 kg upon hospitalization, the patient’s weight
decreased to 49 kg. abdominal cramps, nausea and appears fatigue upon assessment.

Integumentary System

Skin is white and wrinkled, warm and smooth to touch. Poor skin turgor. Seborrheic
warts visible on the lateral side of the neck. No history of any skin allergies. Has a history of
dandruffs. Has a history of chickenpox and measles.

Head, Eyes, Ears, Nose, and Throat (EENT)

Head had no scalp lesions or flaking. No history of any head injuries. Patient had no
history of any abnormalities in the eyes. Patient can still see clearly. Patient is unable to
hear whispered words or watch tick. Patient had no history of otitis media. No problems
upon disseminating various scents. No history of tonsillitis.

Gastrointestinal System

Patient has a history of Peptic Ulcer

Musculoskeletal System

No history of edema at both lower extremities. No deviations, inflammations, or bony

deformities. No joint pain. No muscle pain.

Neurologic System

Patient has no history of memory loss, seizure, dizziness, sensation changes such as
numbness and coldness.

Urinary System

Patient had no history of any urinary tract infection. No pain urination. He had no history
of dysuria, nocturia and hematuria.

Reproductive System Female)

Patient had a history of Caesarian section and sub. Total hysterectomy.

31
Hematologic of lymphatic

Patient has no history of lymph node enlargement. No history of easy bleeding or

bruising.

Endocrine

Patient had no history of polyuria and nocturia. Patient has a history of parathyroid.

Psychiatric

No signs depression. No history of attempted suicides. Has a short term memory.

32
 LABORATORY RESULTS

HEMATOLOGY

COMPLETE BLOOD COUNT

SEPTEMBER 21, 2019

TEST RESULT NORMAL UNIT SIGNIFICANT RATIONALE

VALUES
HEMOGLOBIN 13.3 12.0-17.0 g/dL Normal
HEMATOCRIT 42.6 37-54 % Normal
RBC 4.52 4.0-6.0 10^12/L Normal
MCV 94.2 87 ± 5 fl Increased Infection
MCH 30.3 29 ± 2 pg Increased Infection
MCHC 32.2 34 ±2 g/dL Decreased Infection
RDW 15.5 11.6-14.6 Increased Infection
PLATELET 170 150-450 x10^9/L Normal
COUNT
WBC 14.2 4.5-10.0 x10^9/L Increased Infection
DIFFERENTIA RESULT NORMAL UNIT
L COUNT VALUES
SEGMENTERS 76.0 50-70 % Increased Infection
LYMPHOCYTE 15.6 20-40 % Decreased Infection
MID CELL 17.1 %

ANALYSIS:

The result of the exam with increased MCV and MCH. MCHC is increased caused by
infection. Increased segmenters count of 76.0 that may indicate an infection. Lymphocyte
count decreased that may also indicate an infection.

URINALYSIS

SEPTEMBER 22, 2019

33
 TEST RESULT NORMAL SIGNIFICANT RATIONALE
VALUES
COLOR Yellow Normal
TRANSPARENCY Slightly hazy Normal
PROTEIN Negative Normal
pH 6.8 6.5 Increased Acidic
SPECIFIC GRAVITY 1.025 1.025 Normal
GLUCOSE Negative Normal
BACTERIA Few Few Infection

Analysis:

Urinalysis shown normal urine color amber and slightly hazy, an increased urine specific
gravity indicates that there is a presence of bacteria in the urine. However, a few bacteria is
present in the urine indicating patient is having an infection.

34
 ANATOMY AND PHYSIOLOGY

Anatomy and Physiology

The human digestive system is a complex series of organs and glands that processes food. In

order to use the food we eat, our body has to break the food down into smaller molecules that it

can process; it also has to excrete waste. Most of the digestive organs (like the stomach and

intestines) are tube-like and contain the food as it makes its way through the body.

The digestive system is essentially a long, twisting tube that runs from the mouth to the anus,

plus a few other organs (like the liver and pancreas) that produce or store digestive chemicals.

35
The Normal Digestive Process:

The start of the process - the mouth: The digestive process begins in the mouth. Food is partly

broken down by the process of chewing and by the chemical action of salivary enzymes (these

enzymes are produced by the salivary glands and break down starches into smaller

molecules).

On the way to the stomach:

The esophagus - After being chewed and swallowed, the food enters the esophagus. The

esophagus is a long tube that runs from the mouth to the stomach. It uses rhythmic, wave-like

muscle movements (called peristalsis) to force food from the throat into the stomach. This

muscle movement gives us the ability to eat or drink even when we're upside-down.

In the stomach - The stomach is a large, sack-like organ that churns the food and bathes it in a

very strong acid (gastric acid). Food in the stomach that is partly digested and mixed with

stomach acids is called chyme.

In the small intestine - After being in the stomach, food enters the duodenum, the first part of

the small intestine. It then enters the jejunum and then the ileum (the final part of the small

intestine). In the small intestine, bile (produced in the liver and stored in the gall bladder),

pancreatic enzymes, and other digestive enzymes produced by the inner wall of the small

intestine help in the breakdown of food.

In the large intestine - After passing through the small intestine, food passes into the large

intestine. In the large intestine, some of the water and electrolytes (chemicals like sodium) are

removed from the food. Many microbes (bacteria like Bacteroides, Lactobacillus acidophilus,

Escherichia coli, and Klebsiella) in the large intestine help in the digestion process. The first part

36
of the large intestine is called the cecum (the appendix is connected to the cecum). Food then

travels upward in the ascending colon. The food travels across the abdomen in the transverse

colon, goes back down the other side of the body in the descending colon, and then through the

sigmoid colon.

The end of the process - Solid waste is then stored in the rectum until it is excreted via the anus.

