Gatrointestinal Diseases Manuscript

GASTROINTESTINAL
DISEASES

A Manuscript Presented to the
Faculty of the Nursing Department
San Pedro College, Davao City
Mrs. Jocelyn Cataraja, RN, MN

In Partial Fulfillment of
the Requirements in
Seminar in Nursing 101

Submitted By:
James Nathaniel G. Abedejos, St. N
Nicole Anne M. Alcober, St. N
Tristan Jay M. Amoroso St. N
Maria Ana Cecilia B. Arendain, St. N
John Daniel L. Arguelles St. N
Kristine Joy V. Billones, St. N.
Sachi Megan I. Cang, St. N
Jamie Stefanie G. Chiu St. N
Joennielle Clark I. Colegado, St. N
Laetexia Ysabelle G. Dujon St.N
Vianah Eve A. Escobido, St. N
Justin Joshua C. Espinas, St. N.

March 11, 2022
TABLE OF CONTENTS
PEPTIC ULCER DISEASE…………………………………………………………… 5
Introduction……………………………………………………………………….. 5
Objective………………………………………………………………………….. 6
Definition…………………………………………………………………………. 7
Anatomy and Physiology………………………………………………………... 9
Etiology …….……………………………………………………………………... 13
Symptomatology………………………………………………………………… 18
Schematic Diagram of pathophysiology………………………………………. 24
Narrative of pathophysiology……………………………………………. 26
Diagnostic Laboratories…………………………………………………………..29
Surgical Management…………………………………………………………… 30
Medical Management……………………………………………………………. 30
Nursing Management……………………………………………………………. 49
Related Literature………………………………………………………………… 52
GASTROESOPHAGEAL REFLUX DISEASE…….…………………………………. 55
Introduction……………………………………………………………………….. 55
Objective……………………………………………………………………………56
Definition………………………………………………………………………… 56
Anatomy and Physiology………………………………………………………...57
Etiology……………………………………………………………………………. 62
Symptomatology…………………………………………………………………. 66
Narrative of pathophysiology…………………………………………… 71
Medical Management……………………………………………………………..76
Related Literature……………………………………………………………….. 94
GASTROENTERITIS.………………………………………………………………… 96
Introduction………………………………………………………………………. 96
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Definition………………………………………………………………………… 96
Anatomy and Physiology……………………………………………………….. 97
Etiology……………………………………………………………………………. 98
Symptomatology…………………………………………………………………. 100
Narrative of pathophysiology……………………………………………. 103
Medical Management……………………………………………………………. 105
Nursing Management…………………………………………………………… 112
Related Literature……………………………………………………………….. 118
CROHN’S DISEASE……………………………………………………………………. 121`
Introduction……………………………………………………………………….. 121
Objective…………………………………………………………………………. 123
Anatomy and Physiology…………………………………………………………124
Etiology…………………………………………………………………………….125
Symptomatology…………………………………………………………………. 130
Diagnostic Laboratories…………………………………………………………. 139
Medical Management…………………………………………………………… 147
Related Literature…………………………………………………………………166
ULCERATIVE COLITIS…………………………………………………………………. 169`
Introduction……………………………………………………………………….. 169
Objective…………………………………………………………………………. 170
Etiology…………………………………………………………………………….176
Symptomatology…………………………………………………………………. 180
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HEMORRHOIDS…………………………………………………………………………. 234
Introduction………………………………………………………………………. 234
Objective………………………………………………………………………… 236
Definition…………………………………………………………………………. 237
Etiology…………………………………………………………………………….241
Symptomatology…………………………………………………………………. 244

REFERENCES……………………………………………………………………………278
ASSIGNED TOPICS…………………………………………………………………….. 297

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PEPTIC ULCER DISEASE
Introduction

The endocrine system, which is made up of all of the body's hormones, regulates
all biological processes in the body from conception to adulthood and beyond. It is
comprised of glands that create and secrete hormones, which are chemical messengers
that regulate a variety of physiological functions and activities. This includes metabolism,
which is a chemical reaction or process required for life, such as the conversion of food
into energy. As a result, the digestive tract is the body's biggest endocrine-related organ
system (Hormone Health Network, 2019). This case study will focus on health issues
including the endocrine system, gastrointestinal system, and metabolism, all of which are
essentially interrelated.
The damage to the gastrointestinal tract caused by peptic acid or digestive juices
is known as a peptic ulcer. A thick coating of mucus protects the digestive tract;;
nevertheless, various conditions can cause this protective layer to decrease, allowing
peptic acid to injure the digestive tissues, resulting in a sore or ulceration. It could be a
gastric ulcer, with the ulceration occurring in the stomach lining. It's marked by a gnawing
or searing ache that occurs shortly after eating. If it happens in the duodenum, however,
it is a duodenal ulcer, with pain lasting 2-3 hours after meals. Finally, it's known as an
esophageal ulcer if it affects the esophagus (Felman, 2017). It can lead to consequences
if left untreated. Internal bleeding can occur in rare instances, resulting in a slow or
significant blood loss. It can also be perforated, causing infection by creating a hole in the
stomach or small intestine lining (Higuera, 2020).
Peptic ulcer disease is still a common health problem around the world.
Nonetheless, statistics show that it has been less common in recent years. The condition
affects 4.6 million people in the United States each year. It is also found in 11-14 percent
of males and 8-11 percent of women during the course of their lives (Anand, 2020). In a
global survey conducted in 2018, Spain was shown to have the highest incidence of peptic
ulcer disease, with 141.9 per 100,000 people affected annually. In terms of complications,
the highest rate of bleeding peptic ulcer disease per 100,000 people per year was 79.70
per 100,000 people per year in Spain. Furthermore, the United Kingdom has the grea5test
5

rate of perforated complications, with 12.17 per 100,000 people per year (Hassan et al.,
2018).
Meanwhile in the Philippines, According to the Department of Health's 2018
Philippine Health Statistics, peptic ulcer caused 5,258 deaths across all ages, affecting
5% of the population. According to the 2018 Regional Social and Economic Trends Davao
Region study, the same ailment killed 269 people in Davao Region in 2016. Data on
current morbidity cases in the country is either out of date or unavailable.
With the aforementioned introduction, this case study would be an excellent
opportunity for the student nurses to hone their skills and put their knowledge to use,
contributing to the overall body of nursing education. This would also help gain a better
understanding of the disease and their function as a nurse at the hospital with people who
are in vulnerable positions, in line with enhancing our critical thinking, reasoning skills,
and application of nursing interventions in the capability of the nurses. This case study
could be used as a reference for future research on Peptic Ulcer Disease, as well as
assisting the student in becoming a more effective nurse in the future

Objectives
This case study would let the student nurses, will be able to garner and enhance
sufficient knowledge and understanding from the comprehensive case analysis in line
with Peptic Ulcer Disease;; including its etiology and symptoms, aligning it with the
different nursing theories and management which would be applicable to the given
condition which in turn would help us render the appropriate and relevant nursing
interventions. apply time management and goal setting skills, and develop a sense of
optimism and commitment in the case.

Specifically, the student nurses aims to:
a) Present the definition of the endocrine system and the gastrointestinal tracy, the
assigned case, and the nursing implications that are in line with the case;;
b) formulate the objectives which are specific, measurable, attainable, realistic and
time-bounded
c) identify etiology and symptomatology of Peptic Ulcer Disease;;
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d) create a schematic diagram that represents the disease process of Peptic Ulcer
Disease;;
e) discuss the pathophysiology of Peptic Ulcer Disease;;
f) identify the medical, surgical and nursing management for Peptic Ulcer Disease;;
g) describe the prognosis of the client with Peptic Ulcer Disease;;
h) create a relevant discharge planning for the client Peptic Ulcer Disease using
METHOD approach;;
i) relate significant nursing theories applicable for the management of Peptic Ulcer
Disease;;
j) show a summary on relevant related literature that help support the case analysis
and;;
k) cite references using the APA format

DEFINITION OF DIAGNOSIS
Peptic Ulcer Disease
The lining of the lower half of the esophagus, the stomach, or the upper part of the
small intestine has broken down. When the cells on the exterior of the stomach lining
become inflamed and die, peptic ulcers occur. Helicobacter pylori bugs and certain
medications, such as aspirin and other nonsteroidal anti-inflammatory drugs, are the most
common causes (NSAIDs). Cancer and other disorders may be associated to peptic
ulcers (National Cancer Institute, 2022).
Because of gastric acid secretion or pepsin, peptic ulcer disease is defined by a
discontinuity in the inner lining of the gastrointestinal (GI) tract. It penetrates the gastric
epithelium's muscularis propria layer. It most commonly affects the stomach and proximal
duodenum. The lower esophagus, distal duodenum, or jejunum may be affected (Singh,
Gnanapandithan & Malik, 2021).
Peptic ulcer disease (PUD) is a break in the stomach's inner lining, the first section
of the small intestine, or the lower esophagus in some cases. A gastric ulcer is one that
occurs in the stomach, while a duodenal ulcer occurs in the first part of the intestines
(Najm, 2011).
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Gastric Ulcer
Stomach ulcers (also known as gastric ulcers) are open sores that form on the
stomach lining. Ulcers can also develop just beyond the stomach in the intestine. They
are commonly called duodenal ulcers.
Stomach ulcers, also known as gastric ulcers, are painful lesions on the lining of
the stomach. Peptic ulcer disease includes stomach ulcers. Any ulcer that affects both
the stomach and the small intestine is known as a peptic ulcer. When the thick coating of
mucus that protects your stomach from digestive fluids is weakened, stomach ulcers
develop. This permits the digestive acids to eat away at the stomach's lining tissues,
resulting in an ulcer (Johnson, 2018).
Esophageal Ulcer
An esophageal ulcer is a breach in the mucosal border of the esophagus.

Gastroesophageal reflux disease or severe persistent esophagitis from other sources are
common causes of mucosal injury to the esophagus (Chiejina &Samant, 2021)
A peptic ulcer is a form of esophageal ulcer. It's a painful sore in the lining of the
lower esophagus, near the esophagus's junction with the stomach. The tube that
connects your throat to your stomach is your esophagus. Esophageal ulcers are usually
caused by an infection with the Helicobacter pylori bacteria. Erosion from stomach acid
traveling up into the esophagus can also cause it. Other diseases such as yeast and
viruses can cause esophageal ulcers in some circumstances (Cafasso, 2020).
Duodenal Ulcer
A duodenal ulcer is a lesion that develops in the duodenum's lining. The duodenum
is the initial section of the small intestine, the section of the digestive system through
which food passes immediately after leaving your stomach. Ulcers can develop in both
the stomach and the duodenum (Harding, Kwong, Roberts, Hagler, & Reinisch, 2022).
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When the surface of the duodenum's mucosa is disrupted, duodenal ulcers
develop. Peptic ulcer disease, which affects the stomach and the early section of the
duodenum, causes these ulcers (Quinones & Woolf, 2021).
ANATOMY

Gastrointestinal (GI) Tract
The gastrointestinal (GI) tract's optimal functioning is important for the overall
health and wellbeing. Many chronic health problems can be caused by a non-functioning
or poorly-functioning GI tract, which can have a negative impact on the quality of life. The
digestive system, often known as the gastrointestinal tract, is responsible for breaking
down the foods that a human consumes, releasing nutrients, and absorbing those
nutrients into the body. Although the small intestine is the system's essential part,
performing the majority of digestion and absorbing the majority of released nutrients into
the blood or lymph, each of the digestive system organs plays an important role in the
process.
The gastrointestinal system is basically a long tube that runs through the body,
with specialized parts capable of digesting food introduced at one end, extracting any
useful components, and eliminating waste items at the other. Furthermore, the entire
system is controlled by hormones, with the presence of food in the mouth initiating a
cascade of hormonal responses;; when food is present in the stomach, several hormones
stimulate acid production, enhanced gut motility, enzyme release, and many other
9

functions. The nutrients from the GI tract are not digested on the spot;; instead, they are
transported to the liver, where they are further broken down, stored, and distributed.

Esophagus
The esophagus is a long muscular tube that transports food from the mouth to the
stomach. The pharynx is the throat cavity from which the esophagus originates. Food is
ingested as bolus and passes down the esophagus after it has been chewed and
combined with saliva in the mouth. The esophagus contains a stratified squamous
epithelial lining that protects it from trauma, and the submucosa secretes mucus from
mucous glands to help food pass down the esophagus. The esophagus' lumen is
bordered by layers of muscle, which are voluntary in the upper third and involuntary in the
lower third. Following that, from the pharynx, the food will be pushed into the stomach by
waves of muscle movement known as peristalsis.

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Stomach
The stomach is a muscular, hollow pouch located in the upper gastrointestinal
system. It has two openings - the esophageal and duodenal - and four parts, the cardia,
fundus, body, and pylorus. Each region has a different purpose: the fundus gathers
digestive gases, the body secretes pepsinogen and hydrochloric acid, and the pylorus
secretes mucus, gastrin, and pepsinogen. Within the stomach, the bolus is combined with
digestive acids, which speeds up the breakdown of the bolus, and turns it into a slimy
mess called chyme. The chyme then moves to the small intestine, where it absorbs
nutrients.
Small Intestine
The small intestine is where the majority of chemical and mechanical digestion
takes place, as well as nearly all of the absorption of beneficial nutrients. The absorptive
mucosal type lines the whole small intestine, with minor variations for each section. The
smooth muscle wall of the intestine contains two layers, and rhythmical contractions force
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digestive products through the intestine (peristalsis). The small intestine is divided into
three sections;;

1. Duodenum - The duodenum is the first section of the small intestine, and it is
thought to be the main site of iron absorption. It forms a 'C' shape around the head
of the pancreas. Here, the digestive juices from the pancreas (digestive enzymes)
and the gallbladder (bile) mix together. Proteins and bile are broken down by
digestive enzymes, while lipids or fats are emulsified into micelles. Its primary
function is to neutralize the acidic gastric contents (known as 'chyme') and
stimulate further digestion;; Brunner's glands in the submucosa release an alkaline
mucus that neutralizes the chyme while also protecting the duodenum's surface. It
also produces bicarbonate and pancreatic juice, both of which help the stomach
neutralize hydrochloric acid.
2. Jejunum - The jejunum connects the duodenum with the ileum in the midsection
of the intestine. It has plicae circulares and villi to enhance the surface area of the
GI tract in that area.
3. Ileum - The ileum has villi, which absorb all soluble molecules into the bloodstream
(through the capillaries and lacteals). The jejunum and ileum are two coiled
portions of the small intestine that are about 4-6 meters long when combined;; the
junction between the two is not well-defined. The mucosa of these sections is
highly folded (the folds are called plicae), increasing the surface area available for
absorption dramatically.
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The epithelial surface of the plicae is further folded to form villi. The surface area
of the small intestine is increased even further, and the surface of each villus is covered
in microscopic microvilli to maximize surface area—the area available for absorption is
vast. Each villus has its own blood supply- the vessels can be seen in the submucosa-
and blood containing digestive products from the small intestine is taken to the liver via
the hepatic portal system. The double muscle layer moves food through the intestine by
peristalsis.

ETIOLOGY
PREDISPOSING FACTORS RATIONALE
Advance Age (65 <) Because arthritis is so common in this age
demographic, it's been associated with a
higher intake of NSAIDs, which are
medicines that undermine the stomach's
protective barrier. As a result, gastric acid
has an easier time penetrating and
damaging the digestive tissues, resulting
in ulceration (Felman, 2017).
Blood Type (O) Helicobacter pylori, the most common

cause of peptic ulcers, has a strong affinity
for the H antigen of blood group O
produced in the gastric mucous membrane
(Teshome et al., 2019)
Family History Usually a significant number of people who

suffer from peptic ulcers have relatives
who also suffer from the condition.
Although more research is needed, it has
been linked to the genetic trait familial
hyperpepsinogenemia type I, which
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causes excessive pepsin secretion
(Anand, 2020).
Genetic Factor Peptic ulcer disease is inherited as a

multifactorial trait. Genetic factors may
possibly play a role in the etiology of peptic
ulcer disease. However, the inheritance
pattern is not simple mendelian, and the
genetic basis is complex, According to
some research, family and twin studies,
and numerous genes may be implicated in
its pathogenesis (Malaty, 2000)
PRECIPITATING FACTORS RATIONALE
Helicobacter pylori Infection These bacteria live in the digestive tract's
lining, creating inflammation and
weakening the body's defensive
mechanism, allowing acid to pass through.
They also generate urease, an enzyme
that neutralizes stomach secretions and
makes them less acidic. To compensate,
the stomach generates extra acid, causing
irritation of the stomach lining and ulcer
formation (Felman, 2017)
NSAIDs NSAIDs work by inhibiting enzymes

involved in the formation of prostaglandins,
which relieves pain. Prostaglandins, on the
other hand, are essential in the stomach's
protective barrier. When they are reduced,
the body's defenses against stomach
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acids are suppressed, resulting in
digestive tissue damage and inflammation,
leading to ulceration. It can burst the
capillary blood vessels in the mucosal
lining, leading in bleeding in some
circumstances (Tresca, 2019).
Excessive Alcohol Intake More gastric acid is produced when you

drink too much alcohol. Alcohol in itself is
a risk factor for developing a peptic ulcer.
It can irritate the gastrointestinal mucosa
over time, resulting in inflammation and
ulcers, significantly raising the likelihood
of developing an ulcer (Vertava Health,
2020).
Smoking Cigarette smoking hastens gastric

emptying, increases acid secretion, and
decreases pancreatic bicarbonate
synthesis, which is useful in neutralizing
excess stomach acid, according to a study
(Anand, 2020). Smoking has a mixed
influence on stomach acid output, but it
does have other effects on upper
gastrointestinal function that may
contribute to peptic ulcer disease
development.
Chronic Stress To aid in the digestion of food, the stomach
secretes acid. A person may get ulcer
symptoms if the acidic environment in the
stomach changes or becomes overly
15

acidic. Changes in the body's pH can
cause ulcers in those who are under a lot
of physiological stress. Also, Regardless of
H. Pylori infection, psychological stress
increased the risk of peptic ulcers. NSAID
usage or H. pylori infection. Part of the
increase could be attributed to stress
impacting health risk behaviors linked to
the development of peptic ulcers (Sethi,
2019).
Physical Stress;; Physical stress is thought to be the cause
a) Severe Burns of the ulcer that is commonly referred to as
b) Surgical Procedures a stress ulcer. These physical stresses
c) Increased Intracranial Pressure may come in the form of severe burns,
d) Injury to the Central Nervous some surgical procedures, increased
System intracranial pressure and injury to the
central nervous system (Marcin, 2018).
Severe burns can result in decreased
plasma volume, ischemia, and cell
necrosis of the stomach mucosa, resulting
in a Curling ulcer. Meanwhile, some
surgeries may trigger the need for NSAIDs
and can alter the gastrointestinal function
post surgery. Furthermore, any injury or
brain condition that raises intracranial
pressure can create a Cushing ulcer, in
which the vagus nerve is overstimulated,
resulting in excessive stomach acid output
(Anand, 2020).
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ASSOCIATED HEALTH CONDITIONS
Zollinger Edison Syndrome (ZES) Zollinger-Ellison syndrome is an

uncommon digestive illness characterized
by excessive stomach acid production.
Peptic ulcers in the stomach and intestine
can be caused by too much gastric acid
(John Hopkins Medicine, 2022). The
growth of gastrinomas, which can produce
excessive amounts of gastrin, resulting in
an overproduction of stomach acid, is a
feature of ZES (Christiano, 2017).
Cirrhosis Peptic ulcers are more common in

individuals with liver cirrhosis, are
connected with cirrhosis severity, and
occur without upper abdominal pain in up
to 70% of patients, with consequences in
the remaining 29% (Siringo, 1997). The
ulcerogenic drugs taken can be blamed for
the increased risk of peptic ulcer.
Furthermore, coagulation problems might
lead to bleeding issues (Lu et al., 2019).
Chronic Kidney Disease (CKD) Hemodialysis patients face a risk that is

about ten times higher than people without
CKD. Patients with chronic kidney disease
(CKD) have a higher chance of developing
peptic ulcers (Charnow, 2014). Patients
with CKD who receive hemodialysis
experience inflammatory conditions and
oxidative stress;; also, the drugs used in
17

therapy, such as anticoagulants, might
harm or worsen the digestive system,
increasing the risk of peptic ulcers (Kim et
al., 2019).

Symptomatology
SIGNS AND SYMPTOMS RATIONALE
Anemia Internal bleeding can occur if peptic ulcers

are not addressed. Bleeding can take the
form of slow blood loss, which can lead to
anemia, or catastrophic blood loss, which
may necessitate hospitalization or a blood
transfusion. A bleeding ulcer can lead a
gradual loss of blood.This would
eventually lead to a shortage of red blood
cells and the body's hemoglobin (Berry,
2017)
Fatigue As a result of the increased absence of

blood circulation in the body, tissues and
muscles do not receive enough oxygen,
robbing them of energy, resulting in
weakness and weariness (Brown, 2020).
Syncope Syncope can occur when your blood

pressure drops suddenly, your heart rate
drops, or the amount of blood in different
parts of your body fluctuates. The body
may experience hypotension as a result of
severe blood loss from a bleeding peptic
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ulcer, and less blood will be circulating to
the brain, resulting in syncope or fainting
(Higuera, 2020).
Pallor, Cold and Clammy Skin Similarly, the extremities will turn pale and
lose their warmth due to a lack of
circulating hemoglobin, which is
responsible for the blood's red color
(Brown, 2020)
Melena Peptic ulcer disease, in which painful

ulcers or sores develop in the stomach or
small intestine, is the most prevalent cause
of melena. Melena is the black, tarry stool
passage. The stool may seem black, tar-
like, and sticky if the ulcer has produced
bleeding. The enzymes that break down
and digest the blood as it passes through
the gastrointestinal system are
responsible for this (Cheung, 2020)
Hematesis Hematemesis is the vomiting of blood,

which can be bright red or have a coffee-
ground appearance. Bleeding from the
upper gastrointestinal tract is the cause of
this. This happens when a peptic ulcer has
already injured a blood vessel (Kahn,
2019). Around 60% of cases of
haematemesis are caused by gastric
ulcers. Ulceration can cause erosion of the
blood vessels that supply the upper GI
tract (most typically on the lesser curve of
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the stomach (20%) or the posterior
duodenum (40%), resulting in substantial
bleeding.
Abdominal Distention Infection with H. pylori causes a lot of

peptic ulcers. The bacteria Helicobacter
pylori is a common but potentially deadly
pathogen. Excess gas production might
cause bloating if there are too many
bacteria in your small intestine.
Furthermore, because ulceration is an
injury, inflammation and thick tissue or
scarring may develop over time, causing
the pyloric sphincter to become blocked,
making it difficult for food to pass through
the digestive tract (Higuera, 2020).
Loss of Appetite Individuals with peptic ulcers may develop

an aversion to eating as a result of the
extreme discomfort they experience during
or after eating, as well as bloating (Felman,
2017). Additionally, when your stomach
lining is damaged, scar tissue grows,
obstructing the food passageway and
perhaps causing swelling in the small
intestines.
Unexplained Weight Loss Weight loss is inevitable if patients with

peptic ulcers lose their appetite
completely. Furthermore, due to the
inflammation that stomach ulcers cause,
they can sometimes cause a blockage in
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the digestive tract. This can cause weight
loss and a decrease in appetite by
preventing food from flowing through your
stomach.
Abdominal Pain Acid in the digestive tract eats away at the
inner surface of the stomach or small
intestine, causing peptic ulcers. The acid
might cause an open sore that is
uncomfortable and may bleed. Severe
abdominal pain, with or without bleeding,
could suggest an ulcer perforation through
the stomach or duodenum.
Gnawing & Burning Chest Pain or The strong gastric acid will come into
Heartburn contact with the excavated area of the
mucosal lining, generating a burning
sensation from the navel to the chest
(MacGill, 2018). This is often
misdiagnosed as heartburn. Heartburn is a
symptom that occurs when stomach acid
rises into the esophagus. This causes a
burning sensation beneath your
breastbone or in your upper abdomen.
Feeling of Fullness When the lining of your stomach is

damaged, scar tissue grows, obstructing
the food passageway and possibly causing
swelling in the small intestines. This will
make you feel full despite the fact that you
haven't eaten anything (West
Gastroenterology Medical Group, 2019)
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22

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Narrative
The imbalance of the Gastrointestinal tract’'s aggressive and defensive factors
causes peptic ulcer disease to progress. When one shifts improperly, the body reacts in
an unfavorable way. Predisposing factors (Age, Family History, and Blood Type O) and
precipitating factors (Helicobacter pylori, NSAIDs, Existing Health Conditions, Lifestyle,
and Physiologic Stress) contribute to this imbalance. H. Infection with Helicobacter pylori
can be spread by ingesting infected water, food, or utensils. It has an adhesion property
that allows it to adhere to the mucosa, particularly the foveolar cells. This triggers the
release of an enzyme called protease that breakdowns tissue in the stomach which also
triggers the increased release of gastrin and decreases the somastotatin production.
Together they gradually cause damage to the mucosal cells, they may cause abdominal
pain, loss of appetite and bloating. Another process that are responsible for the disruption
of mucosa are alcohol abuse, smoking and NSAIDs. Long-term use of nonsteroidal anti-
inflammatory drugs (NSAIDs) can cause damage to the stomach mucosa. NSAIDs work
by inhibiting the enzyme cyclooxygenase, which is responsible for the production of
inflammatory prostaglandins. Prostaglandin stimulates mucus formation and bicarbonate
synthesis, which protects the mucosa from gastric acid. Low mucus and bicarbonate
production also translates to a weak protective barrier against hydrochloric acid contact
with the mucosa layer. Because HCL is recognized for digesting or breaking down protein,
it irritates the mucosal layer. Lastly, the vagal stimulation triggers the release of acid and
pepsinogen, this leads to an increase gastric production in which an increase gastric acid
secretion is stimulated, this causes signs and symptoms such as gnawing & burning chest
pain or heartburn and abdominal pain/ Together these 3 factors causes an irritation of the
mucosal layer which furthers damages and erodes the mucosal barrier. As hyperacidity
develops, so does Ulcerations which leads to Peptic Ulcer Disease, excess stomach acid
production can cause mucosal layer irritation and, later, ulcerations.. The decrease in
functionality of the stomach mucus leads to the development of open sores in the stomach
lining, this peptic ulcer disease is called Gastric Ulcer. Meanwhile, the breach in the
mucosal border of the esophagus causes painful sores to develop in the lower lining of
the lower esophagus, this in turns develop Esophageal Ulcers. Lastly, when the surface
mucosa of the duodenum is disrupted, duodenal lesions form in the early section of the
24

duodenum lining, this causes what we call Duodenal Ulcer. Together, gastric ulcer,
esophageal ulcer and duodenal ulcer forms peptic ulcer disease. These ulcers develops
gradual bleeding and hemorrhage as they progress, this leads to a decrease hemoglobin
and a decrease oxygen carrying capacity. They form the generalized and different signs
and symptoms that vary from each other. When you have ulcers, you will have pain, which
is defined by epigastric or abdmonial pain. When the ulceration reaches the muscularis
layer of the stomach, where muscle tissues and blood arteries are present, bleeding
manifests itself as melena and hematemesis. Furthermore, anemia, fatigue, syncope and
pallor develops through gradyal bleeding followed by loss of appetite, feeling of fullness
and unexplained weight loss. Healing of the tissues from the ulcerations results to
scarring;; if this scarring thickens especially on the pyloric sphincter it can cause a
blockage. This blockage resulting to obstruction in the passageway of the gastric
contents can cause an accumulation and build-up of gastric contents. Fullness of the
stomach result to nausea and vomiting. If treated, diagnostic tests are performed such as
physical examination, endoscopy, urea breath test, serologic testing, stool antigen,
gastrin test, barium swallow. With diagnostics done, management follows;; for surgical,
patients go through elective surgery, followed by vagotomy, pyloroplasty, antrectomy,
truncal vagotomy-antrectomy. For the medical management;; administration of antacids,
histamine blockers, proton pump inhibitors, antibiotics, mucosal protective agents are
administered to treat PUD. These treatments slows down the progression of the disease
and decreseas ulcerations. This leads to gradual healing of tissue breaks and ulcertations
which would lead to the overall recovery tissues. This all in all would lead to a good
prognosis of the disease. If left untreated, internal bleeding or hemorrhaging continues
which in time would increase in severity, together with that the ulcers increases in size
which would lead to peritonitis or perforation within the affected area. As the ulcers
increases in size so does the body’s inflammatory response, all would lead to
hypovolemic shock due to severe blood loss and other complications. This would
eventually lead to death and a bad prognosis.