Digestive System Glossary:

Anus - the opening at the end of the digestive system from which feces (waste) exits the body.

Appendix - a small sac located on the cecum.

Ascending colon - the part of the large intestine that run upwards; it is located after the cecum.

Bile - a digestive chemical that is produced in the liver, stored in the gall bladder, and secreted

into the small intestine.

Cecum - the first part of the large intestine; the appendix is connected to the cecum.

Chyme - food in the stomach that is partly digested and mixed with stomach acids. Chyme goes

on to the small intestine for further digestion.

37
Descending colon - the part of the large intestine that run downwards after the transverse colon

and before the sigmoid colon.

Duodenum - the first part of the small intestine; it is C-shaped and runs from the stomach to the

jejunum.

Epiglottis - the flap at the back of the tongue that keeps chewed food from going down the

windpipe to the lungs. When you swallow, the epiglottis automatically closes. When you breathe,

the epiglottis opens so that air can go in and out of the windpipe.

Esophagus - the long tube between the mouth and the stomach. It uses rhythmic muscle

movements (called peristalsis) to force food from the throat into the stomach.

Gall bladder - a small, sac-like organ located by the duodenum. It stores and releases bile (a

digestive chemical which is produced in the liver) into the small intestine.

Ileum - the last part of the small intestine before the large intestine begins.

Jejunum - the long, coiled mid-section of the small intestine; it is between the duodenum and

the ileum.

Liver - a large organ located above and in front of the stomach. It filters toxins from the blood,

and makes bile (which breaks down fats) and some blood proteins.

Mouth - the first part of the digestive system, where food enters the body. Chewing and salivary

enzymes in the mouth are the beginning of the digestive process (breaking down the food).

Pancreas - an enzyme-producing gland located below the stomach and above the intestines.

Enzymes from the pancreas help in the digestion of carbohydrates, fats and proteins in the small

intestine.

38
Peristalsis - rhythmic muscle movements that force food in the esophagus from the throat into

the stomach. Peristalsis is involuntary – you cannot control it. It is also what allows you to eat

and drink while upside-down.

Rectum - the lower part of the large intestine, where feces are stored before they are excreted.

Salivary glands - glands located in the mouth that produce saliva. Saliva contains enzymes that

break down carbohydrates (starch) into smaller molecules.

Sigmoid colon - the part of the large intestine between the descending colon and the rectum.

Stomach - a sack-like, muscular organ that is attached to the esophagus. Both chemical and

mechanical digestion takes place in the stomach. When food enters the stomach, it is churned in

a bath of acids and enzymes.

Transverse colon - the part of the large intestine that runs horizontally across the abdomen.

PHYSIOLOGY

Transverse colon- is the lengthy, upper part of the large intestine, ingested food exits the small

intestine and enters the cecum. As digestion continues, the ingested matter moves up the

ascending colon and into the transverse colon. The transverse colon performs several critical

functions, including moving waste material forward and the absorption of key components for

proper body functioning.

Stomach- the stomach will provide a place for varied amounts of swallowed food to rest and

digest in. Hence, the stomach is a storage site. The stomach will also introduce our swallowed

food to essential acids. The cells in the stomach’s lining will excrete a strong acidic mixture of

hydrochloric acid, sodium chloride, and potassium chloride. This gastric acid, or colloquially

39
known as gastric “juice,” will work to break down the bonds within the food particles at the

molecular level. Pepsin enzyme will have the unique role of breaking the strong peptide bonds

that hold the proteins in our food together, further preparing the food for the nutrient absorption

that takes place in the small (mainly) and large intestines. This brings us to the third task the

stomach has, which is to send off the churned watery mixture to the small intestine for further

digestion and absorption. It takes about three hours for this to occur once the food is a liquid mix.

Sigmoid colon- Its major function is to transport the fecal matters to rectum and anus. It

eliminates all the solid waste and forms of gaseous waste down the gastrointestinal tract. All the

body waste finds its way to get stored in the sigmoid colon until it the time when it can come out

of the body through the anal canal.

Salivary glands- As the only secretion of our salivary glands, it is helpful in creating the food

bolus, or the finely packed ball of food that we roll inside our mouths. This shape facilitates its

safe passage through our alimentary canal. Saliva has lubricating properties that are protective,

as well. Saliva protects the inside of our mouths, our teeth, and our throats as we begin to

swallow the bolus. It also cleanses the mouth after a meal and dissolves food into chemicals that

we perceive as taste.

Rectum- The role of the rectum is to temporarily store feces until defecation.

The food that one consumes is first chewed in the mouth and as a part of the digestion process,

has to pass through the stomach, small intestine, and lastly the large intestine. The undigested

food and waste products that are accumulated during the digestion process, move into the rectum

in the form of fecal matter. It is the function of the rectum to receive this fecal matter and hold it

till one defecates. Thus, the rectum stores fecal matter until defecation, during which the feces

are eliminated from the body through the anus.

40
Peristalsis- Peristalsis is a series of wave-like muscle contractions that moves food to different

processing stations in the digestive tract. The process of peristalsis begins in the esophagus when

a bolus of food is swallowed. The strong wave-like motions of the smooth muscle in the

esophagus carry the food to the stomach, where it is churned into a liquid mixture called chime.

Peristalsis concludes in the large intestine where water from the undigested food material is

absorbed into the bloodstream. Finally, the remaining waste products are excreted from the body

through the rectum and anus.

Pancreas- The pancreas serves two primary functions, according to Jordan Knowlton, an

advanced registered nurse practitioner at the University of Florida Health Shands Hospital. It

makes "enzymes to digest proteins, fats, and carbs in the intestines" and produces the hormones

insulin and glucagon.

Mouth- in the mouth itself, the tongue and teeth help to get the process started by chewing and

chopping the food so it's small enough to be swallowed. Salivary glands secrete saliva, releasing

an enzyme that changes some starches into simple sugars and softens the food for swallowing.

Liver- The liver regulates most chemical levels in the blood and excretes a product called bile.

Bile helps to break down fats, preparing them for further digestion and absorption. All of the

blood leaving the stomach and intestines passes through the liver. The liver processes this blood

and breaks down, balances, and creates nutrients for the body to use. It also metabolized drugs in

the blood into forms that are easier for the body to use.

Jejunum- responsible for absorbing nutrients from digested food into the bloodstream. The

jejunum is able to absorb these nutrients because it is lined with finger-like projections that are

called villi. The villi absorb nutrients in the form of minerals, electrolytes, and carbohydrates,

proteins, and fats that were consumed in the form of food. The nutrients are absorbed into the

41
bloodstream where they can be utilized for energy by the entire body.The jejunum, as well as the

rest of the small intestine, make it possible to change food into energy, powering the body for

daily activities. Without the small intestine, food would pass through the body but we would gain

no nutrients, and would quickly starve.

Ileum- absorb the nutrients from the chyme, or digested food. This is done with the help of villi,

which are finger-like projections found in the inner wall.There are lymph vessels called lacteals

in the villi which absorbs fat in the lymphatic system. This digested fat is then drained into the

bloodstream, which is transported along with other nutrients, to the liver through the hepatic

portal vein. Detoxification takes place and the nutrients are assimilated by the body.

Gall bladder- serves as a reservoir for bile while it’s not being used for digestion. The

gallbladder's absorbent lining concentrates the stored bile. When food enters the small intestine,

a hormone called cholecystokinin is released, signaling the gallbladder to contract and secrete

bile into the small intestine through the common bile duct.The bile helps the digestive process by

breaking up fats. It also drains waste products from the liver into the duodenum, a part of the

small intestine.

Esophagus- The esophagus is an important connection to the digestive system through the

thoracic cavity, which protects the heart and lungs. The esophagus carries food through this

cavity, keeping it separate and moving it through with muscular contractions. Two sphincters on

either side of the esophagus separate food into small units known as a bolus. The size and

complexity of the esophagus varies by species.

Epiglottis- The main function of the epiglottis is to seal off the windpipe during eating, so that

food is not accidentally inhaled. The epiglottis also helps with some aspects of sound production

in certain languages.

42
Duodenum- The duodenum is the first and shortest segment of the small intestine. It receives

partially digested food (known as chyme) from the stomach and plays a vital role in the chemical

digestion of chyme in preparation for absorption in the small intestine. Many chemical secretions

from the pancreas, liver and gallbladder mix with the chyme in the duodenum to facilitate

chemical digestion.

Descending colon - primarily serves to absorb water from fecal matter. It also stores food

particles that are to be emptied into the rectum. While working in a downward movement, this

organ continues to push the digested waste products. The wastes move downwards from the

transverse colon to the sigmoid colon. They ultimately enter the rectum to be expelled during

excretion. While moving the waste material, the descending colon also continues to take out any

remaining nutrients and water from them.

Chyme - There are two major functions of chyme – the first is to increase the surface area of

food to allow digestive enzymes to complete their work, and the second is to stimulate various

digestive glands to release their secretions.The action of enzymes requires direct contact with the

molecules of the substrate. When food is first ingested, it is in the form of large chunks. Such

particles have a very low surface area for their volume, and therefore, enzymes will only have

access to a small proportion of the molecules in the substrate. Mastication of food, and the

subsequent churning through the muscles of the stomach and small intestine repeatedly break

down food through mechanical processes.

Cecum- absorb fluids and salts that remain after completion of intestinal digestion and

absorption and to mix its contents with a lubricating substance, mucus. The internal wall of the

cecum is composed of a thick mucous membrane, through which water and salts are absorbed.

43
Bile- lows into the duodenum and mixes with food contents. Bile has two important functions: It

assists in the digestion and absorption of fats, and it is responsible for the elimination of certain

waste products from the body, particularly hemoglobin from destroyed red blood cells and excess

cholesterol.

Ascending colon- The ascending colon carries feces from the cecum superiorly along the right

side of our abdominal cavity to the transverse colon. In the ascending colon, bacteria digest the

transitory fecal matter in order to release vitamins. The intestinal wall absorbs water, nutrients,

and vitamins from the feces and deposits these materials into our bloodstream.

Appendix- appendix acts as a storehouse for good bacteria, “rebooting” the digestive system

after diarrheal illnesses.

Anus- An aperture for defecation the primary anus function is to serve as an aperture for

defecation. After defecation, the colon and rectum prepare themselves to receive and store the

digestive wastes descending along the alimentary canal .Regulation of excretory process the

internal and external sphincters play a key role in the regulation of excretory process. The

internal involuntary sphincter operates under the command of autonomous nervous system,

voluntary control over feces removal holding feces back for a certain duration is a very important

anus function. Otherwise, you won’t be able to hold the bowels for some time in order to reach

the place of defecation and triggering need for removal of feces sexual arousal.

small intestine- The small intestine is the part of the intestines where 90% of the digestion and

absorption of food occurs, the other 10% taking place in the stomach and large intestine. The

main function of the small intestine is absorption of nutrients and minerals from food.

Digestion involves two distinct parts. The first is mechanical digestion by chewing, grinding,

churning and mixing that takes place in the mouth and the stomach. The second part of digestion

44
is the chemical digestion that uses enzymes, bile acids etc. in order to break down food material

into a form that can then be absorbed, then assimilated into the tissues of the body. Chemical

digestion occurs in the small intestine (and, to a lesser extent, also in some other part of the

gastrointestinal tract.