25

Diagnostic / laboratory confirmatory test
Diagnostic Rationale Nursing responsibilities

test
To assess for pain, epigastric

Physical
tenderness or abdominal
examination
distention
A gastrointestinal endoscopy - Explain the procedure to

Endoscopy
allows your doctor to examine the the client
mucous lining of your upper - Inform the client to fast
gastrointestinal tract. The before the endoscopy (8
examiner will place a tube with a hours)
camera at the end through the - Instruct the client to stop
patient’s mouth down to the taking certain medications
esophagus, then to the (blood-thinning) days
duodenum. Biopsies can also be before the procedure
taken during this time to rule out because this can increase
cancer the risk of bleeding
- After the procedure, inform
the patient that he/she
may experience bloating
and gas, cramping and
sore throat
The urea breath test is used to - Inform the patient not to
Urea breath
detect Helicobacter pylori (H. take antibiotics for atleast
test
pylori), a type of bacteria that 4 weeks before the test
may infect the stomach and is a - Do not take any proton
main cause of ulcers in both the pump inhibitors atleast 2
stomach and duodenum. The weeks before the test
26

patient will be breathing into a - Instruct to be NPO for 4
bag and the laboratory will be horse before the
measuring the amount of carbon procedure
dioxide level. If it is higher then - Explain the procedure to
the patient is positive for H. pylori the client
- Inform the patient that they
may resume normal diet,
unless they are scheduled
for other tests that require
dietary restriction

Serology tests employ enzyme - Define and explain the

Serologic
linked immunosorbent assay to procedure to the client
testing
detect serum H. pylori–specific - State the purpose of the
immunoglobulin G and test
immunoglobulin A antibodies
In this test, a stool sample is - Instruct the patient to have
Stool antigen
collected either solid or liquid to a red-meat free and high
determine if H. pylori antigens are residue diet
present in the gastrointestinal - Proper specimen collection
system. Antigens are substances and handling
that trigger an immune response - Identify the sample
accurately
- Give the specimen to the
laboratory at the right time
- After the test, instruct the
patient to do proper
handwashing
27

Gastrin is a hormone produced - Instruct the client for fast
Gastrin test
by "G-cells" in the part of the for 12 hours before the test
stomach called the antrum. It - Explain the procedure to
regulates the production of acid in the client
the body of the stomach 16 - Ask the medications being
during the digestive process. This taken before the test
test measures the amount of because this can increase
gastrin in the blood to help gastrin levels
evaluate an individual with
recurrent peptic ulcers and/or
other serious abdominal
symptoms. These trophic
changes in the mucosa further
enhance its ability to secrete acid.
The increased acid secretion
results in an increased duodenal
acid load, causing gastric
metaplasia of the duodenal bulb
and eventually the development
of ulceration.
A barium swallow is used to help - Explain the procedure

Barium
diagnose conditions that affect - Intrust the patient to fast
swallow
the throat, esophagus, stomach after midnight before the
and first part of the small intestine test
and this includes ulcers. The - Describe the consistency
patient will be asked to fast after of the barium swallow to
midnight on the night before the prepare the patient
test. A drink that contains barium - Place the patient in an
will be swallowed and this would upright position and let him
swallow the barium
28

allow the radiologist to clearly see - After the test, instruct the
the digestive system. patient to drink plenty of
fluids to help eliminate the
barium
- Instruct the patient to notify
the physician if he/she fails
to expel the barium in 2-3
days
- Inform the patient that the
stools will be chalky and
light colored for 24-72
hours

MANAGEMENT
Surgical Management
Elective surgery is uncommonly needed for peptic ulcer disease in current medical
practice. Currently accepted indications for surgery in the management of peptic ulcer
disease include bleeding, perforation, obstruction, intractable disease, and suspected
malignancy
● Vagotomy
When the stomach produces excessive acid, it can corrode the stomach lining and cause
peptic ulcers. Vagotomy is a surgical operation in which one or more branches of the
vagus nerve of the digestive system are cut, typically to reduce the rate of gastric
secretion. However, this can interfere with the other functions of the stomach. A newer
operation cuts only the part of the nerve that affects acid secretion.
● Pyloroplasty
29

This is done together with vagotomy to widen the opening in the lower part of the stomach
(pylorus) so that stomach contents can empty into the small intestine (duodenum). The
pylorus is a thick, muscular area. When it thickens, food cannot pass through. Thus with
pyloroplasty, there would be encouraged passage of partially digested food and thus acid
production normally stops.
● Antrectomy
This is often done in conjunction with a vagotomy. It involves removing the lower part of
the stomach (the antrum). This part of the stomach produces a hormone that increases
production of stomach acid. Adjacent parts of the stomach may also be removed
● Truncal vagotomy-antrectomy
This type is commonly used with pyloroplasty or abdominal drainage to treat chronic
peptic ulcers. It involves cutting one or more of the branches that split off the main trunk
of the vagus nerve and travel down your esophagus to your stomach and other digestive
organs. Vagotomy-antrectomy, preferably with a Billroth I reconstruction, is the most
effective operation in current use to control recurrent ulceration.
Medical Management

Action Mode of action Side effect/ Nursing intervention

classification adverse effect
Antacid Reduce the acid - Diarrhea or - Monitor patient response to the
reaching the constipation drug (relief of GI symptoms
duodenum by - Flatulence caused by hyperacidity)
neutralizing the - Stomach - Monitor for adverse effects (GI
acid present in cramps effects, imbalances in serum
30

the stomach - Vomiting electrolytes, and acid-base
status).
- Evaluate the effectiveness of the
teaching plan (patient can name
the drug and dosage, as well as
describe the adverse effects to
watch for, specific measures to
avoid them, and measures to
take to increase the effectiveness
of the drug).
- Monitor the effectiveness of
comfort measures and
compliance with the regimen

● H2 inhibitors- H2 blocker antihistamine agents are used in the short-term
treatment of an active duodenal ulcer and as prophylaxis in the long termThese
medications decrease acid secretion
Generic name cimetidine
Brand name Tagamet HB
Action classification H2 inhibitor
Mode of action Competitively inhibits histamine action at

histamine2-receptor sites of gastric
parietal cells, thereby inhibiting gastric
acid secretion
Dose and route Active duodenal ulcer (short-term
31

therapy)
- Adults and children older than age
16: 800 mg P.O. at bedtime, or 300
mg P.O. q.i.d. with meals and at
bedtime, or 400 mg P.O. b.i.d.
Maintenance dosage is 400 mg
P.O. at bedtime.

Active benign gastric ulcer (shortterm
therapy)
16: 800 mg P.O. at bedtime or 300
mg P.O. q.i.d. with meals and at
bedtime

Gastric hypersecretory conditions (such
as Zollinger-Ellison syndrome);;
intractable ulcers
16: 300 mg P.O. q.i.d. with meals
and at bedtime

Erosive gastroesophageal reflux disease
16: 1,600 mg P.O. daily in divided
doses (800 mg b.i.d. or 400 mg
q.i.d.) for 12 weeks

Heartburn;; acid indigestion
32

16: 200 mg (two tablets of over-the
counter product only) P.O. up to
b.i.d. Give maximum dosage no
longer than 2 weeks continuously,
unless directed by prescriber
Indication - Active duodenal ulcer

- Active benign gastric ulcer
- Gastric hypersecretory condition
- Erosive gastroesophageal relux
- Heartburn;; acid ingestion
contraindication - Hypersensitivity to drug

- Alcohol intolerance
Side effects - pain when swallowing;;

- bloody or tarry stools, cough with
bloody mucus or vomit that looks
like coffee grounds;;
- changes in mood, anxiety,
agitation;;
- confusion, hallucinations;; or.
- breast swelling or tenderness.

Adverse effects - CNS: confusion, dizziness,

drowsiness, hallucinations,
agitation, psychosis, depression,
anxiety, headache
- GI: diarrhea
- GU: reversible erectile dysfunction,
gynecomastia
33

Drug interactions Drug-diagnostic tests. Creatinine,
transaminases: increased levels
Parathyroid hormone: decreased level
Skin tests using allergenic extracts: false
negative results (drug should be
discontinued 24 hours before testing)

Drug-food. Caffeine-containing foods and
beverages (such as coffee, chocolate):
increased cimetidine blood level,
increased risk of toxicity
Nursing responsibilities - Monitor creatinine levels in

patients with renal insufficiency or
failure.
- Assess elderly or chronically ill
patients for confusion (which
usually resolves once drug therapy
ends)
- Inform patient with gastric ulcer
that ulcer may take up to 2 months
to heal. Advise him not to
discontinue therapy, even if he
feels better, without first consulting
prescriber. Ulcer may recur if
therapy ends too soon.
- Advise patient not to take over-
thecounter cimetidine for more
than 2 weeks continuously, except
with prescriber’s advice and
supervision.
34

- Do not take antacids within 1 hour
of cimetidine administration
- Avoid tasks that require alertness,
motor skills until response to drug
is established
- Report any blood in vomitus/stool,
or dark, tarry stool

● PPI- Block the three major pathways for acid production. PPIs suppress acid
production much more effectively than H2 blockers. PPIs are the gold standard in
medication therapy of peptic ulcer disease.
Generic name omeprazole
Brand name Prilosec
Action classification Proton pump inhibitor
Mode 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
Dose and route Short-term treatment of active duodenal

ulcer
- Adults: 20 mg P.O. (capsules,
powder) daily for 4 weeks. Some
patients may need 4 additional
weeks of therapy.

35

To reduce risk of duodenal ulcers caused
by Helicobacter pylori
- Adults: 40 mg P.O. (capsules) daily
in morning, given with
clarithromycin t.i.d. for 2 weeks;;
then 20 mg daily for 2 weeks

Gastric ulcers
- Adults: 40 mg P.O. (capsules) daily
for 4 to 8 weeks

Pathologic hypersecretory conditions,
including Zollinger-Ellison syndrome
- Adults: Initially, 60 mg P.O.
(capsules) daily;; may increase up
to 120 mg t.i.d. Divide daily
dosages above 80 mg
Indication - Short-term treatment of active

duodenal ulcer
- Gastric ulcers
- Pathologic hypersecretory
conditions
contraindication hypersensitivity to drug or its component
Side effects
Adverse effects - CNS: dizziness, headache,

asthenia
- GI: nausea, vomiting, diarrhea,
constipation, abdominal pain
36

- Metabolic: hypomagnesemia
- Musculoskeletal: back pain;;
fractures of hip, wrist, spine (with
long-term daily use)
- Respiratory: cough, upper
respiratory tract infection
- Skin:rash
Drug interactions Drug-drug. Ampicillin, cyanocobalamin,

iron salts, ketoconazole: reduced
absorption of these drugs

Drug-diagnostic tests. Alanine
phosphatase, alkaline aminotransferase,
aspartate aminotransferase, bilirubin:
increased levels

Drug-herbs. St John’s wort: substantially
decreased omeprazole concentration
Nursing responsibilities - Assess vital signs.

- Check for abdominal pain, emesis,
diarrhea, or constipation.
- Evaluate fluid intake and output.
- Watch for elevated liver function
test results (rare).
- Monitor magnesium level before
starting drug and periodically
thereafter in patients expected to
be on long-term treatment or who
take proton pump inhibitors with
37

other drugs such as digoxin or
drugs that may cause
hypomagnesemia
- Tell patient to take 30 to 60
minutes before a meal, preferably
in morning.
- Instruct patient to swallow
capsules or tablets whole and not
to chew or crush them.

Generic name lansoprazole
Brand name prevacid
Action classification Gastric acid pump inhibitor
Mode of action Inhibits activity of proton pump in gastric
parietal cells, decreasing gastric acid
production
Dose and route Active duodenal ulcer

- Adults: 15 mg P.O. daily for 4
weeks

Maintenance of healed duodenal ulcer
- Adults: 15 mg P.O. daily

H. pylori eradication, to reduce risk of
duodenal ulcer recurrence
- Adults: In triple therapy, 30 mg
lansoprazole P.O., 1 g amoxicillin
38

P.O., and 500 mg clarithromycin
P.O. q 12 hours for 10 or 14 days.
In dual therapy, 30 mg
lansoprazole P.O. and 1 g
amoxicillin P.O. q 8 hours for 14
days.

Benign gastric ulcer
- Adults: 30 mg P.O. daily for up to 8
weeks

Gastric ulcer associated with NSAIDs
- Adults: 30 mg P.O. once daily for
up to 8 weeks

To reduce risk of NSAID-associated
gastric ulcer
- Adults: 15 mg P.O. daily for up to
12 weeks
Indication - Active duodenal ulcer

- H. pylori eradication, to reduce
risks of duodenal ulcer recurrence
- Benign gastric ulcer
- Gastric ulcer associated with
NSAIDS
- To reduce risks of NSAID-
associated gastric ulcer
contraindication Hypersensitivity to drug or its components
Side effects - headaches.
39

- feeling sick.
- diarrhoea or being sick (vomiting)
- stomach pain.
- constipation.
- wind.
- itchy skin rashes.
- feeling dizzy or tired.
Adverse effects - CNS: headache, confusion,

anxiety, malaise, paresthesia,
abnormal thinking, depression,
dizziness, syncope,
cerebrovascular accident
- CV: chest pain, hypertension,
hypotension, myocardial infarction,
shock
- EENT: visual field deficits, otitis
media, tinnitus, epistaxis
- GI: nausea, diarrhea, abdominal
pain, cholelithiasis, ulcerative
colitis, esophageal ulcer,
hematemesis, stomatitis,
dysphagia, GI hemorrhage
- GU:renal calculi, erectile
dysfunction, abnormal menses,
breast tenderness, gynecomastia
- Hematologic: anemia
- Musculoskeletal: hip, wrist, spine
fractures (with long-term daily use)
- Respiratory: cough, bronchitis,
asthma
40

- Skin: urticaria, alopecia, acne,
pruritus, photosensitivity
Drug interactions Drug-drug.

- Drugs requiring acidic pH (such as
ampicillin esters, digoxin, iron
salts, itraconazole, ketoconazole):
decreased absorption of these
drugs Sucralfate: decreased
lansoprazole absorption
Theophylline: increased
theophylline clearance

Drug-food.
- Any food: decreased rate and
extent of GI drug absorption

Drug-herbs.
- Male fern: inactivation of herb St.
John’s wort: increased risk of
photosensitivity
Nursing responsibilities - Monitor for GI adverse reactions.

- Assess nutritional status and fluid
balance to identify significant
problems.

● Antibiotic
Generic name amoxicillin
Brand name Amoxil
41

Action classification antibiotic
Mode of action kills bacteria by binding to and inactivating
penicillin-binding proteins on the inner
bacterial cell wall, weakening the bacterial
cell wall and causing lysis
Dose and route - PO (adults): 250-500 mg q8 or 875

mg q 12
- PO (children older than 3 mos
weighing 40 kg or less): 20-
90mg/kg/day divided q8-12 hrs
- Otitis media, PO (children):
90mg/kg/day (600 mg/5ml
suspension) in divided doses q12
for 10 days
- PO (neonates children younger
than 3 mos): 30 mg/kg/day (125
mg/5ml suspension) divided doses
q12h
- Renal impairment: do not use 875
mg tablet or extended-release
tablets for creatinine clearance less
than 30 ml/min. Dosage and
frequency are modified based on
creatinine clearance.
- Creatinine clearance 10-30ml/ min:
250-500 mg q12h
- Creatinine clearance less than 10
ml/min: 250-500mg q24h
42

- HD: 250-500 mg q24h , give dose
during and after dialysis
- PD: 250 mg q12h
Indication To treat h.pylori in the digestive tract
contraindication history of severe hypersensitivity

reactions (anaphylaxis or Stevens-
Johnson syndrome) to other beta-lactam
antibiotics, hypersensitivity to amoxicillin
or its components
Side effects diarrhea, loose stools, nausea, skin

rashes, urticaria
Adverse effects - CNS: agitation, anxiety, behavioral

changes, confusion, dizziness,
insomnia, reversible hyperactivity,
seizures
- CV: hypersensitivity vasculitis
- EENT: black, hairy tongue,
mucocutaneous candidiasis, tooth
discoloration
- GI: diarrhea, diarrhea related to
clostridium difficile, elevated liver
enzymes, hemorrhagic or
pseudomembranous colitis,
jaundice, hepatic dysfunction,
nausea, vomiting
- GU: crystalluria, vaginal mycosis
- HEME: agranulocytosis, anemia (
including hemolytic anemia),
43

eosinophilia, granulocytosis,
leukopenia, thrombocytopenia,
thrombocytopenic purpura
- SKIN: erythema multiforme,
erythematous maculopapular rash,
generalized exanthematous
pustulosis, Stevens-Johnsons
syndrome, toxic epidermal
necrolysis, urticaria
- Other: allergic reaction,
anaphylaxis, serum sickness-like
reaction (such as arthralgia,
arthritis, fever, myalgia rash and
urticaria)
Drug interactions - Allopurinol: increased risk of rash

- Chloramphenicol, erythromycins,
sulfonamides, tetracycline: reduced
bacterial effect of amoxicillin
- Methotrexate: increased risk of
methotrexate toxicity
- Oral anticoagulants: possible
prolonged prothrombin time
(increased international normalized
ratio)
- Oral contraceptives with estrogen:
possible reduced effectiveness of
contraceptive
- Probenecid: increased amoxicillin
effects

44

Nursing responsibilities - Monitor patient closely for diarrhea
R: this may indicate
pseudomembranous colitis caused
by clostridium difficile
- Patients with mononucleosis should
not receive amoxicillin
R: this can cause erythematosus
rash
- Monitor hepatic and renal function
in patients with prolonged therapy
R: this is where the drug is
metabolized
- Take the full course of therapy;; do
not stop because the patient feels
better
R: to avoid resistance to the drug
- monitor patient for diarrhea –
bloody stool should be reported
immediately
R: this is one of the adverse effects
of the drug
- Tell the patient to report any
adverse reactions and to notify the
prescriber if infection worsens of
does not improve after 72 hours
- When amoxicillin is prescribed for a
child, instruct parents to place it
directly on the child's tongue to
swallow. If this doesn't work, tell
parents to mix a dose of suspension
45

with formula or cold drink such as
milk, fruit juice and water.
R: For faster and effective

absorption of the drug
- Avoid high fiber food
R: May affect how the stomach

absorbs the medicine
- Provide information on the side

effects of the drug like nausea and
vomiting, GI upset and sore mouth
R: To lessen the side effects

encourage to have small frequent
meals and for the sore mouth
encourage frequent mouth care.
- Tell client to refrigerate client to

refrigerate reconstituted
suspension and to shake well
before each use
R: Temperature can affect the

effectivity of the drug

46

● Mucosal protective agent

Generic name misoprostol
Brand name Cytotec
Action classification Cytoprotective agent
Mode of action Reduces gastric acid secretion and

increases gastric mucus and bicarbonate
production, creating a protective coating
on gastric mucos
Dose and route To prevent gastric ulcers caused by

NSAIDs
- Adults: 200 mcg q.i.d. with food,
with last daily dose given at
bedtime. If intolerance occurs,
decrease to 100 mcg q.i.d.
Indication To prevent gastric ulcers caused by

NSAID
contraindication - Prostaglandin hypersensitivity

- Pregnancy
Side effects - diarrhea;;

- stomach pain, nausea, upset
stomach, gas;;
- vaginal bleeding or spotting, heavy
menstrual flow;; or.
- menstrual cramps.

47

Adverse effects - CNS: headache
- GI: nausea, vomiting, diarrhea,
constipation, abdominal pain,
dyspepsia, flatulence
- GU: miscarriage, menstrual
disorders, postmenopausal
bleeding
Drug interactions - DRUG: Antacids may increase

levels.
- HERBAL: None significant.
- FOOD: None known.
- LAB VALUES: None significant.
Nursing responsibilities - Instruct patient to take with food.

- Advise patient to report diarrhea,
abdominal pain, and menstrual
irregularities.
- Tell patient drug may cause
spontaneous abortion. Stress
importance of using reliable
contraception.
- Instruct female patient using drug
for ulcer treatment to start therapy
on second or third day of normal
menses.
- Caution patient not to take
magnesium-containing antacids,
which may worsen diarrhea.

48

Nursing Management:
Nursing diagnosis Goals Nursing interventions
Acute pain related to After 2 hours of nursing 1. Perform a comprehensive
increased gastric secretions intervention, the patient will assessment of pain. Include
as evidenced by pain scale report relief of pain as evidence location, characteristics,
of 8 out of 10 by pain scale of 2-4 on a scale onset/duration, frequency,
of 0-10 quality, intensity, and
precipitating factors to
determine appropriate
intervention
2. Instruct the client to avoid
NSAIDs such as aspirin.
R: These medications may
cause irritation of the
gastric mucosa.
3. Administer prescribed
medication
R: giving of medications
may lessen the signs and
symptoms being felt by the
patient
4. These medications may
cause irritation of the
gastric mucosa.
R: an irregular schedule of
meals may interfere with
the regular administration of
medications
49

5. Teach the patient non
pharmacologic techniques
(relaxation, music therapy,
distraction)
Imbalanced nutrition: less Within 2 hours of nursing 1. Obtain a nutritional history
than body requirements intervention, the client will R: The client may not eat
related to gastrointestinal demonstrate proper selection of sufficient calories or
bleeding meals essential nutrients as a way
to reduce pain episodes
with peptic ulcer disease.
Because of this, clients are
at high risk for malnutrition.
2. Assess for body weight
changes.
R: weight loss in an
indication of inadequate
nutritional intake. Gastric
ulcers are more likely to be
associated with vomiting,
loss of appetite and weight
loss
3. Assist the client with
identifying foods that cause
gastric irritation
R: clients need to learn
what foods they can
tolerate without gastric
pain. Soft bland, non acidic
foods cause less gastric
irritation
50

4. Encourage the client to limit
the intake of caffeinated
beverages such as tea and
coffee
R: caffeine stimulates the
secretion of gastric acid
5. Teach the client about the
importance of eating a
balanced diet with meals at
regular intervals
R: Specific dietary
restrictions are no longer
part of the treatment for
PUD. During the
symptomatic phase of an
ulcer the client may find
benefit from eating small
meals at more frequent
intervals

Anxiety related to the After 2 hours of nursing - Encourage clients to
nature of the disease and intervention the patient will be express their problems and
long-term management able to decrease anxiety fears and ask questions as
needed
R: open communication
helps clients develop
trusting relationships that
help reduce anxiety and
stress
- Explain the reasons for the
51

planned treatment
schedules such as
pharmacotherapy, dietary
restrictions, modification of
activity levels, reduce or
stop smoking
R: knowledge reduces anxiety
appears to be a sense of fear due
to ignorance. Knowledge can have
a positive effect on behavior
change
- Assist the clients to identify
situations that cause
anxiety
R: stressors need to be
identified so that they can
be overcome
- Teach stress management
strategies such as
distraction

REVIEW OF RELATED STUDIES
Title: Obesity and risk of peptic ulcer disease: A large-scle health check-up cohort study

Summary:
Obesity has been reported to be a risk factor for a person to have Peptic ulcer
disease (PUD). It is not clear whether or not obesity does increase the risk because there
are alot of studies claiming that it does, and some not. With the help of this study, these
researchers are trying to see if there is indeed a relationship. This study was based on
52

the population of patients with PUD at the center for health promotion, samsung medical
center, seoul, korea between january 2005 and june 2017. Participants of this study went
under endoscopy and they have identified patients with a circumscribed mucosal break
5mm or more in diameter, with a well-defined ulcer crater. The peptic ulcer was staged
as active, healing and scarring. The participants were chosen, medications were noted,
smoking status was also asked, alcohol intake, physical measurements, BMI, blood
chemistry tests and serum insulin. As for the statistical analysis results, they have
concluded that the incidence rate of PUD and gastric ulcer (GU) were significantly higher
in the obese group than the non obese group. With the adjustments they made from their
statistical analysis, they had a result that obesity had no significant relationship with
having PUD.

This study had a lot of limitations thus the results were not consistent. . First, the
analysis was limited to those who visited the health check-up center, thus patients might
have better economic status than in the general population. More severe cases of PUD
may have been excluded because usually asymptomatic subjects visit health screening
centers. However, subjects enrolled in this study had considerable percentages of those
in the active (18.9%) or healing (31.8%) gastric ulcers stages, whereas, 86.0% of those
with duodenal ulcer were at the scarring stage. Secondly, Helicobacter pylori infection
status was not examined for all enrolled subjects which is the causative agent of PUD. to
conclude, this study is still in need of more research

Title: Peptic Ulcer disease as a common cause of bleeding in patients with coronavirus
disease 2019
Summary
The risk for bleeding in patients with covid-19 remains unclear and cases were
high in elderly patients with multimorbidity. There were cases of hemorrhagic colitis
related to covid 19. In this case, there were 5 patients presented, they all had a chronic
disease with essential hypertension being present at ⅘ patients and none of these
patients has peptic ulcer disease or a history of h.pylori infection. Upon admission, they
53

all were given heparin and after several days, they all had severe anemia and
manifestations of upper GI bleeding (melena and hypotension). They were given blood
transfusions and underwent upper GI endoscopy and found out that the patients had
gastric and/or duodenal ulcers, other cases had multiple ulcers. All the patients did not
present other risk factors for bleeding other than thromboprophylaxis. But as for this case
presentation, the pathogenesis of peptic ulcer disease might be explained by different
mechanisms like stress resulting from acute illness or it may be from the cytokine storm.
If the management of patients with covid 19 is the thromboprophylaxis then the physicians
should be alert in checking for the GI bleeding of the patient

54

GASTROESOPHAGEAL REFLUX DISEASE
INTRODUCTION
Gastrointestinal conditions are disorders of the digestive system, an extensive and
complex system that breaks down food in order to absorb water and extract nutrients,
minerals and vitamins for the body’s use, while then removing unabsorbed waste.
Gastrointestinal diseases are among the most common problems in tropical countries and
commonly manifest as diarrhea, abdominal pain, abdominal distention, gastrointestinal
bleeding, intestinal obstruction, malabsorption, or malnutrition. GERD (gastroesophageal
reflux disease, or chronic acid reflux) is a condition in which acid-containing contents in
the stomach persistently leak back up into the esophagus, the tube from the throat to the
stomach. Acid reflux happens because a valve at the end of the esophagus, the lower
esophageal sphincter, doesn’t close properly when food arrives at the stomach. Acid
backwash then flows back up through the esophagus into the throat and mouth, giving a
sour taste. The main symptoms are persistent heartburn and acid regurgitation. Some
people have GERD without heartburn. Instead, they experience pain in the chest,
hoarseness in the morning or trouble swallowing.
GERD is one of the most common gastrointestinal disorders, with a prevalence of
approximately 20% of adults in western culture. A systematic review by El-Serag et al.
estimated the prevalence of GERD in the US between 18.1% to 27.8%. However, the true
prevalence of this disorder could be higher because more individuals have access to
over-the-counter acid, reducing medication. The prevalence of GERD is slightly higher in
men compared to women.
Epidemiological data have shown that the prevalence of symptomatic GERD has
been rising in the Asia Pacific Region. In 2005, the prevalence of GERD in Eastern Asia
was approximately 2.5-4.8% and has increased to 5.2-8.5% by 2010. Erosive Esophagitis
(EE), a common complication of GERD, has more than doubled in the past two decades
in the Philippines, according to previously reported time trend studies.
The prevalence of GERD or Gastroesophageal Reflux Disease among Filipinos
has significantly increased over the last decade, according to a study done by the
Endoscopy Unit of the University of Santo Tomas (UST) Hospital in Manila. Meanwhile,
55

in Davao City, Philippines there are no available records of cases and statistics regarding
the epidemiology of gastroesophageal reflux disease.