Large intestine- absorbing water and electrolytes, producing and absorbing vitamins, and

forming and propelling feces toward the rectum for elimination. By the time indigestible

materials have reached the colon, most nutrients and up to 90% of the water has been absorbed

by the small intestine. The role of the ascending colon is to absorb the remaining water and other

key nutrients from the indigestible material, solidifying it to form stool. The descending colon

stores feces that will eventually be emptied into the rectum. The sigmoid colon contracts to

increase the pressure inside the colon, causing the stool to move into the rectum. The rectum

holds the feces awaiting elimination by defecation.

45
 PATHOPHYSIOLOGY
Precipitating factors:
Predisposing factors:
Helicobacter pylori
Age: 81 years old infection
Female Ingestion of gastric
irritant
( Alcohol,caffeine,
sour food )
Use of NSAIDs
Gastric
Hyperacidity

Increased gastrin secretion

Sour eructation Low function of

Hiccuping Increased gastric acid production
mucosal cells, low
quality of mucous

Inflammation of gastric Digestive and

mucosa Damage/ erosion of the mucosa absorptive malfunction

Nausea and vomiting Formation of ulcers

Decrease integrity of
the intestinal wall

Increased Helicobacter Pylori proliferation Infection

Epigastric pain
Loss of appetite

Hemorrhage
Bloody, black mucoid Gastrointestinal bleeding
stool

46
 If Left Untreated

If Left treated

Hemorrhage is prevented
Bleeding continues

Decrease in circulating blood

Normal blood circulation
volume

Hypovolemic Shock ( Inadequate Hypovolemic shock is

brain tissue perfusion prevented

Well
Death

47
LEGEND:

= Disease Process

= Client Manifestation

= Clinical Manifestation

= Treatment/management

= Signs and Symptoms

= If Left Untreated

= If Left Treated

= Well

= Death

48
 Drug Study No. 1

Generic name:

Metoclopromide

Brand name:

PLASIL

Dosage:

2mg/ampoule

Route:

IV

Frequency:

q 8hr

Classification

Anti-emetics

Mechanism of action

It blocks dopamine receptors and makes the GI cells more sensitive to acetylcholine, leading to increased
GI activity and rapid movement of food through the upper GI tract.

Indications

Prevention of chemotherapy-induced emesis, treatment of postsurgical and diabetic gastric stasis,

facilitation of small bowel intubations in radiographic procedures, management of esophageal
reflux, treatment and prevention of postoperative nausea and vomiting when nasogastric
suctioning is undesirable.

49
Contraindications

Hypersensitivity, possible obstruction or hemorrhage, history of seizure disorders,

pheochromocytoma, Parkinson’s disease.

Adverse effect

CNS:

drowsiness, extrapyramidal reactions, restlessness, anxiety, depression, irritability, tardive

dyskinesia

CV:

arrhythmias, hypertension, hypotension

GI:

constipation, diarrhea, dry mouth, nausea

Endo:

Gynecomastia

Nursing Responsibility

 Assess client for abdominal pain distention, bowel sound

 Assess client for extrapyramidal reaction

 Monitor for tardive dyskinesian

50
 Drug Study No. 2

Generic name:

Omeprazole

Brand name:

Omepron

Dosage:

40mg

Route:

PO

Frequency:

OD

Classification

Proton Pump Inhibitor

Mechanism of action

Reduces Gastric Acid Secretion and increases Gastric mucus and bicarbonate production,
creating protective coating on gastric mucosa and easing discomfort from excess gastric acid.

Indications

GERD, Erosive Esophagitis, Short term treatment of Duodenal ulcer, Gastric Ulcer, Pathologic
hypersecretory Conditions, including Zollinger-Ellison Syndrome, Frequent Heartburn

Contraindications

Hypersensitivity to drug, Hepatic Disease, Pregnancy, Children, Posterior Laryngitis

51
Adverse effect

CNS: Headache, irritability, weakness

GI: Nausea, constipation, flatulence

Nursing Responsibility

 Assess Vital Signs

 Check for abdominal pain, emesis, Diarrhea or constipation
 Evaluate fluid and intake
 Watch for elevated liver function test results
 Caution patient to avoid driving and other hazardous activities until he know drugs effects
concentration and alertness.

52
 Drug Study No. 3

Generic name:

Rebamipide

Brand name:

REMAPRIDE

Dosage:

100 mg/tab 1 tab

Route:

Oral

Frequency:

TID

Classification

Anti-ulcer, Antacids

Mechanism of action

Rebamipide is a mucosal protective agent and is postulated to increase gastric blood flow,
prostaglandin biosynthesis and decrease free oxygen radicals.

Indications

Treatment for peptic ulcer and prevention of NSAID-induced gastropathy

Contraindications

Contraindicated with patients who are hypersensitive to the, lactating, pregnant, and children.

Adverse effect

CNS: Anxiety, fatigue, headache, insomnia, pyrexia

53
CV: Hypertension, hypotension, peripheral edema, periorbital edema, tachycardia

GI: Nausea, vomiting, abdominal pain, diarrhea, constipation.

Hematologic: Hemolytic anemia, leukopenia, neutropenia, pancytopenia, thrombocytopenia.

Hepatic: Liver damage, jaundice

Metabolic: Hypoglycemia

Respiratory: Abnormal breath sounds, dyspnea, hypoxia, atelectasis, pleural effusion.

Skin: Rash, urticuria

Nursing Responsibility

 Assess patient’s fever or pain: type of pain, location, intensity, duration, temperature, and
diaphoresis.
 Assess allergic reactions: rash, urticaria; if these occur, drug may have to be
discontinued.
 Teach patient to recognize signs of chronic overdose: bleeding, bruising, malaise, fever,
sore throat.
 Tell patient to notify prescriber for pain/ fever lasting for more than 3 days.

54
 Drug Study No. 4

Generic:

 Hyoscine-N-butylbromide

Brand:

BUSCOPAN

Classification:

Antipasmodic

Dosage:

10 mg, tablet

Route:

Oral

Frequency:

TID

Mechanism of Action:

BUSCOPAN (hyoscine butylbromide) is an antispasmodic agent which relaxes the smooth

muscle of the gastrointestinal, biliary and urinary (parenteral formulation) tracts. It is believed to
act predominantly at the parasympathetic ganglia in the walls of the viscera of these organs.
Structurally, BUSCOPAN exists as a quaternary ammonium compound and as a single positively
charged cation throughout the entire pH range.

Indications

 Spasm in the genitourinary tract

 Spasm in the gastrointestinal tract
 Spasm in the biliary tract

55
  Colic

Contraindications

 Myasthenia gravies, megacolon, hypersensitivity to drug contents, narrow angle glaucoma,

prostate hypertrophy with urinary retention, mechanical stenosis in the GI tract, tachycardia.

Adverse effect

CNS: dizziness, anaphylactic reactions, anaphylactic shock, increased ICP, disorientation,

restlessness, irritability, dizziness, drowsiness, headache, confusion, hallucination, delirium,
impaired memory

CV: hypotension, tachycardia, palpitations, flushing

GI: Dry mouth, constipation, nausea, epigastric distress

DERM: flushing, dyshidrosis

GU: Urinary retention, urinary hesitancy

Resp: dyspnea, bronchial plugging, depressed respiration

EENT: mydriasis, dilated pupils, blurred vision, photopobia, increased intraocular pressure,
difficulty of swallowing.

Nursing Intervention

 Take this drug 30 minutes to 1 hour before meals

 Buscopan will potentiate the effect of alcohol and other CNS depressants.
 Do not take antacids and antidiarrheal 2 to 3 hours prior to raking this drug.
 It is not necessary to take the medication if you are not in pain.
 Avoid driving or operating machinery after parenteral dose.

56
 Drug Study No: 6

Generic Name:

Meropenem

Brand Name:

MERREM

Dosage:

1 mg

Route:

IVTT

Frequency:

q 8 hours

Classification:

Anti-infectives

Mechanism of action:

 Bactericidal, Inhibits synthesis of bacterial cell wall and causes cell death in susceptible
cells.

Indications:

Prescribed for bacterial infections like skin and skin structure infections, bacterial meningitis,
serious nosocomial infections like septicaemia, intraabdominal and pelvic infections. The
medication inhibits cell wall synthesis in bacteria, and thereby leading to cell death.

57
Contraindications:

Contraindicated with hypersensitivity to carbapenem antibiotics

Adverse effect:

CNS: Headache, dizziness, lethargy, paresthesias, insomnia

GI: Nausea, vomiting, diarrhea, anorexia, abdominal pain, flatulence, pseudomembranous colitis, liver
toxicity

Nursing Intervention:

 Culture infected area and arrange for sensitivity tests before beginning therapy.
 Monitor for superinfections and arrange treatment appropriately
 This drug can only be given IV.
 Discontinue drug at any sign of colitis and arrange for appropriate supportive treatment.

58
 NURSING CAREPLAN #1

Assessment
Subjective
“ Hapdos ako tijan pagkatapos mo kaon” as verbalized by the patient
Objective:
 Abdominal guarding
 Restlessness
 Facial grimace
 Pain scale of 7/10
 V/S taken as follows:
 T: 36.5
 P: 65
 R: 18
 BP: 110/80

Nursing Diagnosis:

Acute pain related to irritation of the mucosa and muscle spasms

Planning

After 8 hours of nursing intervention the patient will verbalized relief of pain and able to
sleep/rest appropriately.

Intervention

Nursing intervention Rationale

 INDEPENDENT
 Note reports of pain, including location, duration,
intensity (0-10 scale)
Review factors that aggravate or alleviate pain.
Pain is not always present, but if present should be
compared with patient’s previous pain symptoms.
This comparison may assist in diagnosis of
etiology of bleeding and development of
complications
Helpful in establishing diagnosis and treatment

59
 needs.

Identify and limit foods that create discomfort Food has an acid neutralizing effect and dilutes the
such as spicy or carbonated drink. gastric contents.

Encourage small frequent meals Small meals prevent distension and the release of
gastrin.
Encourage patient to assume position and comfort. Reduces abdominal tension and promotes sense of
control.
 DEPENDENT/COLLABORATIVE

Administered Rebamipide as order by the To relieve pain

Physician

Evaluation:

Goal met. After 8 hours of nursing interventions, patient was able to has verbalized relief of pain
and be able to sleep/rest appropriately

NURSING CAREPLAN #2

60
Assessment
Subjective: “Mag lisod nako mo lakaw nan ako ra isa” as verbalized by the pt.

Objective:
 Leg fractured
 Muscle strength 3/5
 Body malaise

Nursing Diagnosis

Risk for falls related to proprioceptive deficit

Planning

After 8 hours of nursing intervention the patient will be able to verbalized understanding
of individual factors that contribute to possibility of injury.

Intervention

Nursing intervention Rationale

 INDEPENDENT These affect the client’s ability to protect self
Note the client’s age, gender, developmental stage, and/or others, and influence choice of
decision making ability, and level of cognition/ interventions and teachings.
competence.

Assess client’s muscle strength and gross and fine To identify risk for falls. Note: The frequency of
motor coordination falls increases with age and frailty level. Risk
factors for falls lie in four categories: 1.
Biological, 2. Behavioral 3. Environmental 4.
Socioeconomic. In each of these areas, some risk
factors can be modified to decrease the fall risk.
Consider hazards in the care setting and/or home Identifying needs or deficit provide opportunities
environment for intervention or intstruction.
Utilize chairs/bed alarms Alert when client is trying to get up alone

61
 Provide seat raisers for chairs, use of stand-assist, To prevent injury to both client and care provider.
repositioning or lifting devices as indicated
 DEPENDENT To identify high risk tasks, conduct site visits;
Refer to physical or occupational therapist as select, create and modify equipment and assistive
appropriate devices; and provide education about body
mechanics and musculoskeletal injuries in
addition to providing therapies as indicated.