OBJECTIVES
At the end of the virtual seminar, the proponents from BSN 4D Group 1 shall be
able to impart knowledge and acquire further skills and wisdom pertaining to
Gastrointestinal problems, to further understand the factors affecting the health of the
clients having Gastroesophageal Reflux Disease (GERD), and to develop the skills
necessary to provide the utmost quality of care through assessment and nursing
intervention. More specifically, the proponents of this study aim to:
a. Present an introduction which outlines the disease, relevant statistics, and
nursing implications of the study;;
b. composes objectives that are specific, measurable, attainable, realistic, and
time-bounded;;
c. discusses the etiologic factors that lead to the development of GERD;;
d. indicates the symptomatology of the disease;;
e. outlines the disease process of GERD;;
f. trace the pathophysiology of the disease through a schematic diagram;;
g. list potential diagnostic or laboratory confirmatory tests viable to the case
and;;
h. explains the possible medical management, its indication relating to the
disease including diagnostic, laboratory examinations, and possible medications;;
i. presents a summary on a related literature published not earlier than 5 years
from conduct of this study;;

DEFINITION OF THE DISEASE
Gastroesophageal reflux disease, or GERD, is a digestive disorder that affects
the ring of muscle between your esophagus and your stomach. This ring is called the
lower esophageal sphincter (LES) (Bhargava, 2020).
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Gastroesophageal reflux disease (GERD) occurs when stomach acid frequently
flows back into the tube connecting your mouth and stomach (esophagus). This
backwash (acid reflux) can irritate the lining of your esophagus (Mayo Clinic, 2020).
Gastroesophageal reflux disease (GERD) is a more severe and long-lasting
condition in which GER causes repeated symptoms that are bothersome or leads
to complications over time (NIH, 2020).

ANATOMY AND PHYSIOLOGY
Gastrointestinal System
The Gastrointestinal System includes the mouth, pharynx, esophagus, stomach,

small intestine, large intestine, rectum, and anus. It also includes the salivary glands, liver,
gallbladder, and pancreas, which make digestive juices and enzymes that help the body
digest food and liquids.
The principal functions of the gastrointestinal tract are to digest and absorb
ingested nutrients, and to excrete waste products of digestion. Most nutrients are ingested
in a form that is either too complex for absorption or insoluble, and therefore, indigestible
or incapable of being digested.
Mouth
The mouth is the first part of the GI tract. External to the mouth are the lips and
cheeks. Within the mouth are the palate, teeth, and tongue. The palate separates the
oral and nasal cavities. The teeth are used for mastication (chewing). The tongue is
used for taste and speech, and is involved in mastication and swallowing. The lining of
the mouth is made up of epithelial cells. The mouth produces saliva from three sets of
salivary glands: the parotid glands are located between the ears and the jaw, the
submandibular glands under the jaw, and the sublingual glands under the tongue.
Saliva lubricates and begins digestion. The salivary glands produce ptyalin, a type of
amylase, which breakdowns starch, and an antibacterial agent.
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The mouth receives food and drink. Digestion begins in the mouth by mechanical
and chemical means: ingested food is masticated and mixed with saliva and formed into
a food bolus. When the food bolus is voluntarily swallowed, it will pass into the pharynx
Pharynx
The pharynx, also termed the throat, is funnel shaped and connects the mouth and
esophagus. The pharynx also joins the nasal cavity to the larynx, part of the respiratory
system. These two areas are separated by the epiglottis, a flap of tissue that prevents
food getting into the larynx and airway.
Esophagus
The esophagus is a muscular tube about 25 cm long and a little under 2 cm in
diameter. It begins at the pharynx and ends at the stomach, at the cardiac sphincter,
and is situated behind the trachea and close to the greater vessels and left atrium of the
heart. It passes through the diaphragm as it travels to the stomach. The upper portion of
the esophagus is formed of striated muscle to aid the swallowing reflex (voluntary
decision), while the lower two-thirds is formed of smooth muscle to move food towards
the stomach by peristalsis (involuntary). The muscles of the esophagus contract and
relax to move food down to the stomach. Peristalsis is effective and food will pass to the
stomach, even if the person is lying down.
The inner lining of the esophagus is epithelial tissue, the function of which is to
protect the esophagus. Protection of the esophagus is also aided by the mucus
produced from the mucous glands.
Food and fluid are swallowed from the mouth, and pass into the pharynx, the
esophagus, and to the stomach. There are sphincters at the top and bottom of the
esophagus. The upper sphincter is closed except during the swallowing, when it opens
to allow food to enter the esophagus. The lower or cardiac sphincter prevents partially
digested food from re-entering the esophagus.
If the esophagus is involved in the vomiting reflex, the peristaltic action is
reversed.
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Stomach
The stomach is a sac-like organ with strong muscular walls. It secretes acid and
powerful enzymes that continue the process of breaking the food down and changing it
to a consistency of liquid or paste. From there, food moves to the small intestine. Between
meals, the non-liquefiable remnants are released from the stomach and ushered through
the rest of the intestines to be eliminated. Once food is broken down the pyloric sphincter
will allow passage of the semiliquid (chyme) into the duodenum.
Small Intestine
Made up of three segments- duodenum, jejunum, and ileum. The small intestine
also breaks down food using enzymes released by the pancreas and bile from the liver.
The duodenum is largely responsible for the continuing breakdown process, with the
jejunum and ileum being mainly responsible for absorption of nutrients into the
bloodstream.
This process is highly dependent on the activity of a large network of nerves,

hormones, and muscles.
Large Intestine
The large intestine connects the small intestine to the rectum. It is made up of the
cecum, the ascending colon, the transverse colon, the descending colon and the sigmoid
colon, which connects to the rectum. It is a highly specialized organ that is responsible
for processing waste so that defecation is easy and convenient.
Rectum
The rectum is an eight-inch chamber that connects the colon to the anus. The
rectum is the one that receives stool from the colon, letting the person know there is stool
to be evacuated through sensors which sends a message to the brain. The brain then
decides if the rectal contents can be released or not. If they can, the sphincters relax and
the rectum contracts, expelling its contents.
Anus
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The anus is the last part of the digestive tract. It consists of the muscles that line
the pelvis, where it creates an angle between the rectum and the anus that stops stool
from coming out when it is not supposed to and the two other muscles called anal
sphincters (internal and external) that holds the control of stool passage.
Pancreas
Pancreas is the chief factory for digestive enzymes that are secreted into the
duodenum, the first segment of the small intestine. These enzymes break down protein,
fats, and carbohydrates.
Liver
The liver has multiple functions, but two of its main functions within the digestive
system are to make and secrete an important substance called bile and to process the
blood coming from the small intestine containing the nutrients just absorbed. The liver
purifies this blood of many impurities before travelling to the rest of the body.
Gallbladder
The gallbladder is a storage sac for excess bile. Bile made in the liver travels to
the small intestine via the bile ducts. If the intestine does not need it, the bile travels into
the gallbladder, where it awaits the signal from the intestines that food is present. Bile
helps absorb fats in the diet and it carries waste from the liver that cannot go through the
kidneys.
Salivary Glands
Salivary glands play an important role in digestion because they make saliva.
Saliva helps moisten food so we can swallow it more easily. It also has an enzyme called
amylase that makes it easier for the stomach to break down starches in food.
PHYSIOLOGY
The functions of the gastrointestinal system include the following:
1. Ingestion – This is another term for eating—taking food into the body.
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2. Propulsion - Ingested food is moved through the GI tract, initially by swallowing
(voluntary action) and progressing to peristalsis, an involuntary action. In peristalsis, the
gut wall contracts and pushes the food bolus or waste further along the GI tract;; the
muscles then relax and contract again. This combination of contracting and relaxing helps
to break down the food and propels it forward. Peristalsis occurs in the esophagus,
stomach, small bowel, and large bowel.
3. Digestion – Ingested food is broken down into smaller parts in two ways: chemically
and mechanically. In the mouth, the teeth chew the food, breaking it into smaller parts,
and mix it with saliva (mechanical breakdown). The saliva begins to digest the food
(chemical breakdown). The stomach churns the food (mechanical breakdown), and acid
and digestive enzymes are secreted to breakdown it down chemically. Segmentation
contractions in the small bowel mix the food with the digestive enzymes and break it down
(mechanical breakdown), with peristalsis moving food further along the GI tract. There is
further chemical breakdown of the food by bile, which is made in the liver and stored in
the gall bladder and pancreatic juice from the pancreas
4. Absorption – passage of the end products or nutrients of chemical digestion from the
digestive tract into blood or lymph for distribution to tissue cells.
5. Elimination – his is the passage of feces, out of the body via the anus, past the anal
sphincters that control defecation

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PATHOPHYSIOLOGY
A. ETIOLOGY
PREDISPOSING FACTORS RATIONALE

Age Although a person of any age can develop
gastrointestinal reflux disease (GERD) it is
quite common among older adults. The
prevalence of GERD was common in 20-29
years old group and the age group, and the
age group 70-79 years had the lowest
prevalence for both males and females. Due
to the physiological changes that occur with
aging, your sphincter can weaken and stop
function properly. (Cleveland Clinic, 2018)
Sex In terms of GERD symptoms, women are
more likely to have heartburn, regurgitation,
belching, and extra-esophageal symptoms
than men. Anti-inflammatory action of
estrogen and esophageal epithelial
resistance against refluxate are likely to be
associated with the sex and gender
differences in GERD spectrum between
men and women. However, men suffer
pathologic diseases such as reflux
esophagitis, Barrett’s esophagus (BE), and
esophageal adenocarcinoma (EAC) more
frequently than women. (Kim, 2016)
Race The prevalence of GERD appears to be
highest in North America and Europe,
whereas epidemiologic data from the Indian
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subcontinent, Africa, South America, and
the Middle East are sparse (Sharma, 2008).
Genetic Genetic contribution seems to play a major
role in GERD and GERD- related disorders
development such Barrett's esophagus and
esophageal adenocarcinoma. Twin and
family studies have revealed an about 31%
heritability of the disease, but non-genetic
factors were responsible for most cases of
GERD (Davis, 2020).
Hormone Estrogen works via its alpha and beta
receptors and increases nitric oxide
synthesis, a notorious muscle relaxant,
decreasing smooth muscles' tone in the
lower esophageal sphincter. Thus, high
estrogen levels can lead to GERD (Kang,
2020).

PRECIPITATING FACTOR RATIONALE
Smoking The nicotine from tobacco relaxes the valve
between the esophagus and stomach (lower
esophageal sphincter). This can allow
stomach acid and juices, the chemicals that
break down food in the stomach, to back up
(reflux) into the esophagus, which causes
heartburn (Husney, 2020).
Caffeine Caffeinated food and beverages can
increase the acidity and gastric secretions. It
also relaxes the lower esophageal sphincter,
triggering acid reflux or making it worse
(Baum, 2018).
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Alcohol consumption Alcohol is an irritant to the lining of your
stomach because it microscopically disrupts
the membranes of your cells. This disruption
causes inflammation (swelling and redness),
which is the process your body uses to
recruit cells from your bloodstream to heal
damage. Some studies also show that
alcohol impairs the LES’s ability to contract,
or close, which may cause regurgitation of
acid back into the esophagus (Sheehy,
2021).
Overeating Eating too much food requires your organs
to work harder. They secrete extra
hormones and enzymes to break the food
down. To break down food, the stomach
produces hydrochloric acid. If you overeat,
this acid may back up into the esophagus
resulting in heartburn. It also expands yours
stomach beyond normal size, which can
lead to decreased pressure of LES
(Blackburn, 2018).
Medication Nonsteroidal anti-inflammatory drugs
(NSAIDs) include aspirin, Motrin or Advil
(ibuprofen), and Aleve (naproxen), and
gastrointestinal side effects are common
when taking them. These medications are
usually associated with causing peptic
ulcers, and can also make heartburn and
esophageal irritation worse, perhaps by
weakening or relaxing the LES (Chugh,
2021).
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Stress Stress can also deplete the production of
substances called prostaglandins, which
normally protect the stomach from the
effects of acid. This could increase your
perception of discomfort. Stress, coupled
with exhaustion, may present even more
body changes that lead to increased acid
reflux (Luo, 2017).
Obesity Obesity or being overweight is a risk factor
for developing GERD. This may be due to
the additional weight causing pressure on
the stomach which in turn causes stomach
acid and contents to travel back up your
esophagus (Chugh, 2021).
Pregnancy The increase of the hormones estrogen
and progesterone during pregnancy relax
the LES, plus your expanding belly puts
more pressure on your abdomen. Because
of this, it's pretty normal for pregnant women
to experience heartburn, which can lead to
GERD.
Angle of His enlargement The angle of His is an acute angle between
the great curvature of the stomach and the
esophagus, and acts as an anti-reflux
barrier by functioning like a valve. As the
angle of His widened or enlarged more than
60-degree angle, it decreases the pressure
of the LES, thus leading to regurgitation of
stomach contents after meals (Amboss,
2022).
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Hiatal hernia A hiatal hernia occurs when the upper part
of your stomach is above the diaphragm, the
muscle wall that separates the stomach
from the chest. This lowers the pressure on
the LES, which causes reflux (Chugh,
2021).

B. SYMPTOMATOLOGY
SIGNS AND SYMPTOMS RATIONALE

Heartburn Acid reflux occurs when the sphincter
muscle at the lower end of your esophagus
relaxes at the wrong time, allowing stomach
acid to back up into your esophagus and
causing a burning sensation in your chest
(Mayo Clinic, 2020).
Chest pain Chest pain stemming from GERD may affect
your upper body in some cases, but it’s
most often centered either behind your
sternum or just underneath it in an area
known as the epigastrium. When acid reflux
cause damage within the esophagus, the
muscles around the food tube tightens or
also known as esophageal spasms. In turn,
these spasms can cause pain in your throat
and the upper area of your chest (Sullivan,
2018).
Dysphagia The heartburn and regurgitation that are
associated with acid reflux can make it
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difficult to swallow certain foods, thus
leading to dysphagia. The presence of
stomach acid in the esophagus can cause
irritation, and in some cases, scar tissue that
leads to more difficulty swallowing (Minnis,
2018).
Odynophagia When stomach acid leaks back into the
esophagus, you may experience painful
swallowing along with other symptoms, such
as heartburn or chest pain due to irritation of
your esophagus (Minnis, 2018).
Globus sensation One symptom of GERD you might
experience is the feeling that you have
something stuck in the back of your throat,
otherwise known as a globus sensation. The
acid irritates your throat, causing the
muscles to either swell or tense up, which
can create the feeling of a foreign object
lodged in your throat (St. Luke’s Health,
2018).
Water brash/acid regurgitation Regurgitation happens when a mixture of
gastric juices, and sometimes undigested
food, rises back up the esophagus and into
the mouth. When a person produces an
excessive amount of saliva that mixes with
stomach acids that have risen to the throat.
A person experiencing water brash can get
a bad taste in their mouth and feel heartburn
(Brennan, 2021).
Cough As the acid flows up into the esophagus,
and possibly even the throat and lungs, your
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body encourages you to cough up the
substance to remove it from your body (St.
Luke’s Health, 2018).
Hoarseness/Sore throat If acid reflux gets past the upper esophageal
sphincter, it can enter the throat (pharynx)
and even the voice box (larynx), causing
hoarseness or sore throat (Ratini, 2021).
Wheezing/shortness of breath Studies show that stomach acid can inflame
the windpipe, which affects breathing.
However, esophageal acidity can also
trigger the Vagus nerve which tells the lungs
to tighten (bronchoconstriction), and this can
cause GERD wheezing and shortness of
breath (Atlasbiomed, 2021).
Dental erosions When acid reaches your mouth, it can erode
your tooth enamel and cause sensitivity. It
can also instigate to dental erosion since
they may reduce the saliva pH (pH=5.5) to
the levels below the critical pH in which
hydroxyapatite crystals in the dental enamel
dissolves. With a pH of less than 2.0;; gastric
reflux is potentially capable of causing
dental erosion (St. Luke’s Health, 2018).

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C. DISEASE PROCESS
a. Diagram
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70

b. Narrative
Gastroesophageal reflux disease (GERD) is a digestive disorder that occurs

when the acids from the stomach go up to the esophagus. Usually it is greatly
associated with the lower esophageal sphincter problem. We have two factors that
cause or trigger the onset of the disease, the precipitating factors or the modifiable
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factors, and the predisposing factors or the non-modifiable factors. Predisposing
factors include age, sex, race, genetics, and hormones. While precipitating factors
include smoking, caffeine, alcohol consumption, overeating, medication, stress,
obesity, pregnancy, angle of His enlargement, and Hiatal hernia.
In a normal function, the Lower esophageal sphincter (LES) allows food to
transit from the esophagus into the stomach and prevents the reflux of gastric
contents back into the esophagus. In GERD, factors such as alcohol, smoking,
caffeine, and medications can cause an abnormal relaxation of LES. In some
cases, patients with Hiatal Hernia or angle of His enlargement experience
misaligned LES with the level of diaphragmatic contraction, which leads to
decrease in structural support of the LES. For some who are pregnant, overeating,
or obesity, they are experiencing increased pressure on the cardia of the stomach.
The pressure created will stimulate the Vagus Nerve leading to LES relaxation. All
of those factors will decrease the LES pressure to less than 10 mmHg. Normally,
LES pressure varies from 10 to 45 mmHg in adults.
In the long run, there will be a transient lower esophageal sphincter
relaxation (TELSR). TLESR is a physiological mechanism that enables venting of
gas from the stomach. It is also defined as lower esophageal sphincter relaxation
that is induced spontaneously without swallowing. However, If TELSR is prolonged
accompanied with Hydrochloric (HCL) acid in the stomach being pushed up
brought about by increased pressure on the cardia or increased acid production in
the stomach (due to stress, caffeine, and alcohol), this will lead to
Gastroesophageal Reflux Disease (GERD).

As the reflux of gastric content goes into the distal esophagus, this will lead
to symptoms such as Heartburn or the burning sensation on the chest, Water
brash, and acid regurgitation. When the esophageal tissue is repeatedly exposed
to stomach acid, this will signal the pro-inflammatory cells and cytokines to go to
the area being exposed with acid. Both the acid and the cytokines, can damage
the squamous esophageal epithelium, the pharyngeal lining, and airway especially
when aspiration of acid will reach into the larynx, pharynx, and lungs.
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The damaged squamous esophageal epithelium can lead to further irritation
and swelling, which is the cause of having Odynophagia or pain when swallowing,
Dysphagia or difficulty of swallowing, and globus sensation or feeling of lump
inside when swallowing. Damaged squamous esophageal epithelium can also
lead to tightening of muscles in the esophagus. Eventually, it will lead to
esophageal spasms. Esophageal spasms are painful contractions within the
muscular tube in the esophagus. The person may feel sudden, severe chest pain
that lasts from a few minutes to hours. Some people may mistake it for heart pain
(angina).
As the acid reaches the pharyngeal lining and airway which causes damage
to the cells, the cough sensory endings are stimulated as the body encourages
you to cough up the substance to remove it from your body. The vagal reflex is
activated wherein there is an activation of the cough center in the brainstem that
leads to bronchoconstriction. With this, the patient may experience coughing,
wheezing, or even shortness of breath. The irritation and swelling of throat and
vocal folds can also lead to hoarseness and sore throat. When the acid reaches to
the mouth, it can erode your tooth enamel and cause sensitivity. It can also
instigate to dental erosion since they may reduce the saliva pH (pH=5.5) to the
levels below the critical pH in which hydroxyapatite crystals in the dental enamel
dissolves. With a pH of less than 2.0;; gastric reflux is potentially capable of causing
dental erosion.
If treated, the prognosis for acid reflux (GERD) is good in mild to moderate
cases. Chronic cases often respond to prescription drugs, and severe cases may
require surgery to avoid serious complications. However, if GERD is left untreated,
this may lead to different complications. When the Fibroblasts proliferate and
deposit granulation tissue in the airway, this indicates having Chronic Laryngitis. It
has been suggested that chronic inflammation may persist as a result of failure of
the processes involved in wound healing. As the fibroblasts mitigate into the wound
site and proliferate, it tries to reconstitute the various connective tissue
components. As a result, the tissue deposition leads to narrowing of laryngeal and
tracheal space, which indicates Laryngotracheal Stenosis. Laryngotracheal
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stenosis (LTS) is a narrowing of the upper airway between the larynx and the
trachea with potentially devastating consequences, including respiratory failure,
cardiopulmonary arrest, and death.
Also, if left untreated, the squamous esophageal epithelium undergoes
metaplasia to become columnar epithelium. This can lead to Barrett's esophagus,
or the condition wherein the tissue that is similar to the lining of your intestine
replaces the tissue lining of your esophagus. Eventually, the predispose cells will
undergo dysplasia, having premalignant changes, or a generalized state
associated with a significantly increased risk of cancer. This can lead to
Esophageal adenocarcinoma. The overall five-year survival rate for esophageal
cancer is about 20%, but survival rates can range from 5% to 47%.
To add, the increased inflammation of squamous epithelium can lead to
esophagitis. As the ulceration forms, there will be a deposition of collagen as the
ulcers heal. Overtime, the collagen fibers will contract leading to Esophageal
stricture disease. Many patients need more than one dilation over time to keep the
esophagus wide enough for food to pass through. In rare cases, severe and
untreated esophageal strictures can cause perforations (small holes), which can
be life-threatening.
To summarize the situation if GERD is not treated, it can lead to different
complications which causes failure in the function of different organs affected.
Eventually, this can lead to death.

MANAGEMENT
MEDICAL MANAGEMENT
I. DIAGNOSTIC/LABORATORY CONFIRMATORY TESTS
● Physical exam and dietary history – The doctor will ask some questions about the
problems that the patient is having and its medical history. The doctor will also
instruct the client to write down the foods that the patient eat and when he/ she
have symptoms.
o Common physical exam findings in patients with gastroesophageal reflux
disease include:
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o Appearance of the patient - Patients with GERD usually appear ill and
uncomfortable due to the retrosternal pain
o HEENT - Hoarseness of voice, laryngitis, otitis media and d ental erosions
o Lungs – Wheezes and bronchitis
o Abdomen – Epigastric tenderness

● Upper gastrointestinal endoscopy and biopsy - This test allows direct visualization
of the lining of the esophagus and small intestine by the use of an endoscope
passed through the mouth into the esophagus, stomach and small intestine. Direct
visualization of the esophageal lining will allow a check for potential damage
(esophagitis, ulcers). A small sample of tissue may also be taken at the same time
for a biopsy.

● Upper GI series - This is a type of X-ray that shows certain physical abnormalities
that might cause GERD. X-rays are taken after the patient drink a chalky liquid
(barium) that coats and fills the inside lining of the digestive tract. The coating
allows the doctor to see a silhouette of the esophagus, stomach and upper
intestine.

● Esophagram - This is a radiographic study of the esophagus in which the patient
swallows barium (a contrast agent) and the radiologist visualizes the esophagus
and stomach under fluoroscopy. This test can help detect if there is a problem with
a stricture (narrowing) in the esophagus or if a hiatal hernia is present. It can also
give a rough estimate of the degree of esophageal muscle contractions. It is not
helpful, however, in determining if the patient has mild inflammation of the
esophagus or if the patient has Barrett’s esophagus. Additionally, a normal
esophagram does not exclude the fact that the patient may still have GERD.

● Esophageal manometry - This test involves a small diameter tube passed through
the nose into the esophagus. The nose and throat of the patient are numbed prior
75

to this procedure. Once the tube is in position, the patient is asked to swallow.
Measurements of esophageal function are made by the use of pressure readings
of the muscle contractions (motility) of the esophagus. Lower esophageal sphincter
muscle pressure can also be taken. This test will help physicians interpret whether
there is a problem with motility of the esophagus or the function of the lower
esophageal sphincter. The test by itself does not confirm the diagnosis of GERD
but will assist the physician in knowing if esophageal motility problems are
contributing to a patient’s GERD symptoms.

● Esophageal Impedance pH Study - This test is offered at few medical centers. It
involves the same type of procedure as a 24-hour pH test (a tube is passed through
the nose into the esophagus at the level of the LES). It measures liquid movement
from the stomach into the esophagus. This test may be important for people with
reflux symptoms who are having bile reflux, not acid reflux, and therefore have
normal results from a 24-hour pH probe. A 24-hour pH probe reading can be
obtained at the same time as the 24-hour impedance measurement.

● Proton pump inhibitor (PPI) trial therapy - is a brief period of medication to control
stomach acid production. If the patient feels better after being on PPI, he/she
probably have GERD.
II. PHARMACOLOGICAL MANAGEMENT

Medications to reduce acid production: Cimetidine, Famotidine
Medications that block acid production and heal the esophagus: lansoprazole,
Omeprazole
Medication forms a protective film on the surface of your esophagus and stomach:
Sucralfate
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GENERIC NAME: Cimetidine
BRAND NAME: Tagamet

DRUG PHARMACOTHERAPEUTIC: H2-receptor antagonist.
CLASSIFICATION: CLINICAL: Antiulcer, gastric acid secretion inhibitor
MODE OF ACTION: Inhibits histamine action at histamine-2 (H2)-receptor sites
of parietal cells.
Therapeutic Effect: Inhibits gastric acid secretion.
DOSAGE/ROUTE: PO: ADULTS, ELDERLY: 800 mg twice a day
or 400 mg 4 times a day for 12 wks.
INDICATIONS: Treatment of gastroesophageal reflux disease (GERD).
CONTRAINDICATIONS Hypersensitivity to other H2 antagonists.
:
SIDE EFECT: Occasional (4%–2%): Headache. Elderly, pts with renal
impairment, severely ill pts: Confusion, agitation, psychosis,
depression, anxiety, disorientation, hallucinations. Rare
(less than 2%): Diarrhea, dizziness, drowsiness, nausea,
vomiting, gynecomastia, rash, impotence.
ADVERSE EFFECT: None known
DRUG INTERACTION: May increase concentration, decrease metabolism of
warfarin, phenytoin, propranolol, tricyclic antidepressants.
May decrease absorption of itraconazole, ketoconazole.
NURSING 1. Assess for GI bleeding: hematemesis, blood in stool.
INTERVENTIONS: 2. Monitor for changes in mental status in elderly, severely
ill, those with renal impairment.
3. Avoid tasks that require alertness, motor skills until
response to drug is established.
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4. Avoid smoking, excessive amounts of caffeine.
5. Do not take antacids within 1 hr of cimetidine
administration.
REFERENCE: Hodgson, B. B., & Kizior, R. J. (2020) Saunders Nursing
Drug Handbook. Philadephia: Saunders.

GENERIC NAME: Famotidine
BRAND NAME: Pepcid

DRUG PHARMACOTHERAPEUTIC: H2 receptor antagonist.
CLASSIFICATION: CLINICAL: Antiulcer, gastric acid secretion inhibitor
MODE OF ACTION: Inhibits histamine action of H2 receptors of parietal cells.
Therapeutic Effect: Inhibits gastric acid secretion (fasting,
nocturnal, or stimulated by food, caffeine, insulin).
DOSAGE/ROUTE: PO: ADULTS, ELDERLY, CHILDREN 12 YRS AND
OLDER: 20 mg twice a day for 6 wks.
CHILDREN 1–11 YRS: 1 mg/kg/day in 2 divided doses.
Maximum: 40 mg 2 times/day. CHILDREN 3 MOS–11
MOS: 0.5 mg/kg/ dose twice a day. CHILDREN YOUNGER
THAN 3 MOS, NEONATES: 0.5 mg/kg/dose once a day.
INDICATIONS: Short-term treatment of gastroesophageal reflux disease
(GERD)
CONTRAINDICATIONS Hypersensitivity to other H2 antagonists.
:
SIDE EFECT: Occasional (5%): Headache. Rare (2% or less):
Confusion, constipation, diarrhea, dizziness.
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ADVERSE EFFECT: Agranulocytosis, pancytopenia, thrombocytopenia occur
rarely.
DRUG INTERACTION: May decrease absorption of atazanavir, itraconazole,
ketoconazole.
NURSING 1. Assess epigastric/abdominal pain.
INTERVENTIONS: 2. Monitor daily pattern of bowel activity, stool consistency.
3. Monitor for diarrhea, constipation, headache. Assess
confusion in elderly.
4. Avoid excessive amounts of coffee, aspirin.
5. Instruct patient to report headache

GENERIC NAME: Lansoprazole
BRAND NAME: Prevacid

DRUG CLINICAL: Proton pump inhibitor
CLASSIFICATION:
MODE OF ACTION: Selectively inhibits gastric parietal cell membrane enzyme
system (hydrogen-potassium adenosine triphosphatase,
proton pump). Therapeutic Effect: Suppresses gastric acid
secretion.
DOSAGE/ROUTE: Gastric Ulcer
PO: ADULTS: 30 mg/day for up to 8 wks.

NSAID Gastric Ulcer
79

PO: ADULTS, ELDERLY: (Healing): 30 mg/ day for up to 8
wks. (Prevention): 15 mg/ day for up to 12 wks.

Gastroesophageal Reflux Disease (GERD)
PO: ADULTS: 15 mg/day for up to 8 wks.
INDICATIONS: Treatment of gastroesophageal reflux disease (GERD),
NSAID-associated gastric ulcer. OTC: Relief of frequent
heartburn.
CONTRAINDICATIONS None known
:
SIDE EFECT: Occasional (3%–2%): Diarrhea, abdominal pain, rash,
pruritus, altered appetite. Rare (1%): Nausea, headache.
ADVERSE EFFECT: Bilirubinemia, eosinophilia, hyperlipemia occur rarely.
DRUG INTERACTION: May decrease concentration of atazanavir. May interfere
with absorption of ampicillin, digoxin, iron salts,
ketoconazole. Sucralfate may delay absorption. May
increase effect of warfarin. May decrease effect of
clopidogrel.
NURSING 1. Assess for epigastric/abdominal pain, evidence of GI
INTERVENTIONS: bleeding, ecchymosis.
2. Assess for therapeutic response (relief of GI symp-
toms).
3. Question if diarrhea, abdominal pain, nausea occurs.
4. Do not chew/crush delayed-release capsules.
5. For pts who have difficulty swallowing capsules, open
capsules, sprinkle granules on 1 tbsp of applesauce,
swallow immediately.

80

GENERIC NAME: omeprazole
BRAND NAME: Prilosec

DRUG PHARMACOTHERAPEUTIC: Benzimidazole. CLINICAL:
CLASSIFICATION: Proton pump inhibitor
MODE OF ACTION: Converted to active metabolites that irreversibly bind to,
inhibit hydrogen-potassium adenosine triphosphatase, an
enzyme on the surface of gastric parietal cells. Inhibits
hydrogen ion transport into gastric lumen. Therapeutic
Effect: Increases gastric pH, reduces gastric acid
production.
DOSAGE/ROUTE: Erosive Esophagitis, Poorly Responsive Gastroesophageal
Reflux Disease (GERD), Active Duodenal Ulcer,
Prevention/ Treatment of NSAID-Induced Ulcers
PO: ADULTS, ELDERLY: 20 mg/day.
INDICATIONS: Short-term treatment (4–8 wks) of erosive esophagitis
(diagnosed by endoscopy), symptomatic gastroesophageal
reflux disease (GERD) poorly responsive to other
treatment.
:
SIDE EFECT: Frequent (7%): Headache.
Occasional (3%–2%): Diarrhea, abdominal pain, nausea.
Rare (2%): Dizziness, asthenia (loss of strength, energy),
vomiting, constipation, upper respiratory tract infection,
back pain, rash, cough.
ADVERSE EFFECT: Pancreatitis, hepatotoxicity, interstitial nephritis occur
rarely.
81

DRUG INTERACTION: May decrease concentration/ effects of atazanavir. May
increase concentration/effects of diazepam, oral
anticoagulants, phenytoin. May decrease
concentration/effects of clopidogrel.
NURSING 1. Evaluate for therapeutic response (relief of GI
INTERVENTIONS: symptoms).
2. Question if GI discomfort, nausea, diarrhea occurs.
3. Report headache, onset of black, tarry stools, diarrhea,
abdominal pain.
4. Avoid alcohol.
5. Swallow capsules whole;; do
not chew/crush and take before eating

GENERIC NAME: Sucralfate
BRAND NAME: Carafate

DRUG PHARMACOTHERAPEUTIC: Gastrointestinal agent.
CLASSIFICATION: CLINICAL: Antiulcer.
MODE OF ACTION: Forms ulcer-adherent complex with proteinaceous exudate
(e.g., albumin) at ulcer site. Forms viscous, adhesive barrier
on surface of intact mucosa of stomach, duodenum.
Therapeutic Effect: Protects damaged mucosa from
further destruction by absorbing gastric acid, pepsin, bile
salts.
DOSAGE/ROUTE: Active Duodenal Ulcers
82

PO: ADULTS, ELDERLY: 1 g 4 times a day (Before meals
and at bedtime) or 2 g 2 times a day for up to 8 wks.

Maintenance Therapy of Duodenal Ulcers
PO: ADULTS, ELDERLY: 1 g twice a day.

INDICATIONS: Short-term treatment (up to 8 wks) of duodenal ulcer.
Maintenance therapy of duodenal ulcer after healing of
acute ulcers.
:
SIDE EFECT: Frequent (2%): Constipation.
Occasional (less than 2%): Dry mouth, backache,
diarrhea, dizziness, drowsiness, nausea, indigestion, rash,
urticaria, pruritus, abdominal discomfort.
ADVERSE EFFECT: Bezoars (compacted, undigestible material that does not
pass into intestine) have been reported.
DRUG INTERACTION: May decrease absorption of digoxin, ketoconazole,
levothyroxine, phenytoin, quinidine, quinolonesn(e.g.,
ciprofloxacin), ranitidine, tetracycline, theophylline.
NURSING 1. Monitor daily pattern of bowel activity,
INTERVENTIONS: stool consistency.
2. Take medication on an empty stomach.
3. Dry mouth may be relieved by sour hard
candy, sips of tepid water.
4. Advise patient to avoid alcohol and foods that may cause
an increase in GI irritation.
5. Instruct patient to report troublesome side effects such
as severe or prolonged skin reactions (rash, itching) or GI
problems (nausea, diarrhea, constipation, gastric pain,
indigestion, dry mouth).
83


III. NON-PHARMACOLOGICAL MANAGEMENT
SURGICAL MANAGEMENT
● Antireflux Surgery - Surgery for GERD is known as antireflux surgery and involves
a procedure called a fundoplication. The goal of a fundoplication is to reinforce the
LES to recreate the barrier that stops reflux from occurring. This is done by
wrapping a portion of the stomach around the bottom of the esophagus in an effort
to strengthen, augment, or recreate the LES valve. The most common type of
fundoplication is a Nissen fundoplication in which the stomach is wrapped 360
degrees around the lower esophagus. There are also a variety of partial
fundoplication techniques. As the name suggests, these techniques involve a wrap
which does not go entirely around the esophagus. The Nissen fundoplication is
almost always chosen to control GERD. During the procedure, a surgeon creates
a sphincter (tightening muscle) at the bottom of the esophagus to prevent acid
reflux. Most people notice a significant decrease in acid reflux symptoms after the
surgery.

● LINX device. A ring of tiny magnetic beads is wrapped around the junction of the
stomach and esophagus. The magnetic attraction between the beads is strong
enough to keep the junction closed to refluxing acid, but weak enough to allow
food to pass through. The LINX device can be implanted using minimally invasive
surgery.

● Transoral incisionless fundoplication (TIF). This new procedure involves tightening
the lower esophageal sphincter by creating a partial wrap around the lower
esophagus using polypropylene fasteners. TIF is performed through the mouth
with a device called an endoscope and requires no surgical incision. Its
advantages include quick recovery time and high tolerance.
84

NURSING MANAGEMENT
Nursing Rationale Goal of Care Nursing
Diagnosis Interventions
Imbalanced The state in which Within 2 days of 1. Accurately
Nutrition: Less an individual who is nursing care, the measure the
Than Body not on NPO, patient will be able patient’s weight
Requirements experiences or is at to ingest daily and height.
related to inability risk for inadequate nutritional R: For baseline
to intake enough intake or requirements in data.
food because of metabolism of accordance to his
reflux nutrients for activity level and 2. Encourage small
metabolic needs metabolic needs frequent meals of
with or without high calories and
weight loss. It is a high protein foods.
significant health R: Small and
concern that can frequent meals are
lead to serious easier to digest.
diseases and can
make underlying 3. Instruct to remain
medical conditions in upright position
worse. at least 2 hours
after meals;;
avoiding eating 3
hours before
bedtime.
R: Helps control
reflux and causes
less irritation from
reflux action into
esophagus.

85

4. Instruct patient to
eat slowly and
masticate foods
well.
R: Helps prevent
reflux.

5. Obtain a
nutritional history.
R: Determining the
feeding habits of
the client can
provide a basis for
establishing a
nutritional plan.
Acute Pain related The stomach acid Within 2 hours of 1. Administer
to that leaks into the nursing care, the prescribed
gastroesophageal oesophagus in patient will be able medications that
reflux people with GERD to manifest alleviate the
can damage the behaviours of symptoms of
lining of the diminished pain. heartburn/ chest
oesophagus pain
(oesophagitis), R: Antacids are
which can cause helpful in
ulcers to form. neutralizing
These ulcers can stomach acid. H2-
bleed, causing pain receptor blockers
and making it reduce the
difficult to swallow. production of
stomach acid.

86

2. Assess the
patient’s vital signs
and characteristics
of pain at least 30
minutes after the
administration of
medication.
R: To monitor
effectiveness of
medical treatment
for the relief of
heartburn.

3. Carefully assess
pain location and
discern pain from
GERD and angina
pectoris.
R: Pain of
esophageal spasm
resulting from reflux
esophagitis tends
to be chronic and
may mimic angina
pectoris: radiating
to the neck, jaws,
and arms.

4. Elevate the head
of the bed
87

R: To reduce the
backwash of acid
from the
esophagus from
the stomach to
esophagus

5. Encourage
patient to follow
appropriate meal
times and meal
portions.
R: To ensure that
the patient does not
eat a huge meal, or
that he/she does
not eat late at night/
before bedtime as
both of these
contribute to
GERD.

Risk for Aspiration GERD can cause Within 7 hours of 1. Assess patient’s
stomach contents nursing care, the ability to swallow
to flow back into patient will be able and the presence
the esophagus and to maintain patent of gag reflex. Have
dysphagia can airway the patient swallow
cause food and/or a sip of water.
liquid to remain in
the esophagus
after swallowing. If
88

these substances R: Loss of the gag
are inhaled and reflex increases the
move into the risk of aspiration.
lungs, it can lead to 2. Avoid placing
serious respiratory patient in supine
problems, such as position, have the
aspiration patient sit upright
pneumonia. after meals.
R: Supine position
after meals can
increase
regurgitation of
acid.

avoid highly
seasoned food,
acidic juices,
alcoholic drinks,
bedtime snacks,
and foods high in
fat.
R: These can
reduce the lower
esophageal
sphincter pressure.

4. Elevate HOB
while in bed.
R: To prevent
aspiration by
89

preventing the
gastric acid to flow
back in the
esophagus.

5. Instruct the
patient to chew
food thoroughly
and eat slowly.
R: Well-masticated
food is easier to
swallow. Food
should be cut into
small pieces.
Impaired tissue Whether this acid Within 7 hours of 1. Teach patient to
integrity related to reflux is nursing care, the avoid foods that
esophageal accompanied by patient will be able cause pain and or
exposure to gastric GERD symptoms to verbalize can increase acid
acid or not, stomach knowledge of secretions.
acid and chemicals necessity lifestyle R: Foods that can
wash back into the changes cause pain or
esophagus, increase acid
damaging secretion can
esophagus tissue worsen esophageal
and triggering erosion.
changes to the
lining of the 2. If indicated,
swallowing tube recommend
strategies for
smoking cessation.
90

R: Smoking impairs
tissue healing and
is associated with a
higher incidence of
complications that
may necessitate
surgery.

3. Teach the
patient to avoid
NSAIDS, ASA,
chocolate, coffee,
and alcohol.
R: These
medicines and
foods have been
associated with
increased Gl
erosions and
acidity.

4. Administer acid
suppression
therapy as
prescribed.
R: To decrease the
amount of acid that
is produced and
can cause mucosal
erosion.

91

5. Encourage a diet
that meets
nutritional needs.
R: A high-protein,
high-calorie diet
may be needed to
promote healing.
Deficient The state in which Within 7 hours of 1. Provide patient
Knowledge related an individual or nursing care, the with information
to lack of group experiences patient will be able regarding disease
information a deficiency in to have increased process, health
regarding the cognitive knowledge of practices that can
condition knowledge or actions that reduce be changed, and
psychomotor skills reflux. medications to be
concerning the utilized.
condition or R: Provides
treatment plan. knowledge and
facilitates
compliance.

2. Instruct patient
regarding eating
small amounts of
bland food followed
by a small amount
of water. Instruct to
remain in upright
position at least 1–
2 hours after meals,
and to avoid eating
92

within 2–4 hours of
bedtime.
R: Gravity helps
control reflux and
causes less
irritation from reflux
action into the
esophagus.

3. Instruct patient
regarding
avoidance of
alcohol, smoking,
and caffeinated
beverages.
R: Increases acid
production and may
cause esophageal
spasms.

raise both arms,
fully extended
towards the ceiling
prior to eating.
R: Relieves
spasms and allows
for more comfort
when eating.

93

5. Instruct patient in
medications,
effects, side effects,
and to report to
physician if
symptoms persist
despite medication
treatment.
R: Promotes
knowledge,
facilitates
compliance with
treatment, and
allows for prompt
identification of
potential need for
changes in
medication regimen
to prevent
complications.

REVIEW OF RELATED LITERATURE
Title: Stomach Acid & Heartburn Drugs Linked with COVID-19 Outcomes
Bibliography: Yeager, A. (2020). Stomach Acid & Heartburn Drugs Linked with COVID-
19 Outcomes. Retrieved from: https://www.the-scientist.com/news-opinion/stomach-
acid-heartburn-drugs-linked-with-covid-19-outcomes-68026
Summary:
The COVID-19 pandemic's uncertainty has made our stomachs turn, and new
evidence reveals that severe heartburn is connected to worse COVID-19 symptoms.
94

Doctors in the United States discovered that those who took a proton-pump inhibitor twice
a day for acid reflux had a greater risk of testing positive for SARS-CoV-2 than those who
took the medicine once a day or those who took a histamine-2 receptor blocker like Pepcid
AC. Proton-pump inhibitors "may weaken the stomach barrier to SARS-CoV-2 entrance
and reduce microbial diversity in the gut," raising the probability of COVID-19 infection in
patients.

Title: Gastroesophageal reflux disease is linked with higher risks of larynx and
esophageal cancers
Bibliography: Henderson, E. (2021). Gastroesophageal reflux disease is linked with
higher risks of larynx and esophageal cancers. Retrieved from: https://www.news-
medical.net/news/20210222/Gastroesophageal-reflux-disease-is-linked-with-higher-
risks-of-larynx-and-esophageal-cancers.aspx
Summary:
GERD is a gastrointestinal disorder that affects about 20% of Americans. When
stomach acid rushes back into the esophagus, it can cause esophagitis in adults harm
the tissues According to research, this damage may put patients at risk. esophageal
adenocarcinoma is a kind of cancer that affects the esophagus. The researchers
assessed that 24 percent of the subjects had GERD based on Medicare claims data.
Following that, for the next 16 years, 931 people developed esophageal cancer as a result
of their participation in the trial. 876 developed laryngeal squamous cell carcinoma, and
301 developed esophageal squamous cell carcinoma after adenocarcinoma. People with
GERD had a two-fold increased chance of getting each of these conditions. these
cancers, and the increased risk was identical in all groups, smoking status, and alcohol
usage are all factors to consider.

95

GASTROENTERITIS

DEFINITION

One of the most common worldwide health problems that we still face up to this
moment whereas about one out of every five cases is Gastroenteritis. To thoroughly
understand this condition, we can easily break down the word itself to know its certain
definition. The word “Gastro-” refers to the stomach, “-enter-” refers to the small intestine,
and “-itis” refers to inflammation. There are mainly two different types of Gastroenteritis,
Acute gastroenteritis and Chronic gastroenteritis. This condition has been mainly called
“stomach bug” or “stomach flu” since this causes diarrhea and/or vomiting. Symptoms of
Gastroenteritis occur as a result of inflammation of the mucous membranes of the
stomach and intestinal tract, thus stomach pain is a much known symptom. It doesn’t just
solely target the stomach which causes pain, but it can also involve small intestines and
colon. Yet, this has also been affecting mainly the small bowel. Gastroenteritis can be
caused by either viral, which is a more common, bacterial infection, parasites, or toxins.
These viruses causing this condition can mostly infect the lining of the small intestine.
It has already been considered Gastroenteritis is one of the most common causes
of morbidity and mortality worldwide. About more than 20 million people have been
diagnosed with gastroenteritis each year in the United States with an intestinal upset. The
most common cause of this outrage in the United States is virus. In the Philippines, the
World Health Organization (WHO) noted that acute gastroenteritis is the most common
cause of morbidity and it ranks among the top 20 causes of mortality. There was a
diarrhea outbreak last July 2021 at Sto. Tomas, Davao del Norte whereas 47 residents
from the said barangay were rushed to the hospitals, Vomiting and diarrhea were the
common complaints of symptoms by the residents. It was found out in the investigation
of their Quick Reaction Team (QRT) together with their Municipal Health Officer (MHO),
that the reason behind this outbreak was the contamination of water system source of the
barangay in view of the fact that the water’s poor quality due to poor chlorine disinfection.

96

ANATOMY

Gastrointestinal Tract - organs that food and liquids travel through when they are
wallowed, digested, absorbed, and leave the body as feces. These organs include the
mouth, pharynx (throat), esophagus, stomach, small intestine, large intestine, rectum,
and anus. The gastrointestinal tract is part of the digestive system.

Stomach A saclike expansion of the digestive tract of a vertebrate that is located
between the esophagus and duodenum and typically consists of a simple
often curved sac with an outer serous covering, a strong muscular wall
that contracts rhythmically, and an inner mucous membrane lining that
contains gastric glands
Large
The more terminal division of the vertebrate intestine that is wider and
Intestines
shorter than the small intestine, typically divided into cecum, colon, and
97

rectum, and concerned especially with the resorption of water and the
formation of feces.
Small
The narrow part of the intestine that lies between the stomach and colon,
Intestines
consists of duodenum, jejunum, and ileum, secretes digestive enzymes,
and is the chief site of the digestion of food into small molecules which
are absorbed into the body
ETIOLOGY

Predisposing Rationale
Factors
Age Infants as well as young children are at increased risk due to
their underdeveloped immune systems;; while the elderly are
at increased risk due to their weakened immune systems.
Gastroenteritis in the pediatric population is a very common
condition that accounts for around 10 percent of pediatric
deaths and is the second cause of death worldwide. The most
common cause in infants younger than 24 months old
(commonly affects children between 6 months and 18 months
of age) is rotavirus, and after 24 months of age, shigella
becomes the most common cause and rotavirus comes
second. Most people are infected after consuming
contaminated food or water.
Immunocompromising Infectious gastroenteritis is a common, acute illness that is
characteristically self-limiting, but it can become debilitating
and life-threatening in immunocompromised patients. Viruses,
98

(e.g., Noroviruses, Rotavirus) are major pathogens among the
microbes associated with gastroenteritis in both
immunocompetent and immunocompromised hosts.
Immunocompromised hosts are highlighted with potentially
serious outcomes of this illness as they cannot adequately
clear the virus. Generally, anyone suffering from a
compromised immune system is more vulnerable to bacterial,
fungal, viral, and parasitic illnesses, which healthy immune
systems normally conquer.

Precipitating Rationale
Factors
Poor hygiene Poor hygiene is the most common cause of gastroenteritis. It is
possible to contract it through close contact with animals, but it is
more likely to be contracted from bacterially contaminated food or
drink (or the toxic substances they produce).
Improper Infection is more prevalent when there is a lack of proper sanitation
sanitation and hygiene, as well as safe drinking, cooking, and cleaning water,
as these environments promote pathogen growth and spread.
Lack of clean Infectious and parasitic illnesses are still the primary factors of death
water source and illness related to gastroenteritis across the world, owing primarily
to poor water quality, with diarrhea ranking first in morbidity and sixth
in fatality.
Improper food When food is not handled properly, pathogenic contamination is
handling more likely. Not chilling or improper cooking meals, cross-
contamination of cooked and raw foods, and unclean cooking
surfaces, tools, dishes, or hands are all common risk factors. As
such, food poisoning is a prevalent cause of gastroenteritis, which is
distinguished by a set of well-known symptoms.

99

SIGNS AND SYMPTOMS

Symptoms Rationale
Vomiting Although the specific mechanism of vomiting in gastroenteritis is
(and nausea) unknown, it is considered to be caused by peripheral stimuli emerging
from the gastrointestinal tract, especially via the vagus nerve, or by
serotonin activation of the gut's 5-hydroxytryptamine 3 (5HT3)
receptors. In the case of acute gastroenteritis, intestinal irritation can
damage the mucosa of the gastrointestinal tract, causing serotonin to
be released from the enterochromaffin cells. This serotonin binds to the
5HT3 receptors on the vagal afferent nerves in the gastrointestinal tract,
which are subsequently sent directly or via the chemoreceptor trigger
zone to the vomiting center. The vomiting center then sends efferent
impulses to the diaphragm, abdominal muscles, and visceral nerves of
the stomach and esophagus to produce vomiting and/or induce nausea.
Diarrhea In gastroenteritis, viruses infect cells in the lining of the small intestine
where they multiply and cause watery diarrhea (including vomiting, and
fever). In addition, Certain species, such as Vibrio cholerae and
enterotoxigenic strains of E. coli, attach to the lining of the intestines
without invading and produce enterotoxins. These toxins cause the
intestines to secrete water and electrolytes, resulting in watery diarrhea.
Other bacteria (such as Staphylococcus aureus, Bacillus cereus, and
Clostridium perfringens) produce an exotoxin that can be present in
contaminated food. The toxin can cause gastroenteritis without causing
a bacterial infection. These toxins generally cause severe nausea,
vomiting, and diarrhea. Moreover, some bacteria (such as certain
strains of E. coli, Campylobacter, Shigella, Salmonella, and Clostridium
difficile) invade the lining of the small intestine or colon. There, they
damage cells, causing sores (ulcerations) that bleed, and allow a
100

considerable leakage of fluid containing proteins, electrolytes, and
water, constituting diarrhea.
Abdominal Gastroenteritis causes the lining of the stomach or colon to become
pain painful and swollen (inflamed), preventing it from functioning correctly.
Symptoms can range from mild pain to life-threatening.
Bloody stools The body loses fluids and electrolytes as a result of the diarrhea
(dehydration). The watery diarrhea usually lasts approximately a day
before turning into vivid red bloody stools. The infection causes ulcers
in the intestines, resulting in bloody stools.

101

PATHOPHYSIOLOGY

102

Narrative:

“Gastro” refers to stomach, “enter” refers to small intestine and “itis” refers to
inflammation. There are two factors that bring about the onset of the disease, the
predisposing and precipitating factors. Predisposing factors, include age and
immunocomprimisation. While precipitating factors include poor hygiene, improper
sanitation, lack of clean water source, and improper food handling. These factors then
are affected by ingestion of contaminated food and/or water with either viruses, bacteria,
or other pathogens such as parasites, leading to pathogenic infiltration of the
gastrointestinal tract. Then, such infiltration proceeds to pathogenic interaction with the
enteric nervous system, with pathogen toxins stimulating enteric chloride secretion, as
well as irritation of the mucosal lining. Pathogenic infiltration of the enteric nervous system
then leads to increased gastrointestinal fluid secretion including fluid and electrolytes,
inducing vomiting and/or nausea (which can be diagnosed with physical assessment,
stool exam, and blood tests). Irritation of the mucosal lining, on the other hand, leads to
the destruction of the epithelial cells causing noxious stimuli and inflammation of layer
beneath the epithelium of mucosa, and superficial ulceration of mucosa. Noxious stimuli
and inflammation of layer beneath the epithelium of mucosa trigger the stimulation of
visceral nerve afferent and systematic invasion. Together with the superficial ulceration
of the mucosa, stimulation of visceral nerve afferent causes the abdomen to be in pain
(which can be diagnosed with physical assessment and stool exam). Systematic invasion,
on the other hand, triggers the excretion of interstitial fluids leading to diarrhea. In addition,
superficial ulceration of the mucosa causes stool to be bloody or with mucus (which can
be diagnosed with stool exam). Superficial ulceration of the mucosa also leads to the
reduction of mucosal surface area. This reduction of mucosal surface area causes the
alteration of Brush Border activity, and/or structure, impairing the absorption of
substances in the small intestine. As the absorption of substances in the small intestine
is being impaired, osmotically active substances enter the large bowel, leading to the
capacity of water reabsorption in the large intestine to be overwhelmed, causing diarrhea
(which can be diagnosed with physical assessment, stool exam, and blood tests).
Together with vomiting, diarrhea then leads to dehydration and finally a diagnosis of
103

gastroenteritis. If gastroenteritis is treated with medical management (such as
administration of antibiotics and/or antiemetics, and rehydration therapies), and nursing
management (such as education about diet, increasing oral fluid intake, and avoiding
certain foods, a good prognosis could be expected. On the contrary, if gastroenteritis is
not treated, the infection could gain access to the systemic circulation, infecting other
parts of the body, leading to severe complications and poor prognosis, and in more severe
cases, death.