Encourage participation in self-help programs, To enhance self-esteem and sense of self-worth.

such as assertiveness training, positive self-image.

Evaluation:

Goal met. After 8 hours of nursing intervention the patient was able to verbalize understanding
of individual factors that contribute to possibility of injury.

NURSING CAREPLAN #3

Assessment

62
 Subjective: “Mag lisod ko paghingas nan ako ra isa, magpa alalay ko sa ako anak” as
verbalized by the pt.

Objective:
 Fatigue
 Observe body malaise and discomfort
 Difficulty maintain balance

Nursing Diagnosis
Activity intolerance related to immobility

Planning

After 8 hours of nursing intervention the patient will be able to identify techniques to
enhance activity intolerance

Intervention

Nursing intervention Rationale

 INDEPENDENT
Note clients report of weakness, fatigue, pain, Symptoms may be a result of or contribute to
difficulty accomplishing tasks, and/ or insomnia. intolerance of activity
Note treatment related factors such as side effects Which can affect the nature and degree of activity
and interactions of medications intolerance
Increase exercise/activity levels gradually To conserve energy
Assist with activities and provide/monitor client’s To protect the client from injury
use of assistive devices (e.g. crutches, walker,
wheelchair, or oxygen tank)
Provide a positive atmosphere while This helps to minimize the frustration and
acknowledging the difficulties of the situation for rechannel energy.
the client
 DEPENDENT/COLLABORATIVE
Provide referral to other disciplines, such as To develop individually appropriate therapeutic

63
 exercise physiologist, psychological counselling/ regimens
therapy, occupational/physical therapies, and
recreation/leisure therapies, as indicated
Implement a physical therapy/exercise program in A collaborative program with short term
conjunction with the client and other team achievable goals enhances the likelihood of
members. success and may motivate the client to adopt a
lifestyle of physical exercise for the enhancement
of health

Evaluation:

Goal met. After 8 hours of nursing intervention the patient able to identify techniques to enhance
activity intolerance

64
 NURSING CAREPLAN #4

Assessment
Subjective: “Mag lisod nako mo lakaw nan ako ra isa” as verbalized by the pt.

Objective:
 Leg fractured
 Muscle strength 3/5
 Body malaise

Nursing Diagnosis

Risk for falls related to proprioceptive deficit

Planning

After 8 hours of nursing intervention the patient will be able to verbalized understanding
of individual factors that contribute to possibility of injury.

Intervention

Nursing intervention Rationale

 INDEPENDENT These affect the client’s ability to protect self
Note the client’s age, gender, developmental stage, and/or others, and influence choice of
decision making ability, and level of cognition/ interventions and teachings.
competence.

Assess client’s muscle strength and gross and fine To identify risk for falls. Note: The frequency of
motor coordination falls increases with age and frailty level. Risk
factors for falls lie in four categories: 1.
Biological, 2. Behavioral 3. Environmental 4.
Socioeconomic. In each of these areas, some risk
factors can be modified to decrease the fall risk.
Consider hazards in the care setting and/or home Identifying needs or deficit provide opportunities

65
 environment for intervention or intstruction.
Utilize chairs/bed alarms Alert when client is trying to get up alone
Provide seat raisers for chairs, use of stand-assist, To prevent injury to both client and care provider.
repositioning or lifting devices as indicated
 DEPENDENT To identify high risk tasks, conduct site visits;
Refer to physical or occupational therapist as select, create and modify equipment and assistive
appropriate devices; and provide education about body
mechanics and musculoskeletal injuries in
addition to providing therapies as indicated.

Encourage participation in self-help programs, To enhance self-esteem and sense of self-worth.

such as assertiveness training, positive self-image.

Evaluation:

Goal met. After 8 hours of nursing intervention the patient was able to verbalize understanding
of individual factors that contribute to possibility of injury.

66
 NURSING CAREPLAN #5

Assessment
Subjective: “Na fractured man gud ako right leg ugsa maglisod na ako pag panaw”
Objective:
 Muscle strength 3/5
 Impaired ability to walk required distances
 Fractured femur
Diagnosis

Impaired walking related to insufficient muscle strength

Planning

After 8 hours of nursing intervention the patient will be able move about within
environment as needed within limits of ability or with appropriate adjuncts.

Intervention

Nursing intervention Rationale

 INDEPENDENT For differential diagnosis and to guide treatment
Assist with or review result of mobility testing (e.g., interventions.
gait, timing of walking over fixed distance, walked
over set period of time [endurance].
Implement fall precaution for high risk clients. To reduce risk of accidental injury.
Identify appropriate resources for obtaining and To promote mobility.
maintaining appliances, equipment, and
environmental modification.
 DEPENDENT To assess client ability to ambulate safety.
Perform “Timed Up and Go (TUG)” test, as
indicated.
Consult with physical therapist, occupational For individualized mobility program and identify and
therapist, or rehabilitation team. develop appropriate devices.
Involve client/S.O in care, assisting them to learn To enhance safety for clients and S.O/caregiver.
ways of managing deficits.

67
Evaluation:

Goal met: After 8 hours of nursing intervention the patient was able to move about within
environment as needed within limits of ability or with appropriate adjuncts.

NURSING CAREPLAN #6

68
Assessment
Subjective: “Luja ako lawas” as verbalized by the pt.

Objective:
 Drowsiness noted
 fatigue
 body weakness noted
 Inability to maintain usual routines

Diagnosis

Fatigue related to Physiological condition

Planning

After 8 hours of nursing intervention the patient will be able to perform activities of daily
living and participate in desired activities at level of ability.