DIAGNOSTIC/LABORATORY CONFIRMATORY TESTS

Physical The physical exam can assist in determining the cause of
Examination gastroenteritis as well as assess the presence and severity of
dehydration. The severity of the disease can be determined by
temperature, blood pressure, pulse, and body weight. It's also possible
that the temperature will be slightly higher.

Viral Gastroenteritis Clinical Presentation: History, Physical
Examination (medscape.com)
Stool Tests A rapid stool test can detect rotavirus or norovirus, but there are no
quick tests for other viruses that cause gastroenteritis. In some cases,
your doctor may have you submit a stool sample to rule out a possible
bacterial or parasitic infection.

https://www.mayoclinic.org/diseases-conditions/viral-
gastroenteritis/diagnosis-treatment/drc-20378852
Blood Tests In most cases that fit the clinical features of viral gastroenteritis,
laboratory tests are not indicated.
If bacterial or protozoal infection is suspected, stool studies for occult
blood, white blood cell (WBC) count, microscopy for protozoa, C
104

difficile toxin, Giardia lamblia by enzyme immunoassay (EIA), or
bacterial culture may be indicated.
Viral Gastroenteritis Workup: Laboratory Studies (medscape.com)
CT Scan CT scans are used to verify the presence or absence of tumors,
infection, abnormal anatomy, or to examine changes in the body as a
result of trauma. Gastroenterologists may order this scan to evaluate
abdominal pain or to examine organs such as the stomach, small
intestine, liver, pancreas, gall bladder, and colon. An abdominal CT
scan also can be extremely helpful in the diagnosis of conditions like
Crohn’s disease, appendicitis or colon cancer.

CT Scan – Gastroenterology Associates of Central Georgia
(gaocg.com)
MEDICAL MANAGEMENT

A. PHARMACOLOGICAL TREATMENTS (MEDICATIONS)

Generic Name Ampicillin
Brand Name Omnipen
Drug Class Antibiotic
Dose/Route
Penicillins, Amino
Systemic Infections
Adult: PO 250–500 mg q6h IV/IM 250 mg–2 g q6h
105

Child: PO 25–50 mg/kg/d divided q6h IV/IM 25–100 mg/kg/d
divided q6h
Mode of Action The mechanisms of action of ampicillin are interference with cell
wall synthesis by attachment to penicillin-binding proteins (PBPs),
inhibition of cell wall peptidoglycan synthesis and inactivation of
inhibitors to autolytic enzymes.
Indication Infections of GU, respiratory, and GI tracts and skin and soft
tissues;; also gonococcal infections, bacterial meningitis, otitis
media, sinusitis, and septicemia and for prophylaxis of bacterial
endocarditis. Used parenterally only for moderately severe to
severe infections.
Contraindications Hypersensitivity to penicillin derivatives;; infectious

mononucleosis.
Side Effects
acute inflammatory skin eruption (erythema multiforme),redness
and peeling of the skin (exfoliative dermatitis), rash, hives, fever,
seizure, black hairy tongue, diarrhea,inflammation of the small
intestine and colon, inflammation of the tongue, nausea, yeast
infectionin the mouth (oral candidiasis/thrush), swelling or
inflammation of the large intestine/colon,inflammation of the
mouth,vomiting,lowwhite blood cell count (agranulocytosis), low
red blood cell count (anemia), high white blood cell count
(eosinophilia), reduction of white blood cells (leukopenia), acute
allergic reaction (anaphylaxis), elevated aspartate
aminotransferase (AST), inflammation in the kidney, noisy
breathing, allergic reaction, headache, vaginalitching or
discharge, dark urine, easy bruising or bleeding, persistent sore
throat or fever
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Drug Interactions Allopurinol increases incidence of rash. Effectiveness of the
AMINOGLYCOSIDES may be impaired in patients with severe
end-stage renal disease. Chloramphenicol, erythromycin, and
tetracycline may reduce bactericidal effects of ampicillin;; this
interaction is primarily significant when low doses of ampicillin are
used. Ampicillin may interfere with the contraceptive action of oral
contraceptives
Adverse Effects Similar to those for penicillin G. Hypersensitivity (pruritus,
urticaria, eosinophilia, hemolytic anemia, interstitial nephritis,
anaphylactoid reaction);; superinfections. CNS: Convulsive
seizures with high doses. GI: Diarrhea, nausea, vomiting,
pseudomembranous colitis. Other: Severe pain (following IM);;
phlebitis (following IV). Skin: Rash.
Nursing
● Determine previous hypersensitivity reactions to
Responsibilities
penicillins, cephalosporins, and other allergens prior to
therapy.
● Lab tests: Baseline C&S tests prior to initiation of

therapy;; start drug pending results. Baseline and periodic
assessments of renal, hepatic, and hematologic functions,
particularly during prolonged or high-dose therapy.
● Note: Sodium content of drug must be considered in

patients on sodium restriction.
● Inspect skin daily and instruct patient to do the same.
The appearance of a rash should be carefully evaluated to
differentiate a nonallergenic ampicillin rash from a
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hypersensitivity reaction. Report rash promptly to
physician.
● Note: Incidence of ampicillin rash is higher in patients

with infectious mononucleosis or other viral infections,
Salmonella infections, lymphocytic leukemia, or
hyperuricemia or in patients taking allopurinol.
● Take medication around the clock;; continue taking

medication until it is all gone (usually 10 d) unless
otherwise directed by physician or pharmacist.
Generic Name Domperidone
Brand Name Motilium
Drug Class Antiemetics / GIT Regulators, Antiflatulents & Anti-Inflammatories
Dose/Route
Oral
Adult: 10 mg up to 3 times daily. Max: 30 mg daily. Max treatment
duration: 7 days. Use the lowest effective dose for the shortest
possible duration.
Child: <12 years <35 kg: 0.25 mg/kg given up to 3 times daily.
Max: 0.75 mg/kg daily. ≥12 years ≥35 kg: Same as adult dose
Mode of Action Domperidone is a peripheral dopamine-receptor blocker. It

increases oesophageal peristalsis, lower oesophageal sphincter
pressure, gastric motility and peristalsis, and enhances
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gastroduodenal coordination, thereby facilitating gastric emptying
and decreasing small bowel transit time.
Indication
Symptomatic management of gastrointestinal (GI) motility
disorders and to treat gastroesophageal reflux disease
Contraindications Conditions in which stimulation of the GI tract may be dangerous
(eg. gastrointestinal hemorrhage, NEC, mechanical obstruction or
perforation, Hirschsprung's disease
Side Effects insomnia, irritability, lethargy, dry mouth, gynecomastia,

extrapyramidal symptoms (such as agitation, tremor and
increased or decreased muscle movement) are rare,QTc
prolongation at higher doses, especially in patients with other risk
factors such as other medications known to prolong QTc (for
example chloral hydrate, ciprofloxacin, clarithromycin, dopamine,
epinephrine, erythromycin, norepinephrine, salbutamol),
hypokalemia or hyperkalemia, congenital long QT syndrome
Drug Interactions
Bepridil,Cisapride,Darunavir,Dronedarone,Fluconazole,Ketocona
zole,Mesoridazine,Pimozide,Piperaquine,Posaconazole,Saquinav
ir,Sparfloxacin,Terfenadine,Thioridazin,Ziprasidne
Adverse Effects
Significant: Elevated prolactin levels, hypersensitivity reactions
(e.g. anaphylaxis, angioedema). Rarely, neurological or
extrapyramidal side effects (in children).
Eye disorders: Oculogyric crisis.
109

Gastrointestinal disorders: Dry mouth, diarrhoea, transient
intestinal cramps.
General disorders and admin site conditions: Asthenia.
Immune system disorders: Urticaria.
Investigations: Abnormal LFT.
Nervous system disorders: Headache, migraine, dizziness,

convulsions.
Psychiatric disorders: Anxiety, agitation, nervousness, loss of

libido, somnolence.
Renal and urinary disorders: Urinary retention.
Reproductive system and breast disorders: Galactorrhoea, breast

pain or tenderness, gynaecomastia, amenorrhoea.
Skin and subcutaneous tissue disorders: Rash, pruritus.
Potentially Fatal: Serious ventricular arrhythmias, sudden cardiac

death, QT interval prolongation, torsades de pointes.
Nursing
● Assess for nausea, vomiting, abdominal distention,
Responsibilities
and bowel sounds before and after administration.
● Monitor BP (sitting, standing, lying down) and pulse

before and periodically during therapy. May cause
prolonged QT interval, tachycardia, and orthostatic
hypotension, especially in patients older than 60 yrs or
taking >30 mg/day.
110

● Monitor for symptoms related to hyperprolactinemia
(menstrual abnormalities, galactorrhea, sexual
dysfunction).

B. NON-PHARMACOLOGICAL TREATMENTS

Increase Oral Drink plenty of liquid every day, taking small, frequent sips. When
Fluid Intake you have gastroenteritis, your body eliminates large quantities of
water and mineral salts that are essential to your body's proper
functioning. It is therefore important to drink plenty of fluids and to
replenish mineral salts to prevent dehydration and promote
recovery.

Let stomach Stop eating temporarily (for about 3-4 hours). When vomiting
settle subsides, gradually start eating again: eat small amounts of food at
a time, but eat more often.

Commercial To rehydrate, it is best to use a commercial rehydration solution,
Rehydration such as Gastrolyte. Commercial rehydration solutions contain the
Solutions ideal proportion of mineral salts your body needs to recover. They
allow the body to absorb fluids better so that you get plenty of
fluids. They also replace mineral salts lost due to diarrhea or
vomiting.

111

Avoid certain Avoid any caffeine, alcohol, nicotine, and fatty or highly seasoned
foods and food until the client feels better.
substances
Rest Have plenty of rest. The illness and dehydration may make the
client weak and tired.
Maintain good Wash hands well for at least 30 seconds with an antibacterial soap,
personal especially after a bowel movement.
hygiene
IV rehydration IV access should be obtained in severe dehydration and patients
should be administered a bolus of 20-30 mL/kg lactated Ringer
(LR) or normal saline (NS) solution over 60 minutes.

NURSING MANAGEMENT

Nursing Goal of Care Nursing Interventions

Diagnosis
Diarrhea related to Within 8 hours of nursing > Assess for abdominal pain,
bacterial, viral, or care, the patient abdominal cramping, hyperactive
parasitic infection reestablishes and bowel sounds, frequency, urgency,
maintains a normal and loose stools.
pattern of bowel R: These assessment findings are
functioning. commonly connected with diarrhea. If
gastroenteritis involves the large
intestine, the colon is not able to
112

absorb water and the client’s stool is
very watery.

> Submit client’s stool for culture.
R: A culture is a test to detect which
causative organisms cause an
infection.

> Teach the client about the
importance of hand washing after
each bowel movement and before
preparing food for others.
R: Hands that are contaminated may
easily spread the bacteria to utensils
and surfaces used in food
preparation hence hand washing
after each bowel movement is the
most efficient way to prevent the
transmission of infection to others.

> Encourage increase fluid intake of
1.5 to 2.5 liters/24 hour plus 200 ml
for each loose stool in adults unless
contraindicated.
R: Increased fluid intake replaces
fluid lost in liquid stools.

> Administer antidiarrheal
medications as prescribed.
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R: Bismuth salts, kaolin, and pectin
which are adsorbent antidiarrheals
are commonly used for treating the
diarrhea of gastroenteritis. These
drugs coat the intestinal wall and
absorb bacterial toxins.
Imbalanced Within 8 hours of nursing > Measure client weight.

Nutrition: Less care, the patient will have R: This will accurately
Than Body an adequate nutritional monitor the response to therapy.
Requirements intake.
related to > Monitor the client’s food intake.
malabsorption of R: To determine the amount of food
nutrients that is consumed.

> Provide parenteral fluids, as
ordered.
R: To ensure adequate fluid and
electrolyte levels.

> Provide a diverse diet according to
client’s needs.
R: This will stimulate the appetite of
the client.

> Refer to a dietitian if indicated.
R: Collaboration with the dietician in
order to guide the client about proper
nutrition.
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Risk for Fluid Within 8 hours of nursing > Assess the client’s skin turgor and
Volume Deficit care, the patient will mucous membranes for signs of
related to diarrheal manifest normovolemia. dehydration.
stools R: A loss of interstitial fluid causes the
loss of skin turgor. Assessment of the
skin turgor in adults is less accurate
since their skin normally loses its
elasticity. Therefore the skin turgor
assessed over the sternum in the
forehead is best. Several longitudinal
furrows and coating may be noted
along the tongue.

> Assess the consistency and
number of bowel movements.
R: Gastroenteritis is associated with
an increased frequency of very loose
or watery bowel movements. The
inflammation in the large intestine
limits the colon’s ability to absorb
water, leading to fluid volume deficit.

> Encourage increase fluid intake of
1.5 to 2.5 liters/24 hour plus 200 ml
for each loose stool in adults unless
contraindicated.
R: Increased fluid intake replaces
fluid lost in the liquid stool. Being
creative in selecting fluid sources
(e.g., flavored gelatin, frozen juice
115

bars, sports drink) can facilitate fluid
replacement. Oral hydrating solutions
(e.g., Rehydrate) can be considered
as needed.

> For the client who is unable to take
sufficient oral fluids, consider
administration of parenteral fluids as
ordered.
R: Fluids are needed to maintain
hydration status. Determining the
type and amount of fluid to be
replaced and the infusion rates will
vary depending on the client’s clinical
status.

> Administer antidiarrheal
medications as ordered
R: These drugs will reduce diarrheal
frequency and the risk for fluid
volume deficit.
Deficient Within 8 hours of nursing > Assess client’s knowledge of

Knowledge related care, the patient will gastroenteritis, its mode of
to unfamiliarity of verbalize understanding transmission, and its treatment.
the disease of causes of R: Clients who experience diarrhea
gastroenteritis, mode of and vomiting may not correlate the
transmission, and symptoms with an acquired intestinal
management of infection. The client may not realize
symptoms. the risk for transmitting the infection
to others.
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> Assess the client’s knowledge on
safe food preparation and storage.
R: The client may not understand the
relationship of gastroenteritis to the
consumption of inadequately cooked
food, food contaminated with bacteria
during preparation, and foods that
are not maintained at appropriate
temperatures

> Educate the client and the family
about the causes of and treatments
for gastroenteritis.
R: Knowledge about the possible
cause of this episode of
gastroenteritis will help the client
initiate to prevent future episodes.
The client needs to recognize that the
use of antibiotics is controversial in
managing diarrhea. The client needs
to understand the importance of fluid
replacement.

> Educate the client about the
importance of hand washing after
toileting and perianal hygiene and
before preparing food for others.
R: Proper hand washing will prevent
the spread of infectious agents.
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> Educate the client about food
preparation and storage methods to
reduce contamination by
microorganisms.
R: Raw meats should be kept
separate from other ready-to-eat
foods. All utensils and surfaces that
have been in contact with the raw
meat need to be washed with hot,
soapy water. Raw fruits and
vegetables must be washed before
eating if they will not be cooked. Only
pasteurized milk, fruit juices, and
ciders should be consumed. Bacteria
contamination or growth is more
likely to occur in foods that are not
maintained at appropriate
temperatures until eaten.


Title: Multicenter Trial of a Combination Probiotic for Children with Gastroenteritis
Summary:
Every year, roughly 1.7 million children attend the emergency department (ED) in
the United States due to gastroenteritis. There isn't enough data to see if giving these
kids probiotics improves their results. The researchers performed a randomized, double-
blind research with 886 children aged 3 to 48 months who presented to six pediatric
118

emergency departments in Canada with gastroenteritis. A 5-day course of a combination
probiotic product comprising Lactobacillus rhamnosus R0011 and Lactobacillus
rhamnosus L0011 was given to participants. helveticus R0052, twice daily at a dosage of
4.0109 colony-forming units, or placebo.
The primary outcome was moderate-to-severe gastroenteritis, which was defined
as a symptom score of 9 or above on the modified Vesikari scale after enrolment. The
length of diarrhea and vomiting, the percentage of children who had unscheduled medical
visits, and the presence or absence of adverse events were all secondary outcomes.The
result of the study showed that in children with gastroenteritis who presented to the
emergency room, twice-daily treatment of a combination L. rhamnosus–L. Within 14 days
of enrolment, the helveticus probiotic did not prevent the onset of moderate-to-severe
gastroenteritis.

Title: Global Trends in Norovirus Genotype Distribution among Children with Acute
Gastroenteritis

Summary:
Noroviruses are the most common cause of acute gastroenteritis (AGE) in both
adults and children all over the world. NoroSurv is a worldwide network that monitors
norovirus strains in children under the age of five who have AGE. During the period 2016–
2020, participants from 16 countries on six continents followed established techniques for
dual typing (genotype and polymerase type) and uploaded 1,325 dual-typed sequences
to the NoroSurv online platform. This virus is a non-invasive monitoring system that relies
on voluntary submissions from laboratories. As a result, their findings aren't always
consistent with national surveillance records. Furthermore, the number of sequences
provided by each nation varies;; this quantity is influenced by a variety of factors, including
time and laboratory capability. Low-income nations, as well as those in Africa and Central
America, are currently underrepresented in NoroSurv.
NoroSurv allows for the identification of worldwide norovirus genotype trends and
diversity in children under the age of five with AGE in near real time. Childhood norovirus
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immunization will most likely minimize the occurrence of norovirus-associated AGE in
children and stop community transmission in people of all ages.

TITLE: The Role of Human Coronavirus Infection in Pediatric Acute Gastroenteritis
BIBLIOGRAPHY: Xiong, Li-Jing MD;; Zhou, Meng-Yao MD;; He, Xiao-Qing MD;; Wu,
Ying MD;; Xie, Xiao-Li MD The Role of Human Coronavirus Infection in Pediatric Acute
Gastroenteritis, The Pediatric Infectious Disease Journal: July 2020 - Volume 39 - Issue
7 - p 645-649 doi: 10.1097/INF.0000000000002752
SUMMARY:
The link between HCoV and juvenile gastrointestinal disease has been known
since human coronavirus (HCoV)–like particles were discovered in stool specimens of
children with acute gastroenteritis and necrotizing enterocolitis using electron
microscopy. Overall detection rates have indeed been low in recent years, and they have
varied by location. In pediatric acute gastroenteritis, HCoVs have not been identified as
a major pathogen. 229E, OC43, HKU1, NL63, and severe acute respiratory syndrome
coronavirus have all been found in children with acute gastroenteritis. Middle East
Respiratory Syndrome Coronavirus and severe acute respiratory syndrome coronavirus-
2 were also linked to gastrointestinal symptoms in children.Despite the fact that the
digestive system has been identified as an infection pathway, because to the small
number of pediatric cases, it has been unable to adequately explore the link between
HCoVs infection and gastrointestinal symptoms. Furthermore, pathologic characteristics
have remained a mystery.
These case studies showed that gastrointestinal symptoms might be one of the
most relevant clinical aspects in SARS-CoV-2 infection in children, especially in newborns
and infants. In order to detect infected children early and prevent children with moderate
symptoms from being the source of infection, it is critical to examine the route of
gastrointestinal transmission and symptoms while managing pediatric cases.

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CROHN’S DISEASE
INTRODUCTION
Gastrointestinal diseases are disorders of the digestive system, an extensive and
complex system that breaks down food in order to absorb water and extra nutrients,
minerals and vitamins for the body’s use, while then removing unabsorbed waste. A type
of gastrointestinal disease is the Inflammatory Bowel Disease (IBD). According to CDC
(2020), Inflammatory Bowel Disease is a term for determining two chronic inflammatory
disorders, Crohn's Disease and Ulcerative Colitis. Ulcerative colitis only affects the large
intestines while on the other hand, Crohn’s disease can affect the whole gastrointestinal
tract, from mouth to anus, but it usually affects the small intestines. If it is not treated, the
disease will worsen and may progress to colon cancer.
Chron’s disease is a disorder that causes inflammation to the digestive tract, often
manifested clinically by abdominal pain, severe diarrhea, fatigue, weight loss, and
malnutrition. This disease can be painful since the inflammation often spread into the
deeper layers of the bowel and sometimes may lead to life-threatening complications.
The etiology of Crohn's disease remains unknown. Studies have shown that diet and
stress may aggravate the development of Crohn's Disease but are not identified as the
leading cause of the disease. Several factors, such as heredity and a malfunctioning
immune system, likely play a role in its development. The treatment for Chron’s disease
is still non-existent at present, however, therapies are there to reduce the sign and
symptoms and aid in long-term remission and healing of the inflammation.
According to Rowe (2020), prevalence of IBD is assumed high in developed
countries and considered low in developing regions. Internationally, the incidence of
Chron’s disease is 0.1-16 cases per 100,000 persons annually. In North America, the
prevalence of this disease is 319 per 100,000 persons, meanwhile in Europe, it was 322
per 100,000 persons. In the Philippines, Castro (2019) stated that there was an increasing
incidence of patients diagnosed with inflammatory bowel disease at the University of the
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East Ramon Magsaysay Memorial Medical Center from 2012 to 2018. A total of 24
patients had a diagnosis of IBD admitted in UERMMMC and 15 among those patients
have Chron’s disease (62.5%). An average of 2-3 patients were diagnosed every year
with 5-6 new cases diagnosed over the last 2 years in the medical center. Inflammatory
bowel disease was an emerging worldwide epidemic. A 2019 study in Taiwan reported
that there was a higher mortality rate in the country compared to Western countries.
Between 2001 and 2015, a total of 3806 patients having Crohn’s disease were registered
as having catastrophic illness, and 8.2% of these patients died during follow-up. Elderly
individuals and pneumonia were identified through a multivariate Cox proportional
hazards analysis to be the causative risk factors for death due to IBD (Lin et.al, 2019).
This case analysis can give nursing implications towards the student nurses,
specifically to nursing education, nursing practice, and nursing research. For nursing
education, this will help student nurses to have more comprehensive understanding in
the topic of Gastrointestinal Disorders, specifically the Chron’s disease. In nursing
practice, the different nursing interventions and medications mentioned in this case
analysis will help us to provide an enhanced nursing care towards our patients diagnosed
with Crohn’s disease. Lastly, in nursing research, this case analysis may serve as a
related literature to other researchers relating to these different types of cancer.

122

OBJECTIVES
At the end of the virtual seminar conducted by the BSN 4D Group 1, BSN
participants will be able to gain a better understanding and knowledge that will allow them
to grasp the understanding of Crohn’s Disease and create new limits to optimize nursing
practice, research, and education.
Specifically, the proponents aim to:
a) Present an introduction composing brief overview of the disease and relevant
statistics.
b) compose objectives that are specific, measurable, attainable, realistic, and time-
bounded;;
c) define Crohn’s Disease;;
d) discuss the etiologic factor that lead to the development of the disease;;
e) identify the symptomatology of the disease;;
f) trace the pathophysiology of the disease through a schematic diagram;;
g) list the possible medical, surgical, and nursing management, its indication
relating to breast cancer including diagnostic, laboratory examinations, and
possible medications;;
h) present a summary on a related literature published not earlier than 5 years;; and
i) arrange an alphabetical list of references used in the study using APA format.

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DEFINITION OF THE DISEASE

Crohn's disease (CD) is an idiopathic, chronic regional enteritis that predominantly
affects the terminal ileum but can actually impact any part of the gastrointestinal tract from
the mouth to the anus. Crohn, Ginzburg, and Oppenheimer described this condition in
1932, but it was not medically, histologically, or radiographically differentiated from
ulcerative colitis (UC) until 1959 (Rendi, 2017). Crohn's disease, like ulcerative colitis, is
a recurrent and remitting condition. It may affect only a small portion of the gastrointestinal
system at first, but it has the potential to spread widely (Hopkins Medicine, 2013).
Crohn’s disease comes in many forms. Ileocolitis is a form of Crohn’s disease that
causes inflammation and irritation of the ileum (the lower part of the small intestine) and
colon, Ileitis causes inflammation and irritation of the ileum only – the last part of the small
intestine, Gastroduodenal Crohn’s disease affects the stomach and duodenum – the first
part of the small intestine, Jejunoileitis is where area of inflammation occurs in the jejunum
– the second part of the small intestine, and lastly, the Crohn’s Colitis which affects the
colon, which is the main part of the large intestine causing fistulas, ulcers, and abscess
formation around the anus (Cirino, 2021).

124

ANATOMY AND PHYSIOLOGY
The digestive tract is a long chain of organs that runs from the mouth to the anus,
and it includes the esophagus, stomach, small intestine, and large intestine and an adult's
digestive tract is around 30 feet long. The digestive process starts in the mouth, where
saliva begins to break down food. Food is swallowed from the mouth and passes through
the esophagus, which carries the partially digested food to the stomach. The stomach's
muscular walls mix and churn food with acid and enzymes (known as gastric juice),
breaking it down into smaller portions.

Organs of the digestive system include the:
• Mouth – also known as the oral cavity, is the opening section of the digestive tract.
It is designed to receive food through swallowing, break it down into little particles
through mastication, and mix it with saliva. The boundaries are created by the lips,
cheeks, and palate.
125

• Esophagus – is a muscular tube that links the pharynx (throat) to the stomach
(esophagus). The esophagus is around 8 inches in length and is covered with
mucosa, a moist pink tissue. The esophagus is located behind the windpipe
(trachea), in front of the heart, and behind the spine.
• Stomach – is a muscular organ found on the upper abdomen's left side. The
esophagus delivers food to the stomach. When food reaches the end of the
esophagus, it passes through a muscular valve known as the lower esophageal
sphincter and into the stomach. The
stomach produces acid and enzymes that
aid in the digestion of food.

The semiliquid food, known as chyme, is
transferred slowly from the stomach into
the small intestine where most of the
digestion and absorption occurs (Williams,
2021).

• Small Intestine (Duodenum, Jejunum, Ileum) – also known as the small bowel, is
an organ in the gastrointestinal tract that is responsible for the majority of nutritional
absorption from food. It is located between the stomach and the large intestine,
and it gets bile and pancreatic juice from the pancreatic duct to help in digestion.
The first part of the small intestine is the duodenum. Food go into the duodenum
after mixing with stomach acid, and there they mix with bile from the gallbladder
and digestive secretions from the pancreas. The second part is the jejunum, and
the third part is the ileum. Ileum is the one which is connected to the cecum and it
aids in the further digestion of food.
Found in the inner walls

Villi
of the small intestines
126

where absorption of
nutrients occurs.
Microvilli

• Pancreas – The pancreas is responsible for the production of digestive juices,
insulin, and other hormones related to digestion. The exocrine pancreas is the
section that creates digestive fluids. The endocrine pancreas is the organ that
generates hormones, including insulin.
• Liver – The liver is a large, fleshy organ located on the right side of the abdominal
cavity. It is reddish-brown in appearance and rubbery to the touch, weighing
roughly 3 pounds. The liver processes blood, breaks it down, balance, and
produce nutrients. It also metabolizes drugs into forms that are easier to use or
harmless for the human body.
• Large Intestine (Colon) – a long, tube-like organ that links the small intestine on
one end and anus on the other. The large intestine is divided into four sections:
cecum, colon, rectum, and anal canal. Partially digested food passes through the
cecum into the colon, where water, nutrients, and electrolytes are eliminated.
• Anus – is the rectum's opening, by which stool exits the body. Complications in the
anus are common which includes hemorrhoids, abscesses, fissures, and cancer.

Any food which has not been digested makes its way to the large intestine. The major
function of the large intestine is to extract water and salts (electrolytes) from undigested
food and generate excretable solid waste (feces). The remainder of the large intestine's
contents travel into the rectum, where feces are held until they pass through the anus as
a bowel movement (Williams, 2021).
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PATHOPHYSIOLOGY
A. Etiology
PREDISPOSING
RATIONALE
FACTORS
Crohn's disease has a bimodal distribution in terms of onset
age. The first peak occurs between the ages of 15 and 30 (late
adolescence and early adulthood), and the second occurs
most frequently in women between the ages of 60 and 70.
AGE Nevertheless, most cases begin before the age of 30, and
approximately 20-30% of all Crohn's disease patients are
diagnosed before the age of 20. Older patients have a higher
proportion of colonic and distal Crohn disease, while younger
patients have prevalently ileal disease (Ghazi & Roy, 2019).
Although the condition is not hereditary, it appears to run in
some families, as it is present in more than one family in
roughly 15% of cases. Variations in certain genes, such as the
ATG16L1, IL23R, IRGM, and NOD2, have been discovered to
affect the likelihood of getting Crohn's disease in recent
GENETIC
studies. These genes give instructions on how to make
PREDISPOSITION
proteins that help the immune system work. Variations in any
of these genes may hamper intestinal cells' ability to respond
to germs, resulting in chronic inflammation and, as a result, the
condition's signs and symptoms (Genetic and Rare Diseases
Information Center , 2018).
White populations, notably those who live in Western countries
and those people of European Jewish descent, have
historically had the highest prevalence rates, with black and
ETHNICITY
Asian communities in these or any other foreign country
having substantially lower rates. However, according to a
recent article by William Faubion (2020), Crohn's disease is
128

becoming more common among Black people in North
America and the United Kingdom.
Women are more likely than men to have Crohn's disease, but
men are more likely to develop ulcerative colitis. Crohn's
SEX
disease is 1.1-1.8 times more common in women than in men
(Ehrlich, 2021).

PRECIPITATING
RATIONALE
FACTORS
Those who live in cooler regions have been found to be at a
higher risk in developing Crohn’s Disease. High sun exposure
was reported to be linked with a significantly lower incident risk
ENVIRONMENT/
of Crohn's Disease, according to the researchers. A longer-
LOCATION
term study found that women with low vitamin D levels had a
higher risk of developing Crohn's disease over the next two
decades (Team, 2018).
Crohn's disease is not caused by food, and no specific diet has
been shown to be beneficial in treating it. Certain foods, on the
other hand, may provoke flare-ups in Crohn's disease
DIET
symptoms in certain people. Foods heavy in dietary fiber and
fat, dairy, and carbonated beverages are some of the foods
that are more probable to cause symptoms (Zibdeh, 2020).
Smoking can alter the bacteria that live in the gut, affects how
a person's genes function, and alter the immune system, all of
SMOKING
which may increase a person's risk of developing Crohn's
disease (Crohn's and Colitis UK, 2017).
NONSTEROIDAL The risk of NSAIDS for IBD [inflammatory bowel disease] has
ANTI- long been postulated due to their effects in lowering barrier
INFLAMMATORY function of the gut epithelium (Yin, 2020).
DRUGS

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B. SYMPTOMATOLOGY
SYMPTOMS RATIONALE MANAGEMENT
Abdominal pain is due to the o Encourage the

inflammation in the gut or due to the patient to a
stricture. The pain usually manifests in comfortable
the right lower side of the abdomen, position (knees
since most of the disease and flexed).
massive inflammation located as o Provide comfort
ulcers occurs commonly in the measure (deep
ABDOMINAL PAIN terminal ileum and cecum. breathing,
repositioning,
diversional
activities).
o Administer
medications as
prescribed
(corticosteroids).
Inflammation in the intestine makes o Encourage to
food pass through faster, leading to increase oral fluid
less time for the absorption of water. intake unless
Crohn’s induced inflammation can contraindicated;;
also cause the affected parts of your consider nutritional
digestive tract to become hyperactive support.
DIARRHEA and spasm too much, which can force o Administer
food to move through your system far antidiarrheal
too quickly, resulting in those really medications as
loose, watery stools. ordered.
o Weigh daily and
note for the
changes in weight.
130

Bleeding in Crohn’s disease can vary o Provide sitz bath
depending on the location of as tolerated.
inflammation. If it takes place in the o Encourage small
colon or rectum, there will be more frequent feedings.
ANAL FISSURES blood present in stools. Blood loss in o Provide perianal
AND BLOOD IN THE Crohn’s disease may be due to anal care after each
STOOL fissures that develop as a bowel movement.
complication of Crohn’s disease. Anal
fissures on the other hand is formed
because integrity of the skin is broken
due to the frequent diarrhea.
About one-fifth of patients with o Recommend small
Crohn's disease and one-tenth of frequent feedings.
those with ulcerative colitis report o Consider meal
losing their appetite. IBD patients' replacement
eating difficulties are exacerbated shakes.
during flares, which is expected.
LOSS OF APPETITE
During remission, the majority of
people's appetite improve. The fact
that eating is frequently connected
with symptoms such as nausea, pain,
bloating, and diarrhea is one of the
major issues.
Even with sufficient caloric intake, o Weigh frequently
weight loss can happen because of and note for the
the inflammatory process in Crohn’s changes in weight.
WEIGHT LOSS/
disease. nutrition absorption happens o Encourage to
MALNOURISHMENT
within the small intestines, and create a daily meal
intestinal villi within the area are being plan.
damaged leading to an impaired
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absorption of nutrients, thus cause
malnutrition.
For people with Crohn’s, strictures — o Encourage for
narrowed areas in the small intestine some physical
— can cause abdominal pain, activities and
CONSTIPATION cramping, and vomiting. Strictures exercise
can also block food from passing
through the digestive tract, thus cause
constipation.
Another cause of fatigue-related to o Promote sufficient
Crohn’s disease could stem from nutritional intake.
nutritional shortfalls, particularly
ANEMIA/FATIGUE anemia. People with anemia don’t
have enough healthy red blood cells to
carry oxygen throughout their body,
which can lead to fatigue.
Canker sores are the result of poor o Orajel
vitamin and mineral absorption in o Encourage
your GI tract from Crohn’s disease. frequent oral
CANKER SORES You may notice canker sores most hygiene.
when your disease is flaring. o Discontinue
flossing if pain
persists.
In IBD-related arthritis (Crohn's o Encourage
disease, ulcerative colitis), bacteria in frequent changes
the intestines are thought to invade in position.
the bloodstream which o Provide a firm
JOINT PAINS
triggers arthritis. This type of arthritis mattress and
mainly affects larger joints in the body, elevate linens with
such as the knees, ankles, elbows, bed cradle as
wrists, and hips. Joint pain is needed.
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commonly associated with stomach
and bowel flare-ups.
It has elevated nodules or patches o Prednisone
that are reddish or violet in color and o Cold wet compress
may be tender to the touch. It's o Bed Rest
ERYTHEMA
generally idiopathic, but it comes and
NODOSUM
goes with intestinal inflammation.
When you have an IBD flare, it
also flares up.
It is the second most common o Optimal wound
extraintestinal manifestation that care
affects the skin of patients suffering o Maintain a moist
from IBD. The true mechanism of wound
PYODERMA pyoderma gangrenosum is unknown. environment
GANGRENOSUM The condition is not infectious nor
contagious, and it is frequently
associated with autoimmune diseases
including ulcerative colitis, Crohn's
disease, and arthritis.

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C. SCHEMATIC DIAGRAM
PREDISPOSING FACTORS PRECIPITATING FACTORS
• Age • Environment
• Genetics • Diet
• Ethnicity ETIOLOGY • Smoking
Pancreas
• Sex • NSAIDS

Impaired barrier M-cell sample antigens
function in the lumen

Translocation of
microbial products

Immune cells activation

Chronic Inflammation

Transmural systemic
inflammation of the GI tract lining

CROHN’S DISEASE Period of remissions
C
Period of flare-ups

Scarring of Inflammatory cytokines Healing ↑ permeability
the small damage mucosal impairment of blood vessel
intestinal villi epithelial cells in the GI tract

Excess
extracellular
Impaired Apoptosis & Leakage of
absorption ulceration matrix deposition fluid into the
of nutrients GI tract

Weight
loss
A
Management: Tissue scarring
Daily food log
Consider patient’s
food choice
Monitor weight B
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135

D
IF TREATED IF NOT TREATED
Medical Management:
• Corticosteroids Organ Cell turnover
• Antibiotics Sepsis in the
• Oral gel intestinal
• Eye drops lining
• Antispasmodic drugs
• Vitamins and supplements

Surgical Management: Colorectal
• Bowel Ressection Cancer

Nursing Management:
• Provide emotional support to the patient and his family.
• Schedule patient care to include rest periods DEATH
throughout the day.
• If the patient is receiving parenteral nutrition, provide
meticulous site care. Poor Prognosis
• Give iron supplements and blood transfusion as
ordered.
• Administer medications as ordered
• Provide good patient hygiene and meticulous oral care.
• Record fluid intake and output, weigh the patient daily.
• If the patient is receiving TPN, monitor his condition
closely.
• Evaluate the effectiveness of medication administration.
• Emphasize the importance of adequate rest.
• Give the patient a list of foods to avoid, including
lactose-containing milk products, spicy or fried high-
residue foods.
• Teach the patient about the prescribed medications,
their desires effects and possible adverse reactions.

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D. NARRATIVE
Crohn's disease is an inflammatory bowel disease that causes inflammation and ulcer
formation in the GI tract. Although the disease can be found anywhere in the GI tract,
from the mouth to the anus, it is most commonly found in the terminal ileum and the
beginning of the colon in a skip lesion pattern or scattered patches. Another characteristic
that distinguishes Crohn's disease from ulcerative colitis is its transmural inflammation,
which occurs throughout the entire intestinal layer, from the mucosa down to the serosa,
unlike ulcerative colitis which only affects the mucosal layer. The etiology of the disease
is still unknown and the mechanism of IBD is not fully understood yet, all that is known is
that it is caused by a faulty immune system. However, there are several factors that
contribute to the progression of the disease, and one of them is thought to be
environmental factors, lifestyle, smoking, and the use of NSAIDS. Another factors include
the non-modifiable ones which includes the age, genetic predisposition, ethnicity, and
gender.
These factors can either lead to an impaired barrier function or activate m-cells in
sampling antigen which is the principal pathway in initiating mucosal immunoglobulin A
(IgA) production – the one responsible in protecting mucosal tissues from microbial
invasion – to commensal enteric bacteria. This action of the m-cells causes translocation
of the microbial products, where antigens from the lumen are being transported to the
mucosal tissues to initiate immune cell activation. Once activated, B cells are activated to
produce immunoglobulins, which travel through the bloodstream, permeate other bodily
fluids, and bind specifically to the foreign antigen that triggered their production. Once the
antigen binds to the receptor, it causes the release of inflammatory mediators. The
antigen-presenting cell, which is the macrophage, will process these antigens and present
them to the CD4 T cells. The CD4 T-cell is then activated, which can lead to two
outcomes. First, the CD4 T cell stimulates and activates further the nearby macrophages
and second, both CD4 and macrophages will begin releasing plenty of cytokines,
including TNF alpha and interleukin 1&6. As these cytokines are continuously being
released, it could lead to a chronic inflammation. Tumor necrosis factor alpha plays a big
role in this chronic inflammation. TNF alpha is one of the inflammatory cytokine that, when
released, causes a variety of effects in the body. It it stimulates angiogenesis – formation
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of new blood vessels, it induces panneth cells necrosis which also destroys the
antimicrobials, is stimulates epithelial intestinal cell (IEC) death and impairs barrier
function, and it also increases immune response causing further damage.
Essentially, it is the production of cytokines and chronic inflammation that causes
the local and systemic complications associated with inflammatory bowel disease. What
happens after the chronic inflammation is there will be a transmural systemic inflammation
within the GI tract lining which means that there’s already damage within the entire later
intestinal layer, from the mucosa down to the serosa. This could happen in the entirety of
the GI tract from the mouth down to the anus in scattered patches but is only common in
the terminal part of the ileum up to the cecum, and that’s what we call now the Crohn’s
disease. The mechanism behind the skipping pattern of lesions is still unclear however,
this is a distinguishing characteristic of Crohn’s disease to Ulcerative colitis. A person
suffering from Crohn’s disease can have periods of remissions and flare-ups which can
also be triggered by food, lifestyle, and certain environmental factors. This period of
remissions and flare-ups can cause further intestinal damage which increases the
permeability of blood vessels within the GI tract which will cause leakage of fluids into the
GI tract. The chronic inflammation on the other hand caused an impairment in healing
leading to a deposition of extracellular matrix to aid in maintaining the body’s
homeostasis. However, an excessive extracellular matrix along with the fluids that had
leaked within the GI tract can cause tissue scarring which will eventually lead to a stricture
– a narrowing of GI lumen that can cause bowel obstruction. Crohn’s disease damages
mucosal epithelial cells thus lead to apoptosis and ulceration within the affected area.
This event could cause prolonged bleeding which can lead to complications like anemia,
disappearing transport proteins because of the programmed cell death and can lead to
inability of the lumen to absorb sodium and water causing diarrheal problems, and
microperforations through the intestinal wall because of the ulcerations. The initial
problem that had occurred because of the stricture and these microperforations could
predispose abscess formation – a swollen area containing pus that might actually leak.
When abscesses are drained, a passage may remain between the anal gland and the
skin, resulting in a fistula. Anal fistula can be painful and can actually cause bleeding
within the anal area. Since Crohn’s disease affects the entirety of the GI tract, it can also
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cause damage within the small intestine and could lead to the scarring of the intestinal
villi within the area. Villi is the one responsible in the absorption of nutrients in the small
intestines and a damage to these structures could cause an impaired absorption of
nutrients which could actually lead to patient’s weight loss.
All of these when not treated could lead to further complications related to the
joints, skin, eyes, mouth and liver and can actually cause organ sepsis, or colorectal
cancer when turnover of cells within the intestinal lining occurs, which could all lead to
death, a poor prognosis. Crohn’s disease doesn’t have a cure however, when managed
with certain medications and surgical management, along with some changes in lifestyle
and diet to prevent flare-ups could lead to a good prognosis.

Diagnostic, Laboratory, and Confirmatory Test
Doctors use some tests to confirmed Crohn’s disease. Some are used to help diagnose,
screen, or monitor a specific disease.
Diagnostic, Laboratory, Significance of the Nursing Responsibilities
and Confirmatory Test Result

Computed Tomography Normal size and Pre-Procedure:
Scan- also known as contour of body 1. That the procedure requires
computed axial tomography structures and organs;; from 45 minutes to 2 hours,
or computed transaxial no pathology such as depending on the extent of the
tomography, is a noninvasive masses or abnormal imaging and whether a
procedure that uses accumulation of body contrast medium is used.
tomographic radiography (x- fluids or substances 2. Those foods and fluids are
ray) combined with a special withheld for 4 hours before the
scanning machine, detectors procedure if a contrast medium
that determine the amount of is used;; otherwise, there are
radiographic beams no food or fluid restrictions.
absorbed by tissues, and a 3. Those medications can be
computer that processes continued, insulin can be
these readings and administered, diet can be
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reconstructs a body region followed, and study scheduled
by calculating the differences around this need.
in tissue absorption of the 4. That clothing, including
radiographic beams. It belts, jewelry, and all metallic
produces a series of three- objects, is removed and a
dimensional, cross-sectional hospital gown without snaps or
anatomic views of the tissue other metallic closures will be
structure of solid organs as worn.
well as differences between 5. That a contrast medium can
soft tissue and water. be given IV or orally before the
study if better visualization of
Magnetic Resonance an area is desired.
Imaging- also known as 6. That, if a contrast medium is
nuclear magnetic resonance given, nausea, flushing, and
imaging, is a noninvasive sweating experienced after
procedure that uses a administration should be
magnet, radio waves to reported to the physician.
create a field of energy, and 7. That the client is encircled
a computer that allows by the scanning camera during
visualization of a body the study while the pictures are
region. The use of the word taken and that claustrophobia
nuclear has been generally is not uncommon.
excluded to reduce the 8. That the only discomfort
anxiety provoked by the term experienced is undergoing the
that is often present in clients venipuncture to administer the
needing this study. The study contrast medium and lying in
produces one position on the hard table
cross-sectional, multiplanar for a long period.
images of the entire body, a 9. Administer ordered
body part, and specific body medications for sedation and
organs. anxiety, such as diazepam
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(Valium) for claustrophobia,
steroids, or antihistamines
such as diphenhydramine
(Benadryl) or prednisone
(Deltasone) for known
allergies to the contrast
medium before the study.
10. Have the client void.
11. If the procedure is closed,
known claustrophobia should
be reported to the physician
before the study.
During the Procedure:
1. Instruct the patient to remain
very still because movement
results in blurring of the
picture.
After the Procedure:
1. Care and assessment after
the procedure include the
return of clothing and personal
items.
2. Advise the client to resume
food intake and to increase
fluid intake to eliminate the
contrast medium, if one was
used.
3. Note and report nausea,
skin rash, sweating,
palpitations, respiratory
changes, and changes in vital
141

signs. Administer ordered
antihistamines if needed. Have
resuscitation equipment on
hand.
Complete Blood Count- The values must be in Before the procedure:
enumeration of the cellular normal range. 1. The purpose of the test
elements of the blood, 2. The procedure, including the
evaluation of RBC indices, Hematocrit and site from which the blood
and determination of cell hemoglobin levels sample is likely to be obtained
morphology by means of (which may be 3. That momentary discomfort
stained smears. decreased in Crohn’s may be experienced when the
disease) as well as the skin is pierced.
white blood cell count After the procedure:
(may be elevated). 1. After bleeding has stopped,
apply an adhesive
bandage.

Erythrocyte Sedimentation The values must be in Before the procedure:
Rate- measures the rate at normal range 1. The purpose of the test
which RBCs in 2. The procedure, including the
anticoagulated blood settle In Crohn’s disease site from which the blood
to the bottom of a calibrated ESR is usually sample is likely to be obtained
tube. In normal blood, elevated 3. That momentary discomfort
relatively little settling occurs may be experienced when the
because the gravitational pull skin is pierced.
on the RBCs is almost After the procedure:
balanced by the upward 1. After bleeding has stopped,
force exerted by the plasma. apply an adhesive
bandage.
2. The sample should be
transported promptly to the
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laboratory, because the test
must be performed within 3
hours of collecting the sample.
Delays may retard the ESR
and cause abnormally low
results.
Upper Gastrointestinal Normal esophageal, Before the procedure:
Series with Barium stomach, and small 1. That a physician or a
Studies- series involves intestine motility;; technician will perform the
radiologic examination of the normal size and shape Study.
lower esophagus, stomach, of the stomach and 2.That the procedure requires
duodenum, and upper small intestine;; no about 45 minutes to 1 hour.
jejunum after ingestion of a ulcerations, 3. Those foods and fluids are
solution of barium sulfate. inflammation, tumors, withheld for at least 8 hours
The entire small bowel can strictures, ruptures, before the procedure and
also be evaluated by this foreign bodies, or should continue to be
study. hiatal hernia. restricted until the study has
been completed.
4. That the client will be
requested to swallow a
flavored barium solution while
standing in front of a
fluoroscopy x-ray screen and
that films will be taken while
the barium moves down the
esophagus.
5. That no pain is associated
with the procedure, although
swallowing of the contrast
medium can be unpleasant.
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6. Ensure that dietary and fluid
restrictions have been
followed.
7. Ensure that all jewelry and
clothing are removed from the
waist up and provide the client
with a gown without metal
closures.
8. Assess baseline vital signs
to compare with later readings
or to determine any deviations
that can warrant
postponement of the study.
After the procedure:
1. Resume food and fluids if no
additional films are to be taken.
2. Monitor vital signs and
compare with baselines for
changes that indicate
complications.
3. Administer, or advise client
to take, a mild laxative and
increase fluid intake to aid in
the elimination of the barium.
4. Inform the client that feces
will be whitish or light in color
for 2 to 3 days and to notify the
physician if the normal color
does not return or if the client
is unable to eliminate the
barium.
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Endoscopy- A visual Normal intestinal Before the procedure:
examination of the interior mucosa with no polyps 1. Explain the purpose and
through the use of special or other abnormal what to expect.
instruments called tissues;; no bleeding or 2. Instruct the patient to fast
endoscopes. In relation to inflammation. and restrict fluids for 6 to 8 hr
the digestive system, the prior to the procedure to
term endoscopy is used to reduce the risk of aspiration
describe visual examination related to nausea and
of the inside of the GI tract. vomiting.
3. The patient may be required
to be NPO after midnight
4. Check the doctor's order.
5. Let the patient sign for the
consent.
6. The patient may be
instructed to take a laxative, an
enema, or a rectal laxative
suppository.
7. Instruct the patient to
cooperate and follow
directions.
8. Prepare the instruments,
equipment and supplies
needed for the procedure.
9. Clean and sterilize
equipment before use.
10. Regarding the patient's risk
for bleeding, the patient should
be instructed to avoid taking
natural products and
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medications with known
anticoagulant, antiplatelet, or
thrombolytic properties or to
reduce dosage, as ordered,
prior to the procedure.
1. Ask the patient again about
her name and age for
verification.
2. Check Vital signs
3. Assist with patient
positioning as necessary.
4. Encourage the patient to
take slow, deep breaths
5. Administer medications as
ordered.
6. Change the position of the
patient
7. Assist the physician
throughout the procedure.
After the procedure:
1. Observe the patient closely
for signs of bowel perforation.
2. Obtain and record the
patient’s vital signs.
3. Instruct patient to resume a
normal diet, fluids, and activity
as advised by the health care
provider.
4. Assess if there are any signs
of bleeding
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5. Provide privacy while the
patient rest after the
procedure.
6. Encourage increased fluid
intake.

Management
Medical treatment for Crohn’s disease is aimed at reducing inflammation, suppressing
inappropriate immune responses, providing rest for a diseased bowel so that healing may
take place, improving quality of life, and preventing or minimizing complications. Most
patients have long periods of well-being interspersed with short intervals of illness.
Management depends on the disease location, severity, and complications.
Medical Management
PROCEDURE RATIONALE
Nutritional therapy Oral fluids and a low-residue, high-protein,
high-calorie diet with supplemental vitamin
therapy and iron replacement are
prescribed to meet nutritional needs,
reduce inflammation, and control pain and
diarrhea. Fluid and electrolyte imbalances
from dehydration caused by diarrhea are
corrected by IV therapy as necessary if the
patient is hospitalized or by oral fluids if the
patient is managed at home. Any foods
that exacerbate diarrhea are avoided. Milk
may contribute to diarrhea in those with
lactose intolerance. Cold foods and
smoking are avoided because both
147

increase intestinal motility. Parenteral
nutrition may be indicated.
Pharmacological therapy -Sedatives and antidiarrheal and
antiperistaltic medications are used to
minimize peristalsis in order to rest the
inflamed bowel.
-Aminosalicylates such as sulfasalazine
(Azulfidine) are often effective for mild or
moderate inflammation and are used to
prevent or reduce recurrences in long-
term maintenance regimens.
-Sulfa-free aminosalicylates (e.g.,
mesalamine [Asacol, Pentasa]) are
effective in preventing and treating
recurrence of inflammation.
-Antibiotics (e.g., metronidazole [Flagyl])
are used for complications such as
abscesses or fistula formation.
-Corticosteroids are used to treat severe
and fulminant disease and can be given
orally (e.g., prednisone) in outpatient
treatment or parenterally (e.g.,
hydrocortisone [Solu-Cortef]) in
hospitalized patients.
-Immunomodulators (e.g., azathioprine
[Imuran], mercaptopurine [6- MP],
methotrexate [MTX], cyclosporine
[Neoral]) have been used to alter the
immune response. The exact mechanism
of action of these medications in treating
IBD is unknown.
148

-Newer biologic therapies incorporate
monoclonal antibodies, including
infliximab (Remicade), adalimumab
(Humira), certolizumab pegol (Cimzia),
and natalizumab (Tysabri) for treating
Crohn’s disease.

Sulfasalazine
Generic Name: Sulfasalazine
Brand Name: Azulfidine
Drug Classification: Anti-inflammatory
Mode of Action: Modulates local mediators of inflammatory response. Therapeutic

Effect: Decreases inflammatory response, interferes with GI secretion. Effect appears
topical rather than systemic.
Contraindications: Hypersensitivity to sulfasalazine, sulfa, salicylates;; porphyria;; GI or

GU obstruction.
Suggested Dose:
PO: ADULTS, ELDERLY: Initially, 3-4 g/day in divided doses q8h. May initiate at
1-2 g/day to reduce GI intolerance. Maximum: 6 g/day. Maintenance: 2 g/day in divided
doses at intervals less than or equal to q8h.
CHILDREN 6 YRS AND OLDER: Initially, 40–60 mg/kg/day in 3–6 divided doses.
Maximum (initial dose): 4 g/day. Maintenance: 30 mg/kg/day in 4divided doses at intervals
less than or equal to q8h. Maximum (maintenance dose): 2 g/day.
Side effects:
Frequent (33%): Anorexia, nausea, vomiting, headache, oligospermia (generally

reversed by withdrawal of drug). Occasional (3%): Hypersensitivity reaction (rash,
149

urticaria, pruritus, fever, anemia). Rare (Less Than 1%): Tinnitus, hypoglycemia,
diuresis, photosensitivity.
Adverse Effects:
Anaphylaxis, Stevens-Johnson syndrome, hematologic toxicity (leukopenia,

agranulocytosis), hepatotoxicity, nephrotoxicity occurs rarely.
Drug Interactions:
DRUG: Hepatotoxic medications (e.g., acetaminophen, isoniazid, ketoconazole,

simvastatin, SSRIs) may increase risk of hepatotoxicity.
Nursing Responsibilities:
Assessment and Baseline Data

1. Question for hypersensitivity to medications.
2. Check initial urinalysis, CBC, serum renal function, LFT.

Intervention/evaluation
1. Monitor I&O, urinalysis, renal function tests;; ensure adequate hydration (minimum
output 1,500 mL/24 hrs) to prevent nephrotoxicity.
2. Assess skin for rash (discontinue drug, notify physician at first sign).
3. Monitor daily pattern of bowel activity, stool consistency. (Dosage increase may be
needed if diarrhea continues, recurs.)
4. Monitor CBC closely;; assess for and report immediately any hematologic effects
(bleeding, ecchymoses, fever, pharyngitis, pallor, weakness, purpura).
5. Monitor LFT;; observe for jaundice.