Intervention

Nursing intervention Rationale

 INDEPENDENT
Assess vital signs To evaluate fluid status and cardiopulmonary
response to activity.
Evaluate aspect of “learned helplessness” that Can perpetuate a cycle of fatigue, impaired
may be manifested by giving up. functioning, and increased anxiety and fatigue.
Note daily energy patterns This is helpful in determining pattern/timing of
activity.
Accept the reality of fatigue and do not For example clients with severe disease are prone
underestimate effect on client’s quality of life to more frequent and severe fatigue following
minimal energy expenditure and require a longer
recovery period than the usual
Encourage the use of assistive devices (ex. To extend active time/conserve energy for other
Wheeled walker. Wheelchair, Cane) as needed tasks

69
  DEPENDENT/COLLABORATIVE
Refer to comprehensive rehabilitation program, To improve stamina, strength, and muscle tone
physical/occupational therapy for programmed and to enhance sense of well being
daily exercises and activities
Provide supplemental oxygen as indicated The presence of anemia and hypoxia reduces
oxygen available for cellular uptake and
contributes to fatigue.

Evaluation:

Goal met. After 8 hours of nursing intervention, client was able to perform activities of daily
living and participate in desired activities at level of ability.

70
 NURSING CARE PLAN #7

Assessment

Subjective: “wala man siya’y gana mukaon tapos kung mukaon kay musuka man dayon” as

verbalized by the SO

Objective:

weight loss of .55kg after 2 days (from 49kg)

Vomiting

Weakness ( Muscle strength 4/5 )

Decreased appetite

Normal BMI for adult 18.5-24)

Patient BMI: 18 (underweight)

Nursing Diagnosis: Imbalanced Nutrition: less than body requirements related to inability to

ingest or digest food and inability to absorb nutrients.

Planning: Within 2 hours of rendering my nursing intervention the patient will be able to: a)

Verbalize food preference which is not contraindicated to his underlying disease to promote good

appetite. b) Improve appetite from poor to fair by eating ½ share from ¼ share and reduce the

occurrence of vomiting.

71
 Nursing Intervention Rationale
INDEPENDENT

Use flavoring agents To determine enhance food satisfaction and

stimulate appetite
Encouraged client to choose foods. Have To stimulate appetite.

family members bring foods that seen

appealing (which are not contraindicated)

Promote pleasant, relaxing environment, To enhance food intake

including socialization when possible.

Prevent/minimize unpleasant odors To reduce the occurrence of nausea and

vomiting.
Dependent
Administered medication (metoclopramide 1 To decrease the occurrence of vomiting.

ampule IVTT), as ordered

1. Collaborative
Referred to dietician for modification of diet To gradually stimulate appetite for fast

(General Liquids) recovery

Evaluation: Goal met within 2 hours of rendering nursing intervention the patient was able to

verbalize food preference which are not contraindicated to hr underlying disease to promote

good appetite. b) Improve appetite from poor to fair by eating ½ share from ¼ share and reduce

the occurrence of vomiting.

Nursing Care Plan # 8

Assessment

Objective:

Irritable

Fatigue

72
 Itching

Anxiety

Nursing diagnosis: Self-Care Deficit related to in ability to perform activities of daily living

Planing: Within 2 hours of rendering my nursing intervention the patient will be able to perform

self-care activities within level of his own ability.

Nursing Intervention Rationale

Independent
Performed or assessed with meeting client’s Personal care assistance is part of nursing care and

needs should not be neglected while self care

independence is promoted and integrated.

Bathed or assessed client in bathing, providing for Type and purpose of bath is determined by

any or all hygiene needs as indicated individual need.

Obtained hygiene supplies for specific activity to To provide visual cues and facilitate completion of

be performed and place in the SO easy to reach activity.

Certain individuals ( especially infants, the

Provided for adequate warmth. elderly, and very thin or debilitated persons are

prone to hypothermia and can experience

evaporative cooling during and after bathing.

Determined that client can perceive water To prevent chilling and burns.

temperature, adjust water temperature safely.

Assessed client in and out of shower or tub as To promote safety of the patient

indicated
Use adaptive clothing as indicated ( e.g., clothing These may be helpful for client with limited arm

with front closure, wide sleeves and pant legs. or leg movement or impaired fine motor skills.

73
Evaluation: Within 2 hours of rendering my nursing intervention the patient was be able to

performed self-care activities within level of his own ability.

DISCHARGE PLAN
MEDICATIONS:

 Take medication exactly as directed.

 Inform the S.O about the possible side effects of the medications.
 Continue taking the medicines prescribed by the physician such as:
 Omeprazole 40mg 1 cap OD
 Metoclopromide 2mg/ampule q 8 hours
 BUSCOPAN 10mg TID
 Rebamipide 100mg/ 1 tab TID
 Advised patient don’t skip doses

74
  Continue taking antibiotics as directed until they are all gone.

ENVIRONMENT

 Advice patient or SO by providing quiet environment, and avoiding stressful Situation.

 Advice patient to avoid contaminated area.
 Advice S.O to clean up the room regularly
 Advice patient smell fresh air such as: go to beach.
 Avoid polluted area.

TREATMENT

 Instructed patient to follow proper instructions medications prescribed by the

physician.
 Comply with medication.
 Increased fluid intake
 Observe adverse effect that need to report such as: dizziness, fatigue, headache.

HEALTH TEACHINGS

Activities

 Bed rest upon arrival at home from the hospital.

 Light exercise every morning.
 Eventually the patient can return to its normal activities of daily living.
 Clinic appointment schedule
 Understanding and knowing what to do with side effects of medications.