Patient and Family Education
1. May cause orange-yellow discoloration of urine, skin.
2. Space doses evenly around the clock.
3. Take after or with food with 8 oz of water;; drink several glasses of water between
meals.
150

4. Swallow enteric-coated tablets whole;; do not chew, crush, dissolve, or divide tablets.
5. Continue for full length of treatment;; may be necessary to take drug even after
symptoms relieved.
6. Routinely monitor blood levels.
7. Inform dentist, surgeon of sulfasalazine therapy.
8. Avoid exposure to sun, ultraviolet light until photosensitivity determined (may last for
mos after last dose).
Metronidazole
Generic Name: Metronidazole
Brand Name: Flagyl, Metrogel
Drug Classification: Antibacterial, antiprotozoal.
Mode of Action: Disrupts DNA, inhibiting nucleic acid synthesis. Therapeutic Effect:
Producesbactericidal, antiprotozoal, amebicidal, trichomonacidal effects. Produces anti-
inflammatory, immunosuppressive effects when applied topically.
Contraindications: Hypersensitivity to metronidazole. Pregnancy (first trimester with

trichomoniasis), use of disulfiram within 2 wks, use of alcohol during therapy or within 3
days of discontinuing metronidazole
Suggested Dose:
IV: ADULTS, ELDERLY: 500 mg q6h. Maximum: 4 g/day.
Side effects:
Frequent: Anorexia, nausea, dry mouth, metallic taste. Occasional: Diarrhea,

constipation, vomiting, dizziness, erythematous rash, urticaria, reddish-brown urine. Rare
: Mild, transient leukopenia;; thrombophlebitis with IV therapy.
Adverse Effects:
Oral therapy may result in furry tongue, glossitis, cystitis, dysuria, pancreatitis. Peripheral
neuropathy (manifested as numbness, tingling of hands/feet) usually is reversible if
151

treatment is stopped immediately upon appearance of neurologic symptoms. Seizures
occur occasionally.
Drug Interactions:
DRUG: Alcohol may cause disulfiram-type reaction (e.g., abdominal cramps,

nausea, vomiting, headache, psychotic reactions). Disulfiram may increase risk of toxicity.
May increase effects of oral anticoagulants (e.g., warfarin).

1. Obtain baseline CBC, LFT. Question for history of hypersensitivity to metronidazole,
other nitroimidazole derivatives.
2. Obtain specimens for diagnostic tests, cultures before giving first dose (therapy may
begin before results are known).

1. Monitor daily pattern of bowel activity, stool consistency.
2. Monitor I&O, assess for urinary problems. Be alert to neurologic symptoms
(dizziness, paresthesia of extremities)
3. Assess for rash, urticaria.
4. Monitor for onset of superinfection (ulceration/change of oral mucosa, furry tongue,
vaginal discharge, genital/anal pruritus).

1. Urine may be red-brown or dark.
2. Avoid alcohol, alcohol-containing preparations (cough syrups, elixirs) for at least 48 hrs
after last dose.
3. Avoid tasks that require alertness, motor skills until response to drug is established.
Prednisone
Generic Name: Prednisone
Brand Name: Rayos
152

Drug Classification: Anti-inflammatory, immunosuppressant
Mode of Action: Inhibits accumulation of inflammatory cells at inflammation sites,

phagocytosis, lysosomal enzyme release/synthesis, release of mediators of
inflammation. Therapeutic Effect: Prevents/suppresses cell-mediated immune reactions.
Decreases/prevents tissue response to inflammatory process.
Contraindications: Hypersensitivity to prednisone. Acute superficial herpes simplex

keratitis, systemic fungal infections, varicella, administration of live or attenuated virus
vaccines.
Suggested Dose:
PO: ADULTS, ELDERLY: 5–60 mg/day in divided doses. CHILDREN: 0.05–
2 mg/kg/day in 1–4 divided doses.
Side effects:
Frequent: Insomnia, heartburn, nervousness, abdominal distention, diaphoresis, acne,

mood swings, increased appetite, facial flushing, delayed wound healing,increased
susceptibility to infection, diarrhea, constipation. Occasional: Headache, edema, change
in skin color, frequent urination. Rare: Tachycardia, allergic reaction (rash, urticaria),
psychological changes, hallucinations, depression.
Adverse Effects:
Long-term therapy: Muscle wasting (esp. in arms, legs), osteoporosis, spontaneous

fractures, amenorrhea, cataracts, glaucoma, peptic ulcer, HF. Abrupt withdrawal
following long-term therapy: Anorexia, nausea, fever, headache, rebound
inflammation, fatigue, weakness, lethargy, dizziness, orthostatic hypotension. Sudden
discontinuance may be fat.
Drug Interactions:
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DRUG: CYP3A4 inducers (e.g., carbamazepine, phenytoin, rifampin) may
decrease effects. Live virus vaccines may increase vaccine side effects, potentiate virus
replication, decrease pt’s antibody response to vaccine. May increase effect of warfarin.

1. Question medical history as listed in Precautions.
2. Obtain baselines for height, weight, B/P, serum glucose, electrolytes.
3. Check results of initial tests (tuberculosis [TB] skin test, X-rays, EKG).
1. Monitor B/P, serum electrolytes, glucose, results of bone mineral density test, height,
weight in children.
2. Be alert to infection (sore throat, fever, vague symptoms);; assess oral cavity daily for
signs of Candida infection.
3. Monitor for symptoms of adrenal insufficiency, immunosuppression.

1. Report fever, sore throat, muscle aches, sudden weight gain, swelling, loss of appetite,
or fatigue.
2. Avoid alcohol, alcohol-containing preparations (cough syrups, elixirs) for at least 48 hrs
after last dose.
3. Maintain fastidious oral hygiene.
4. Do not abruptly discontinue without physician’s approval.
5. Avoid exposure to chickenpox, measles.
6. Long-term use may significantly increase risk of serious infections.
Azathioprine
Generic Name: Azathioprine
Brand Name: Azasan, Imuran
Drug Classification: Immunosuppressant.
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Mode of Action: Antagonizes purine metabolism, inhibits DNA, protein, and RNA
synthesis. Therapeutic Effect: Suppresses cell-mediated hypersensitivities;; alters
antibody production, immune response in transplant recipients.
Contraindications: Hypersensitivity to azathioprine. Pregnant women with RA, pts

previously treated for RA with alkylating agents (cyclophosphamide, chlorambucil,
melphalan) may have a prohibitive risk of malignancy with azathioprine.
Suggested Dose:
PO: ADULTS, ELDERLY: Initially, 1 mg/kg/day (50–100 mg) as a single dose
or in 2 divided doses for 6–8 wks. May increase by 0.5 mg/kg/day after 6–8 wks
at 4-wk intervals. Maximum: 2.5 mg/kg/day
Side effects:
Frequent: Nausea, vomiting, anorexia (particularly during early treatment and with large
doses). Occasional: Rash. Rare: Severe nausea/vomiting with diarrhea, abdominal pain,
hypersensitivity reaction.
Adverse Effects:
Increases risk of neoplasia (new abnormal-growth tumors). Significant leukopenia and

thrombocytopenia may occur, particularly in pts undergoing renal transplant rejection.
Hepatotoxicity occurs rarely.
Drug Interactions:
DRUG: Allopurinol, sulfamethoxazole/trimethoprim may increase activity, toxicity.

Bone marrow depressants may increase myelosuppression. Other immunosuppressants
may increase risk of infection or development of neoplasms. May increase effects of live
virus vaccines.
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1. CBC, LFT should be performed weekly during first mo of therapy, twice monthly
during second and third mos of treatment, then monthly thereafter
2. If WBC falls rapidly, dosage should be reduced or discontinued.
3. Assess particularly for delayed myelosuppression.
4. Routinely watch for any change from baseline.
1. Contact physician if unusual bleeding/bruising, sore throat, mouth sores, abdominal
pain, fever occurs.
2. Therapeutic response in rheumatoid arthritis may take up to 12 wks.
3. Women of childbearing age must avoid pregnancy.
Infliximab
Generic Name: Infliximab
Brand Name: Remicade
Drug Classification: Antibacterial, antiprotozoal.
Mode of Action: Binds to tumor necrosis factor (TNF), inhibiting functional activity of TNF
(induction of proinflammatory cytokines, enhanced leukocytic migration, activation of
neutrophils/eosinophils). Therapeutic Effect: Prevents disease and allows diseased joints
to heal.
Contraindications: Hypersensitivity to infliximab. Moderate to severe HF (Doses greater
than 5 mg/kg should be avoided). Sensitivity to murine proteins, sepsis, serious active
infection
Suggested Dose:
IV Infusion: ADULTS, ELDERLY, CHILDREN 6 YRS AND OLDER: 5 mg/kg
followed by additional doses at 2 and 6 wks after first infusion, then q8wks thereafter. For
adults who respond then lose response, consideration may be given to treatment with 10
mg/kg.
Side effects:
Frequent (22%–10%): Headache, nausea, fatigue, fever. Occasional (9%–5%):
Fever/chills during infusion, pharyngitis, vomiting, pain, dizziness, bronchitis, rash,
rhinitis, cough, pruritus, sinusitis, myalgia, back pain. Rare (4%–1%): Hypotension or
hypertension, paresthesia, anxiety, depression, insomnia, diarrhea, UTI.
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Adverse Effects:
Serious infections, including sepsis, occur rarely. Potential for hypersensitivity reaction,
lupus-like syndrome, severe hepatic reaction, HF.
Drug Interactions:
DRUG: Anakinra, abatacept may increase risk of infection. Immunosuppressants
may reduce frequency of infusion reactions, antibodies to infliximab. Live virus vaccines
may decrease immune response (do not give concurrently).
1. Evaluate baseline hydration status (skin turgor urinary status).
2. Screen for active infection.
1. Monitor urinalysis, erythrocyte sedimentation rate (ESR), B/P.
2. B/P. Monitor for signs of infection.
3. Monitor C-reactive protein, frequency of stools.
4. Assess for abdominal pain.
1. Report persistent fever, cough, abdominal pain, swelling of ankles/feet.
2. Treatment may depress your immune system and reduce your ability to fight infection.
3. Do not receive live vaccines.

Surgical Management
1. Bowel Resection- Bowel resection is a type of surgical procedure that removes the
affected part of the colon. It is used to treat obstruction in the large intestine, which may
affect the normal function of the colon, and is also used in treating fistulas. A fistula is an
abnormal tunnel that forms between two different parts of the intestine or connects the
intestine to another organ. Fistulas can occur following severe inflammation of the
intestinal wall and can become infected. During a bowel resection, the surgeon will focus
on removing this tunnel and the damaged tissues around it.
As a healthcare provider, encourage the patient to do deep breathing exercises and
resume oral food and fluids as ordered. Initial feedings may be clear liquids, progressing
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to full liquids, and then frequent small feedings of regular foods. Before the procedure,
educate the patient for the possible changes in bowel function. Alert the patients to the
prospect that they will have to adjust to the new normal in which they don’t have the same
bowel habits they had before surgery. Monitor bowel sounds and abdominal distention
frequently during this period. Oral feedings are reintroduced slowly to minimize abdominal
distention and trauma to the suture lines.
2. Strictureplasty- is a surgical procedure in which it repairs strictures in the intestine
caused by Crohn’s Disease through widening or narrowing the area without removing any
part of your intestines. Strictures are caused by inflammation and medicines are the initial
treatment in improving the narrowing of the intestines. Surgery is a necessary option if
initial treatment is not effective.
Strictureplasty complements Bowel resection because it reduces the risk of developing
short-bowel syndrome and its associated complications. Short bowel syndrome is a
condition in which your body is unable to absorb nutrients from food intake because it
does not have enough small intestine which is responsible for the absorption of nutrients.
Patients with nutritional problems should receive preoperative supplements or parenteral
nutrition in order to optimize postoperative wound healing. Preoperative CT or Magnetic
Resonance Enterography should be obtained to define the extent and location of small-
bowel strictures, to visualize any unsuspected fistulas or perforations, and to obtain an
estimate of small-bowel length.
3. Colectomy/Proctocolectomy- Colectomy is a surgical procedure to remove the colon.
The large intestine is a long tubelike organ at the end of your digestive tract. Colectomy
may be necessary to treat or prevent diseases and conditions that affect your colon. The
surgeon will connect the ileum to the rectum in order to continue to pass stool through
your anus without the need for an external pouch. On the other hand, Proctocolectomy is
a surgical procedure to remove the rectum and colon.
Patients with Crohn’s Disease is usually recommended with Proctocolectomy with end
ileostomy. As a healthcare provider, Monitoring bowel sounds and the degree of
abdominal distention is essential in the care of post-operative patients. Bowel sounds and
the passage of flatus indicate a return of peristalsis. Educate the client that patients who
have undergone Proctocolectomy, men may experience sexual dysfunction, and women
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may feel pain during intercourse but ensure that these are only temporary. also,
encourage the patient to eat foods high in pectins such as bananas, and peanut butter.
this will help thicken the stool output and control diarrhea.
4. End Ileostomy- With an end ileostomy, the small intestine is inverted through a stoma
or an artificial hole made in the abdominal wall to divert waste into an ileostomy bag. The
common site for an ileostomy is the lower abdomen to the right of the navel just below
the beltline. Some patients may still feel as if they need to have a bowel movement after
surgery, just as people who have lost a limb sometimes still feel as if the limb is still there.
It Is called Phantom rectum and it is completely normal. It does not require any treatment
and often subsides over time.
5. Abscess Drainage- In Crohn’s Disease, the collection of pus or abscesses often
develops around the anal area or in the abdomen. An abscess is an area that fills with
pus and becomes red, swollen, and painful. In patients with Crohn’s disease, abscesses
are most often found in the abdomen or rectal areas which may further develop into fistula
which is common in Crohn’s disease. It requires antibiotic drugs to treat infections but it
is recommended to do surgical drainage of the pus cavity to ensure that the area heals
completely. The surgeon will make a small incision into the abscess and insert a thin tube
in order to drain the pus. The tube may be left for a week or more to allow the abscess to
completely drain and begin healing. As a health care provider, it is important to examine
the skin for breaks or irritation, signs of infection because disruptions of skin integrity at
or near the operative site are sources of contamination to the wound. Careful shaving or
clipping is imperative to prevent abrasions and nicks in the skin. Maintain dependent
gravity drainage of indwelling catheters, tubes, and/or positive pressure of parenteral or
irrigation lines in order to prevent stasis and reflux of body fluids and identify breaks in
aseptic technique and resolve immediately on occurrence because contamination by
environmental or personnel contact renders the sterile field unsterile, thereby increasing
the risk of infection.
6. Intestinal Transplant- This technique is now available to children and to young and
middle-aged adults who have lost intestinal function from disease. It may provide
improvement in quality of life for some patients. The associated technical and
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immunologic problems remain formidable, and the costs and mortality rates continue to
be high.

Nursing Management
Nursing Rationale Outcome Nursing Intervention
Diagnosis
Diarrhea The cells in the After 8 hours 1. Observe and document stool
related to lining of the of nursing frequency, characteristics,
inflammatory intestine become intervention amount, and precipitating factors.
process as inflamed, the patient R. Helps differentiate individual
evidenced by meaning the will be able disease and assesses severity of
liquid stools intestine can't to report episode.
absorb all the reduction in
nutrients and fluid. frequency of 2. Promote bedrest, if indicated,
This results in stools and and provide bedside commode.
stools being loose return to R. Rest decreases intestinal
and watery, or more normal motility and reduces the metabolic
even entirely stool rate when infection or hemorrhage
liquid, causing consistency is a complication. Urge to defecate
diarrhea. may occur without warning and be
uncontrollable, thus increasing risk
of incontinence and falls if facilities
are not close at hand.

3. Remove stool promptly. Provide
room deodorizers
R. Reduces noxious odors to avoid
undue client embarrassment.

4. Discuss client’s usual diet. Have
client/SO identify foods and fluids
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(if any) that precipitate client’s
diarrhea and/or cramping pain.
R. There is no one single food or
group of foods that precipitates
problems for everyone with IBD.
Dietary needs and restrictions
must be individualized, depending
on which disease the client has
and what part of the intestine is
affected.

5. Restart oral fluid intake
gradually, if client has been on
bowel rest (NPO) during
treatment. Offer clear liquids
hourly and avoid cold fluids.
R. Provides colon rest by omitting
or decreasing the stimulus of foods
and fluids. Gradual resumption of
liquids may prevent
cramping and recurrence of
diarrhea;; however, cold fluids can
increase intestinal motility.

6. Provide opportunity to vent
frustrations related to disease
process.
R. Presence of disease with
unknown cause that is difficult to
cure
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and that may require surgical
intervention can lead to stress
reactions that may aggravate
condition.

7. Administer medications, as
indicated

8. Prepare for surgical
intervention, such as colectomy,
proctocolectomy, or ileostomy.
R. Two-thirds to three-quarters of
patients with Crohn’s disease will
require surgery at some point
during their lives perforation or
bowel obstruction occurs or
disease is unresponsive to
medical treatment. Surgery can
cure UC, and can help, but not
cure, Crohn’s disease. Surgery to
remove the colon and rectum
(proctocolectomy) is followed by
ileostomy, or ileoanal
anastomosis. If the client isn’t
critically ill and the anal sphincter
is free from lesions, the surgeon
may remove the colon and rectum
but leave the anus intact. An
internal pouch is then formed from
the distal ileum and connected to
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the anal sphincter, allowing the
client
to have continent bowel
movements
Risk for Inflammation of After 8 hours 1. Monitor I&O. Note number,
deficient fluid the intestine in of nursing character, and amount of stools;;
volume Crohn’s Disease intervention estimate insensible fluid losses
related to can cause the patient (e.g., diaphoresis). Measure urine
excessive disruption of will be able specific gravity and observe for
losses absorbing fluids. to maintain oliguria.
through Hence, extra adequate R. Provides information about
normal fluids will be fluid volume overall fluid balance, renal
routes- eliminated as evidenced function, and bowel disease
diarrhea through bowel by moist control, as well as guidelines for
movements like mucus fluid replacement.
diarrhea membrane,
good skin 2. Assess vital signs (blood
turgor, and pressure [BP], pulse,
capillary temperature).
refill. R. Hypotension (including
postural), tachycardia, and fever
can indicate response to and effect
of fluid loss.

3. Observe for excessively dry skin
and mucous membranes,
decreased skin turgor, and slowed
capillary refill.
R. Indicates excessive fluid loss
and resultant dehydration.

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4. Weigh daily or per protocol.
R. Indicator of overall fluid and
nutritional status.
5. Administer IV fluids and
electrolytes, as indicated.
R. May be needed to replenish
fluid volume and reduce risk of
complications associated with
electrolyte imbalances.

Imbalanced After 7 days 1. Assess weight, age, body mass,
Nutrition: less of nursing strength, and activity and rest
than body intervention levels. Ascertain stage of disease
requirements the patient process and its effects on
altered will be able client’s nutritional status.
absorption of to R. Provides comparative baseline.
nutrients as demonstrate
evidenced by progressive 2. Evaluate client’s appetite.
weight loss weigh gain R. Appetite may be suppressed
because of altered taste, early
satiety, meal-related cramping,
diarrhea, or medications,
or a combination of these factors.

3. Weigh frequently.
R. Provides information about
dietary needs and effectiveness
of therapy.

4. Recommend rest before meals.
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R. Quiets peristalsis and increases
available energy for eating.
5. Encourage client to eat a
healthy, varied diet as much as
possible, incorporating several
small meals and snacks per day.
R. Will promote achieving and
maintaining healthy weight and a
more strong, active lifestyle.

6. Encourage client to avoid or limit
foods that might cause or
exacerbate abdominal cramping
and other uncomfortable
symptoms, such as dairy products
R. Individual tolerance varies,
depending on stage of disease
and area of bowel affected.

7. Resume or advance diet as
indicated—clear liquids
progressing to bland, low-residue,
and then high-protein, high-
calorie, caffeine-free, nonspicy,
and low-fiber, as indicated.
R. Allows the intestinal tract to
readjust to the digestive process.
Protein is necessary for tissue
healing integrity. Low bulk
decreases peristaltic response to
meal.
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8. Provide nutritional support, for
example: Enteral feedings, such
as Ultra Clear Plus via nasogastric
(NG) tube, percutaneous
endoscopic gastrostomy (PEG),
or J-tube
R. Many clinical studies have
shown early enteral feeding is
beneficial in reducing the effects of
malabsorption and providing
essential nutrients. Although
elemental enteral solutions cannot
provide all needed nutrients, they
can prevent gut atrophy.


Title: People with Crohn’s Disease Have More Microplastics in their Feces
Summary:
Microplastics -- tiny pieces of plastic less than 5 mm in length -- are everywhere,
from bottled water to food to air. According to recent estimates, people consume tens of
thousands of these particles each year, with unknown health consequences. Now,
researchers have found that people with inflammatory bowel disease (IBD) have more
microplastics in their feces than healthy controls, suggesting that the fragments could be
related to the disease process.
The team obtained fecal samples from 50 healthy people and 52 people with IBD
from different geographic regions of China. Analysis of the samples showed that feces
from IBD patients contained about 1.5 times more microplastic particles per gram than
those from healthy subjects. The microplastics had similar shapes (mostly sheets and
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fibers) in the two groups, but the IBD feces had smaller (less than 50cm) particles. The
two most common types of plastic in both groups were polyethylene terephthalate (PET;;
used in bottles and food containers) and polyamide (PA;; found in food packaging and
textiles). People with more severe IBD symptoms tended to have higher levels of fecal
microplastics. Through a questionnaire, the researchers found that people in both groups
who drank bottled water, ate takeaway food and were often exposed to dust had more
microplastics in their feces. These results suggest that people with IBD may be exposed
to more microplastics in their gastrointestinal tract. However, it's still unclear whether this
exposure could cause or contribute to IBD, or whether people with IBD accumulate more
fecal microplastics as a result of their disease, the researcher say.

Title: Western Diet may Increase Risk of Gut Inflammation and Infection
Summary:
Eating a Western diet impairs the immune system in the gut in ways that could
increase risk of infection and inflammatory bowel disease, according to a study from
researchers at Washington University School of Medicine in St. Louis and Cleveland
Clinic. It showed that a diet high in sugar and fat causes damage to Paneth cells, immune
cells in the gut that help keep inflammation in check. When Paneth cells aren't functioning
properly, the gut immune system is excessively prone to inflammation, putting people at
risk of inflammatory bowel disease and undermining effective control of disease-causing
microbes.
In relation to that, Paneth cell impairment is a key feature of inflammatory bowel
disease. For example, people with Crohn's disease, a kind of inflammatory bowel disease
characterized by abdominal pain, diarrhea, anemia and fatigue, often have Paneth cells
that have stopped working. Hence, the researchers found that high body mass index
(BMI) was associated with Paneth cells that looked abnormal and unhealthy under a
microscope. The higher a person's BMI, the worse his or her Paneth cells looked. The
association held for healthy adults and people with Crohn's disease. In people, obesity is
frequently the result of eating a diet rich in fat and sugar. So, the scientist discovers in
which 40% of the calories came from fat or sugar, similar to the typical Western diet after
167

two months on this chow, the person had become obese and their Paneth cells looked
decidedly abnormal. It's possible that if you have Western diet for so long, you cross a
point of no return and your Paneth cells don't recover even if you change your diet.

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ULCERATIVE COLITIS
INTRODUCTION
Gastrointestinal (GI) conditions are disorders of the digestive system,

wherein it is made up of the digestive tract and other organs working together to
break down food into nutrients and energy needed by the body. The GI diseases
can be divided into functional or structural. For functional, the GI tract appears
normal upon examination, but it does not function properly. Some diseases in this
group includes constipation, GERD, and irritable bowel syndrome (IBS). On the
other hand, structural indicates that the GI tract both appears abnormal, does not
work properly, and may even require surgical intervention. Some diseases in this
group includes inflammatory bowel disease (Cleveland Clinic, 2021).
Inflammatory Bowel Disease (IBD) is a group of chronic disorders that
includes Crohn’s disease and Ulcerative colitis (UC). Both of these disorders lead
to either inflammation or ulceration (or even both) of the bowel. One of the main
differences between the two is their location. While Crohn’s disease can affect the
entire GI tract, ulcerative colitis occurs in the large intestine. In particular, the latter
is a systemic disease affecting the mucosal and submucosal layers of the colon
and rectum that is characterized by unforeseeable periods of remission and
exacerbation and bouts or flare-ups of abdominal cramps, bloody or purulent
diarrhea, and the frequent and immediate need to empty the bowels (Hinkle &
Cheever, 2018).
In relation with this disease, there are also different types of ulcerative colitis
according to their location. The first is ulcerative proctitis, which is considered mild
in terms of severity. This is because it only occurs in the area closest to the rectum
or anus, with rectal bleeding as its significant sign of the disease. Another type is
the proctosigmoiditis, affecting the rectum and sigmoid colon. Left-sided colitis
occurs from the rectum up through the sigmoid and descending colon. Abdominal
cramping can be felt on the left side of the abdomen. Lastly, pancolitis is a severe
type as this affects the entire colon (Mayo Clinic, 2021).
According to Basson (2022), ulcerative colitis is three times more common
than Crohn’s disease. In the United States alone, there are about one million
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people affected by ulcerative colitis. The prevalence rate is 35-100 cases per
100,00 people, with an incidence of 10.4-12 cases per 100,000 people.
Specifically, about 20%-25% of all ulcerative colitis cases occur in individuals 20
years or younger. Ulcerative colitis is more common in the Western and Northern
hemispheres, while the rate of incidence is low in Asian countries. In Japan, there
are more than 160,000 people with ulcerative colitis. In the Philippines, there was
no available data showing how the percentage of ulcerative colitis cases. However,
IBD Philippines reported that its prevalence in the country is 1.22 per 100,000
persons.
A. OBJECTIVES
At the end of the second virtual seminar conducted by the BSN 4D Group
1, the BSN participants will be able to gain better synthesis of information and
knowledge that can grasp the understanding about ulcerative colitis and create
new frontier to enhance the nursing practice, research, and education.
a. Present an introduction composing brief overview of the disease
and relevant statistics.
b. compose objectives that are specific, measurable, attainable,
realistic, and time-bounded;;
c. define the ulcerative colitis;;
d. discuss the etiologic factor that lead to the development of the
disease;;
e. identify the symptomatology of the disease;;
f. trace the pathophysiology of the disease through a schematic
diagram;;
g. list the possible medical, surgical, and nursing management, its
indication relating to ulcerative colitis including diagnostic, laboratory
examinations, and possible medications;;
h. present a summary on a related literature published not earlier
than 5 years;; and
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i. arrange an alphabetical list of references used in the study using
APA format.