Hygiene

 Encourage personal hygiene regularly

 Proper handwashing is necessary
 Bath regularly
 Oral care
 Perineal care

75
OPD- FOLLOW-UP:

 Instruct patient to follow scheduled check up

 Instruct patient to seek medical attention when adverse reactions and sign and symptom
occurs.

DIETARY MANAGEMENT:

 Maintain high fiber and low fat and sugar diet

 Eat more fruits and vegetables to facilitate easy bowel movement.
 Drink several glasses of water a day.
 Eat a balance diet so your body can work its best and heal quickly.

 Increase oral fluid intake: To prevent dehydration.

 Avoid juices and coffee, To prevent abdominal pain

 Light soups, toast, rice and eggs are good foods; eat foods high in fiber and

carbohydrates.

SPIRITUAL

 Encourage patient to be more faithful and have trust in God

 Encourage SO to pray for the patient’s early recovery.
 Spiritual counseling
 Anger management
 Supportive counseling

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 APPENDICES

Summary of IVF

Date # of Solution Volume Additive Rate of Time

Bottle Drop
09/21/19 1 1L PNSS 80 cc/hr 07:00 pm

09/22/19 2 1L PNSS 80 cc/hr 07:00 am

77
09/23/19 3 1L PNSS 80 cc/hr 07:00 pm

09/24/19 4 1L PNSS 80 cc/hr 10:00 am

78
 Summary Vital Signs

Date Time BP PR RR Temp

09/21/19 8 pm 110/80 66 18 36
12 mn 110/80 70 20 36.5
4 am 120/70 72 20 36.6
09/22/19 8 am 110/80 62 18 36.5
12 nn 120/70 70 28 36.8
4 pm 120/70 66 18 36.7
8 pm 110/70 63 20 37.7
12 mn 100/80 64 20 36.5
4 am 120/70 80 20 37.6
09/23/19 8 am 110/70 73 18 36.7
12 nn 120/70 81 20 37.2
4 pm 110/80 64 20 36
8 pm 110/80 75 20 36.5
09/24/19 12 mn 120/80 62 18 36.3
4 am 120/70 81 20 36.1
8 am 120/90 88 20 36.5
12 nn 120/80 87 18 36.3

I AND O SHEET

Date IVF Oral Total Urine Total Output

79
 Credit Consumed fluid Take Output Vomitu Bm

take n s

n
9/21/19

7am7p 340 1160 120 1280 1050 2x 2x 1050+2x BM

m
450 890 200 1090 1500 1x 1x 1500/2550

7pm7a

9/22/19

7am7p 800 790 400 1190 1400 2x 3x 1400+3x BM

m
200 600 400 1000 1650 - - 1650

7pm7a

m
9/23/19

7am7p 600 600 200 800 3600 - - 3,600

m 600 -
180 700 400 1900 2x 4200+1x BM

7pm7a

m
9/24/19

80
7am7p 600 500 1000 1200 1500 - 2x 2300+5x BM

m
7pm7a 900 650 600 1280 1800 - 2x 1800+1x BM

81
 CFAC

COLOR FREQUENCY AMOUNT CHARACTERISTICS

09/21/19 BLACK 2X MEDIUM MUCOID WITH
(7AM) BLOOD STREAK
09/21/19 BLACK 2X FEW MUCOID WITH
(7PM) BLOOD STREAK
09/22/19 BLACK 1X MODERATE MUCOID

(7AM)
09/22/19 YELLOW 2X MODERATE SOFT

(7PM)

GENOGRAM

82
 78 y/o
62y/o
HTN
Liverchirrosis
Deceased
Deceased

37 y/o

A&W

81 y/o
78 y/o
With Peptic
Ulcer Disease With Diabetes

Deceased

38 y/o
32 y/o
A&W 28 y/o
A&W
A&W

LEGENDS:

83
Mother HTN, Deceased

Father Liverchirrosis, Deceased

Patient’s with Peptic Ulcer Disease

Patient’s Husband with Diabetes

Patients Son, Alive & Well

LE
Patients Daughter, Alive & Well
GE

LE Patients Daughter, Alive & Well

GE

REFERENCES

84
 Books

 Medical Surgical Nursing 10th edition by Brunner and Suddarth

 Nurse’s Pocket Guide 14th edition by Doenges, Moorhouse and Murr.
 Davis’s Drug Guide for Nurses 11th
Journals / Articles
 Maysoun Freij, et. al. (2017) Clinical Decision Support for Peptic Ulcer Disease
 Manolito L. Chua, M.D., et. al., (2010) Philippine Clinical Practice Guidelines on the
Diagnosis, Empiric Management, and Prevention of Peptic Ulcer Disease
 Clinical Infectious Diseases, Volume 31, Issue 4, October 2000, Pages 1066–1078
 https://medlineplus.gov/ency/article/000145.htm?
fbclid=IwAR2EUNZI_y2cz9L97VqnDsb9mJcXj4aIHJYOGbhu5P2yoWZboiGzxUAIem
8 Peptic Ulcer Disease
 Electronic Sources
 https://www.cedars-sinai.org/health-library/diseases-and-
conditions/c/PepticUlcerDisease-adults.html?
fbclid=IwAR2EUNZI_y2cz9L97VqnDsb9mJcXj4aIHJYOGbhu5P2yoWZboiGzxUAIem
8-Pepticulcerdisease
 World Health Organization 2005( A manual for Physicians and other Senior Health
Workers by Ellis D. Avner, MD page 40-41 Chapter 3 Vol. 1 15th edition)
 Centers for Disease Control and Prevention or CDC(Gastroenteritis outbreaks in Health
Care Settings by Kurt B. Stevenson, MD page 55-58 Chapter 22 volume 1 7th Edition)
 Baby and Child Health Care by Dr. Miriam Stoppard page 140 volume 1 3rd edition

85