B. ANATOMY AND PHYSIOLOGY
ANATOMY
Gastrointestinal System
The Gastrointestinal System includes the

mouth, pharynx, esophagus, stomach, small intestine,
large intestine, rectum, and anus. It also includes the
salivary glands, liver, gallbladder, and pancreas, which
make digestive juices and enzymes that help the body digest food and liquids (National
Institutes of Health, n.d.).
The Gastrointestinal System is optimally designed and intricately regulated by

neurological and hormonal systems to take in food and beverages, to extract nutrients
and other substances from food, to transport nutrients and these substances through
complex mechanisms to the circulation for further delivery and use by all tissues, and
finally to excrete waste products from the body (Vorster, H., 2019).
Mouth
The mouth is the beginning of the digestive system

and digestion starts here. The smell of food triggers the
salivary glands in your mouth to secrete saliva, causing
your mouth to water.
Once you start chewing and breaking the food down

into pieces small enough to be digested, other mechanisms
come into play, therefore, more saliva is produced. It contains substances including
enzymes that begin the process of breaking down food into a form your body can absorb
and use.
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Pharynx
This is the portion of the digestive tract that
receives the food from your mouth. Branching off the
pharynx is the esophagus, which carries food to the
stomach, while the trachea or windpipe carries air to
the lungs.
The act of swallowing takes place in the

pharynx as a reflex and under voluntary control. The
tongue and soft palate push the food into the
pharynx, which closes off the trachea. The food then
enters the esophagus.
Esophagus
The esophagus is a muscular tube extending from the pharynx and behind the
trachea to the stomach. Food is pushed through the esophagus and into the stomach by
means of a series of contractions called peristalsis.
Just before the opening to the stomach is an important ring-shaped muscle called
the lower esophageal sphincter. This sphincter opens to let food pass into the stomach
and closes to keep it there. If your lower esophageal sphincter does not work properly,
you may suffer from a condition called gastroesophageal reflux disease (GERD) which
causes heartburn and regurgitation.
Stomach
The stomach is a sac-like organ with strong

muscular walls. It secretes acid and powerful
enzymes that continue the process of breaking the
food down and changing it to a consistency of liquid
or paste. From there, food moves to the small
intestine. Between meals, the non-liquefiable remnants are released from the stomach
and ushered through the rest of the intestines to be eliminated.
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Small Intestine
Made up of three segments- duodenum,

jejunum, and ileum. The small intestine also breaks
down food using enzymes released by the
pancreas and bile from the liver. The duodenum is
largely responsible for the continuing breakdown
process, with the jejunum and ileum being mainly
responsible for absorption of nutrients into the
bloodstream.
This process is highly dependent on the activity of a large network of nerves,

hormones, and muscles.
Large Intestine
The large intestine connects the small intestine to the rectum. It is made up of the
cecum, the ascending colon, the transverse colon, the descending colon and the sigmoid
colon, which connects to the rectum. It is a highly specialized organ that is responsible
for processing waste so that defecation is easy and convenient.
Appendix
It is a hollow tube that is closed at one end and is attached at the other end to the
cecum. It is still not clear whether the appendix serves any useful purpose in humans.
Rectum
The rectum is an eight-inch chamber that connects the colon to the anus. The
rectum is the one that receives stool from the colon, letting the person know there is stool
to be evacuated through sensors which sends a message to the brain. The brain then
decides if the rectal contents can be released or not. If they can, the sphincters relax and
the rectum contracts, expelling its contents.
Anus
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The anus is the last part of the digestive tract. It consists of the muscles that line
the pelvis, where it creates an angle between the rectum and the anus that stops stool
from coming out when it is not supposed to and the two other muscles called anal
sphincters (internal and external) that holds the control of stool passage.
Pancreas
Pancreas is the chief factory for digestive

enzymes that are secreted into the duodenum,
the first segment of the small intestine. These
enzymes break down protein, fats, and
carbohydrates.

Liver
The liver has multiple functions, but two of its main functions within the digestive
system are to make and secrete an important substance called bile and to process the
blood coming from the small intestine containing the nutrients just absorbed. The liver
purifies this blood of many impurities before travelling to the rest of the body.
Gallbladder
The gallbladder is a storage sac for excess bile. Bile made in the liver travels to
the small intestine via the bile ducts. If the intestine does not need it, the bile travels into
the gallbladder, where it awaits the signal from the intestines that food is present. Bile
helps absorb fats in the diet and it carries waste from the liver that cannot go through the
kidneys.
Salivary Glands
Salivary glands play an important role in digestion because they make saliva.
Saliva helps moisten food so we can swallow it more easily. It also has an enzyme called
amylase that makes it easier for the stomach to break down starches in food.
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PHYSIOLOGY
The functions of the gastrointestinal system include the following:
1. Ingestion – the oral cavity allows food to enter the digestive tract then mastication
occurs by mouth, and the resulting food bolus is swallowed. Saliva lubricates food and
provides enzymes for digestion.
2. Propulsion - since food is to be processed by more than one digestive organ, they
must be propelled from one organ to the next. The major means of propulsion is
peristalsis, a series of alternating contractions and relaxations of smooth muscle that lines
the walls of the digestive organs and that forces food to move forward.
3. Mechanical Digestion – muscular movement of the digestive tract physically breaks
down food into smaller particles. Physical processes are mixing of food in the mouth by
the tongue, churning of food in the stomach, and segmentation in the small intestine.
4. Chemical Digestion – hydrolysis reactions aided by enzymes chemically break down
food particles into nutrient molecules, small enough to be absorbed. It is the sequence of
steps in which large food molecules are broken down into their building blocks by
enzymes.
5. Absorption – passage of the end products or nutrients of chemical digestion from the
digestive tract into blood or lymph for distribution to tissue cells.
6. Elimination – the undigested materials will be released through the rectum and anus
by defecation.
D. PATHOPHYSIOLOGY
a. ETIOLOGY
Ulcerative colitis occurs in the large intestine and is a systemic disease affecting
the mucosal and submucosal layers of the colon and rectum. (Hinkle & Cheever, 2018).
The exact etiology of ulcerative colitis is unknown, but certain factors have been found
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to be associated with the disease. The table below indicates the predisposing and
precipitating factors that contribute to the occurrence of ulcerative colitis.
PREDISPOSING RATIONALE
FACTORS
Age Ulcerative colitis can occur at any age, but it is more likely to
develop in people between the ages of 18-30, or older than
50 years of age (Gastroenterology of Rockies, 2021).
Doctors believe that when the condition strikes younger
people, it is more likely to have a genetic component. In older
patients, it is believed to be related to changes in the immune
system that come with aging (Washington University School
of Medicine in St. Louis, 2010).
Gender Males aging above 45 years of age appear to have a 20%
higher incidence rate of UC compared to women (Greuter,
T., et al., 2020).Some studies show a slight predilection for
men, most studies note no preference regarding sex (Lynch,
W. & Hsu, R., 2021).
Family History Family history is a composite of shared environmental

exposures and genetic factors. A first-degree relative of a
patient with ulcerative colitis has a four times higher risk of
developing the disease. Among 71 studies, 12% of ulcerative
colitis patients have a family history of inflammatory bowel
disease. A recent study by Jostins showed that there are
many shared loci between ulcerative colitis and crohn’s
disease;; the study found a higher concordance of a
ulcerative colitis family history among ulcerative colitis
patients compared to a crohn’s disease family history, which
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may suggest that specific loci influence the type of
inflammatory bowel disease (Childers, R., et al., 2014).
Race Prevalence is higher among Jewish people

born in Europe and the Ashkenazi Jews in the United
states than among those born in Asia and Africa.
(source) Inflammatory bowel disease is closely linked to a
westernized environment and lifestyle (Lynch, W. & Hsu, R.,
2021). The increased genetic risk factors seen in Ashkenazi
jews appear to be rooted in a history of migrations,
catastrophic reductions in population, and then re-population
from a small number of surviving founder families over many
centuries (Sedars-Sinai, 2018).
These results further suggest that Jewish patients with
inflammatory bowel disease probably represent a
nonrandom genetically predisposed subset of the Jewish
population. This provides further evidence for the genetic
contribution to inflammatory bowel disease in general, and to
its higher risk in the Jewish population (Roth, M., et al., 1989)
Childhood 25% out of 21,852 Canadian patients with ulcerative colitis
Abuse reported that they had been physically abused and about
20% stated that an adult had forced them into unwanted
sexual activity. Researchers have determined that the risk of
ulcerative colitis was more than 2 times higher for patients
who had experienced childhood abuse than it was for those
who were not (Pharmacy Times, 2016).
PRECIPITATING RATIONALE
FACTORS
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Diet Diet does not cause the development of ulcerative colitis
nor can any special diet cure the disease. However, it
plays a role in managing symptoms and lengthening the
time between flare ups (Cleveland Clinic, 2020). An
increased consumption of polyunsaturated fatty acids
may contribute to issues with digestive health (University
Hospitals, 2021).As dietary trends and the cost of
processed food, refined carbohydrates, and higher-fat
foods which can irritate your digestive tract and trigger
symptoms like cramping, bloating, and diarrhea, have
enabled more widespread consumption of these items.
Thus, the incidence of ulcerative colitis has started to
increase significantly (Miller, B., 2019).
Lifestyle Exercise is one candidate complementary intervention

that may prevent relapses of disease. Further, lack of
exercise may be an important risk factor for the
development of inflammatory bowel disease. Exercise
has demonstrated beneficial effects on bone mineral
density, muscle mass, and functional capacity. This is
also of particular interest to the field of inflammatory bowel
diseases, as patients are known to suffer from issues with
low bone mineral density and low muscle mass due to
side effects of medications and the disease process itself.
According to research, moderate-intensity exercise exerts
an anti-inflammatory effect by both decreasing visceral fat
and subsequent release of pro-inflammatory cytokines
and releasing myokines such as interleukin 6 with each
exercise session. Interleukin 6 is released during exercise
and has been shown to increase the release of glucagon-
like peptides, which are trophic factors associated with
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repair of damaged intestinal mucosa (Engels, M., Cross,
R. K., & Long, M. D., 2017)
Immune System When your immune system tries to fight off an invading
Reactions virus or bacterium, an abnormal immune response
causes the immune system to attack the cells in the
digestive tract too. (Mayo Clinic, 2022) Immune reactions
that compromise the integrity of the intestinal epithelial
barrier may contribute to ulcerative colitis. Serum and
mucosal autoantibodies against intestinal epithelial cells
may be involved. The presence of antineutrophil
cytoplasmic antibodies and anti– Saccharomyces
cerevisiae antibodies is a well-known feature of
inflammatory bowel disease (Basson, M., 2019).
The characteristics of the
inflammatory response are different, with ulcerative
colitis, the inflammation is usually confined to the
mucosa. Both UC and CD exhibit a relapsing and
remitting course and there is a significant, often
dramatic, reduction in quality of life
during exacerbations of the disease (Talley N., et al.,
2011).
Nonsteroidal Anti- NSAIDs work by blocking the enzymes cyclooxygenase-1

Inflammatory Drug and cyclooxygenase-2. NSAIDs dampen the cycle of
(NSAID) Use inflammation and pain, they also cause the digestive
system to lose some of its normal protective substances.
This could create problems for people who already have
inflammation, or the potential for inflammation, in their
digestive tract (Tresca, A., 2020).
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b. SYMPTOMATOLOGY
Bloody The immune system attacks healthy cells in the digestive

Diarrhea tract. The attack increases white blood cells in your colon
and rectum, and repeated attacks lead to chronic
inflammation. Inflammation causes your colon to contract
and empty frequently which causes frequent diarrhea and
urgent bowel movements. When inflammation destroys the
cells lining your colon, sores or ulcers can develop. These
ulcers can bleed and produce pus, resulting in bloody
diarrhea (Higuera, V., 2020).
Loss of Body Ulcerative colitis causes inflammation and sores in the
Fluids and intestine, where the body absorbs most of its nutrients from
Nutrients food. Thus, having inflammation in the intestine prevents
from absorbing enough nutrients, fluid, and electrolytes.
Also, diarrhea and some of the drugs prescribed to manage
IBD can make it harder for the body to absorb nutrients from
foods (Watson, S., 2021).
Dehydration Ulcerative colitis inflames the lining of the intestine and

prevents it from absorbing fluid. The extra water exits your
body in watery bowel movements or diarrhea. A patient can
lose fluids with every watery bowel movement, which could
lead to dehydration (Watson, S., 2021).
Tenesmus Tenesmus occurs because it is believed that inflammation in
the bowel may affect the nerves that control the excretion of
waste. When these nerves are overstimulated, they may
send a signal to the brain saying there's still material in the
bowel. Basically, it can trigger the muscles in the gut that are
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used to push out feces. Those muscles contract, so the body
thinks it needs to have a bowel movement (Bolen, B., 2022).
Passing Mucus The large intestine produces mucus to protect the lining of
through the colon, creates a healthy environment for good gut
Rectum bacteria, and eases the passage of stool. In ulcerative colitis,
the mucus membrane of the large intestine is inflamed. Thus,
it develops small sores called ulcers. These ulcers can bleed
and produce pus. They can also make enough mucus to be
seen in the stool (Tresca, 2021).
Constipation Inflammation in the rectum increases the risk of constipation
in ulcerative colitis. This is called the ‘Proctitis’ where the
pelvic floor doesn’t relax due to spasm. This interferes with
normal bowel activity, making it difficult to pass stools
(Higuera, V., 2019).
Abdominal Pain Pain may arise due to partial blockage and gut distention as
well as severe intestinal inflammation (Bielefeldt, K., Davis,
B., & Binion, D. G., 2009).
Rectal Pain Ulcerative colitis is where inflammation involves the entire

rectum and extends continuously up the colon (Washing
University School of Medicine in St. Louis, 2022). Patients
with ulcerative colitis, ulcers and inflammation of the inner
lining of the colon lead to symptoms of pain (Wedro, B.,
2019).
Rectal Bleeding The inflammation often involves the rectum because it is at
the end of the large intestine, blood from this source is quite
visible in or on the stool. Bleeding occurs because it attacks
the lining of the large intestine. The ulcers that form in the
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mucosa of the large intestine tend to bleed (Tresca, A.,
2022).
Iron Deficiency When inflammation destroys the cells lining your colon,
Anemia sores or ulcers can develop which may cause bleeding and
produce pus (Higuera, V., 2020). Inflammation in active
inflammatory bowel disease causes ongoing blood loss from
the digestive tract. Blood loss is considered the most
significant cause of anemia in inflammatory bowel disease.
In addition, the presence of inflammation affects the body’s
ability to absorb iron and other nutrients from the food
(Werner, C., 2020).
Dyspnea Hemoglobin is a protein that makes up part of a red blood
cell. Its job is to carry oxygen around the body. Iron is
required to make hemoglobin. When there is iron deficiency
anemia, the patient cannot make hemoglobin thus will not
carry enough oxygen around the body which then causes
dyspnea (Werner, C., 2020).
Weight Loss Frequent diarrhea strips your body of nutrients and can lead
to weight loss. Aside from that, an increased demand for
protein is often the result of chronic inflammation. When this
happens, your body may start to break down muscle and
other fat-free areas of mass. The decrease in muscle mass
can cause you to lose weight (Watson, S., 2021).
Loss of There are many factors as to why ulcerative colitis patients
Appetite loss their appetite: One, symptoms of nausea and diarrhea
tend to make ulcerative patient feel less like eating;; mouth
sores can also prevent them from eating certain types of
foods and;; fatigue can also be a factor because if the patient
182

is tired, they are less likely to prepare and consume healthy
meals (Tresca, A., 2020).
Fatigue In some cases, fatigue is caused by the body’s response to
inflammation in the colon. Chemical signals produced during
inflammation can directly act on the brain to cause tiredness
and lack of energy (Geer, K., 2021).
Fever Fever develops as part of the inflammatory process

(Inflammatory Bowel Disease, 2015).
Sores The immune system thinks food, good gut bacteria, and the
cells that line your colon are the intruders. White blood cells
that usually protect you attack the lining of your colon
instead. Thus, causing inflammation and ulcers (web MD,
2021). Mouth ulcers can possibly occur due to vitamin and
mineral deficiencies but can also be a side effect of some
ulcerative colitis medications that cause dry mouth and
swelling in the mucous membranes (Watson, S., 2020).
Joint Pain When the body’s immune system overreacts, it seems that
(Arthritis) this inflammation spreads to the joints and other parts of the
body (Whitbourne, K., 2020).

183

c. SCHEMATIC DIAGRAM

184

185

186

187

d. NARRATIVE
Ulcerative Colitis (UC) and Crohn’s Disease (CD) are the two common forms of
Inflammatory Bowel Diseases (IBD). UC is an idiopathic inflammatory bowel disease that
affects the colonic mucosa and is clinically characterized by diarrhea, abdominal pain,
and rectal bleeding. Even though the cause of the disease is still not known, there are
risk factors that have been known or identified to provide in its development. In the
predisposing factors, it includes: age, gender, family history, race, and childhood abuse.
On the contrary, the precipitating factors are: diet, lifestyle, immune system reactions, and
NSAIDs use.
The first-line of defense of the mucosal immune system is the epithelial barrier,
which is covered by a mucinous layer. It provides physical separation between the host
immune cells and luminal microbes;; it also synthesizes antimicrobial microbes. In
ulcerative colitis, there are alterations and synthesis of mucin sulfation is decreased.
Moreover, there is a disruption and defect in the layers. Permeability is increased due to
the damage to the epithelial barrier. This barrier loss allows for increased luminal antigen
uptake into the lamina propria. Via contact with macrophages and dendritic cells, antigens
stimulate the innate immune response. Dendritic cells, interdigitated in the intestinal
epithelial cells, may send dendrites outside the epithelium to sample bacteria and other
lumen antigens. Macrophages and dendritic cells (innate immune cells) change their
functional status from tolerogenic to an active phenotype by recognizing non-pathogenic
bacteria through molecular pattern recognition receptors. Toll-like receptors (TLR)
activation activates innate and adaptive immune responses that lead to the activation of
the nuclear factor transcription factor (NF- 3B) and other transcription factors that are
essential for inflammatory cascade activation. Activation of NF-kB pathways induces pro-
inflammatory gene transcription, leading to increased development of pro-inflammatory
cytokines (TNF-alpha, interleukins12,23,6, and 1β). Macrophages and dendritic cells that
present antigens to B cells and T cells populate the lamina propria, so the rise in
proinflammatory components contributes to the activation of adaptive immune reactions.
In due course with increased stimulatory capacity, the numbers of active and mature
dendritic cells increase and their circulating numbers correlate with disease activity. After
188

antigens, macrophages and dendritic cells are processed, they are introduced to naive
CD4 T-cells, promoting differentiation into Th2 effector cells, characterized by interleukin
4 development. The major source of interleukin13, which has been associated with
destruction of the epithelial cell barrier, is natural-killer T cells. This results in an atypical
Th2 response mediated by the development of interleukins 5 and 13 by non-classic
natural killer T-cells. Interleukin 13 is especially significant because it exerts cytotoxic
functions against epithelial cells, including apoptosis induction and alteration of tight-
junction protein composition. In the lamina propria of an inflamed colon, natural killer T-
cells are increased and are capable of producing several Th2 cytokines;; first, interleukin
4, which is then soon superseded by interleukin 13. Interleukin 13 can have a positive
feedback effect on T-cells of the natural killer, thus amplifying tissue injury. There is a
subsequent rise in the population of B-cells and plasma cells as the immune response
progresses, leading to increased production of IgG, IgM, and IgA.
With more disruption to the colon's epithelial defenses, leukocyte recruitment

stimulates further immune response. On two fronts, leukocyte recruitment is impaired. In
ulcerative colitis, there is an upregulated release of the chemoattractant CXCL8, 3 and 1
in order to recruit leukocytes from the systemic circulation into the mucosa. In addition,
mucosal addressing cellular adhesion molecule-1 (Mad-CAM1) on the endothelium of
mucosal blood vessels is upregulated. Via MadCAM-1, circulating T cells carrying
integrin- alpha4β7 bind to colonic microvasculature endothelial cells, whose expression
is enhanced in the inflamed intestine, leading to increased entry into the lamina propria
of gut-specific T cells. These two fronts of recruitment amplify the inflammatory response
and prolong the mucosal wall inflammation loop.
The persistent damage results in diffuse friability on the colonic wall and superficial
erosions associated with bleeding and numerous ulcerations in the colonic wall
associated with abdominal pain in the lower left quadrant and pus, serum, blood passage
in the stool. It is possible to grossly diagnose the entailing bleeding that is a hallmark
symptom of UC and is related to anemia, pallor and exhaustion symptoms with the stool
or with the occult fecal blood examination. It is also possible to display and histologically
test the ulcerations by endoscopy, MRI/CT scans, and biopsy. The crypt abscess, in
189

which the crypt epithelium breaks down and the lumen is filled with polymorphonuclear
cells, is the usual histological (microscopic) lesion of ulcerative colitis. The damage to the
colonic walls contributes to the failure of the capacity of the colon to absorb water and
nutrients, resulting in diarrhea (watery stool) and dehydration that can be treated by
fluid/hydration therapy. Many of these implications relate to the diagnosis of ulcerative
colitis. Usually, the diagnosed disease is gradual, and patients will likely experience
periods of spontaneous recovery, and subsequent relapse and prolonged ulceration
cycles will lead to the projection of scar tissue masses that form during the healing
process from the granulation tissue. In addition to the hallmark UC manifestation, certain
extraintestinal manifestations (EIMs) are also present in 10 percent to 30 percent of
ulcerative colitis patients.
The mucosal wall becomes edematous and inflamed as the disease progresses.
Tenesmus, which gives off a cramping feeling of an immediate need to defecate, will
illustrate this. Tests such as sigmoidoscopy, barium enema, and blood tests may verify
inflammation. Various sections of the colon may be involved in the spread of infectious
lesions on the wall. Rectum-limited involvement is known as Proctitis, manifested by
tenesmus and rectal bleeding. Proctosigmoiditis, the presence of the rectum and sigmoid
colon, is manifested by tenesmus, LLQ pain and bloody diarrhea. Colitis manifested by
persistent inflammation and architectural distortion is referred to as left-sided colitis from
the rectum to the descending colon. Pancolitis, which can be manifested by extreme
bloody diarrhea, pain, fever, and weight loss, is also called the involvement of the entire
colon. Lastly, distal ileum involvement can lead to Ileitis backwash, which is manifested
by fever, abdominal pain, diarrhea and bleeding. For patients with ulcerative colitis, the
option of treatment is dependent on both the extent of the condition and the severity. The
prognosis is mostly relatively positive for the first decade after diagnosis, and most
patients go into remission. Sulfasalazine and 5-Aminosalicylates, delivered orally or
rectally, are the first- line therapy, with a remission rate of around 50 percent. Ulcerative
colitis care consists primarily of mesalamine, corticosteroids, immunosuppressive
medications, and TNF-al monoclonal antibodies, which are part of pharmacological
therapy.
190

For patients with ulcerative colitis, the option of treatment is dependent on both the
extent of the condition and the severity. The prognosis is mostly relatively positive for the
first decade after diagnosis, and most patients go into remission. First-line therapy
includes anti-inflammatory drugs such as orally or rectally administered aminosalicylates,
which have a remission rate of around 50%, antibiotics and corticosteroids. Surgical
management may also be included in the treatment of the disease. Surgical management
such as proctocolectomy, specifically Proctocolectomy with Ileostomy and Restorative
Proctocolectomy with Ileal Pouch Anastomosis, colectomy, ileostomy, proctectomy, and
continental ileostomy. Nursing management may run from VS control, bowel movements,
hydration, daily weight monitoring, GI assessment, initial simple full meals diet.
Significant damage to the mucosal wall may continue in the absence of treatment,
which may lead to complications such as severe bleeding leading to anemia or
hypovolemia that may lead to hypovolemic shock. Progression of precursor dysplastic
lesions that lead to dysplasia and adenocarcinoma and subsequently to colorectal cancer
can also occur. The bowel can rupture with repeated ulcerations, resulting in peritonitis
and sepsis. The nerve plexus may be impaired with the intervention of the muscularis
propria, leading to colonic dysmotility and dilatation that may result in infarction and
gangrene or toxic megacolon. Total paralysis occurs with TM and bowel content can
accumulate with the absence of peristalsis, leading to colon rupture. Post-surgical issues
such as anastomotic leakage and rupture, which can then lead to sepsis, are included in
the complications. Complications may contribute to shock, multi-organ failure, systemic
shutdown and death. The prognosis is mostly usually positive within the first decade after
diagnosis, although a certain percentage of patients also develop serious problems,
resulting in bad results and poor quality of life.
E.MEDICAL MANAGEMENT
a. DIAGNOSTIC/LABORATORY TESTS
Diagnostic Test Definition Nursing Responsibilities
191

This test is used to measure Before the Procedure:
different type of cells in the • Explain the
person’s withdrawn blood procedure and
sample. what to expect
Doctors use blood tests to after.
check for signs of ulcerative
colitis and complications, After the Procedure:
Complete
such as anemia. Blood tests • Monitor puncture
Blood Count
can also show signs of site for oozing or
(CBC)
infection or other digestive hematoma
diseases. Moreover, with formation.
IBD, the lining of the large • Apply manual
intestine becomes inflamed pressure and
which causes ulcers and dressing over
Laboratory bleeding to occur in the puncture site.
Tests colon or rectum.
White blood cells or certain Before the Procedure:
proteins in the stool can • Explain purpose of
indicate ulcerative colitis. A the procedure.
stool sample can also help • Advise patient to
rule out other disorders, avoid laxatives, and
such as infections caused by follow a high-
Fecalysis
bacteria, viruses and residue diet.
(Stool
parasites. • Assess patient’s
Analysis)
level of comfort.
• Encourage patient
to urinate before
collecting.

192

• Instruct patient to
wash hands.
• Wear gloves when
transporting the
specimen to the
lab. Label the
specimen and note
its consistency and
date and time of
collection.
A procedure in which the Before the Procedure:
doctor uses specialized • Obtain informed
instruments to view and consent.
operate on the internal • Explain the
organs and vessels of the procedure.
body without making large • Check for
incisions. hypersensitivity to
local anesthetic.
Types: • Advise patient to
1. Colonoscopy – an follow a clear-liquid
Endoscopy exam used to detect diet at most 2 days
changes or before the test, and
abnormalities in the take nothing by
large intestine (colon) mouth the midnight
and rectum. A biopsy before.
(a test that takes • Instruct to void and
small samples of remove metal
tissue for laboratory objects before the
analysis) may also be test.
performed to make a
diagnosis.
193

2. Flexible During the Procedure:
Sigmoidoscopy – • Assist with patient
used to view the positioning.
lower part of the large • Administer sedative
intestine (colon). or pain
medications.
• Instruct to bear
down when tube is
inserted inside.
• Encourage patient
to take deep, slow
breaths.

• Observe for signs
of bowel perforation
(e.g. abdominal
pain, nausea and
vomiting, fever).
• Take and record
vital signs.
• Tell patient normal
diet and activity
may be resumed as
prescribed.
• Encourage
increased oral fluid
intake as
prescribed.
194

• Monitor for rectal
bleeding.
• Assist in collecting
and transporting of
biopsy sample to
the laboratory, if
appropriate.
A safe and painless test that Before the Procedure:
uses a small amount of • Ensure that patient
radiation to make an image is not pregnant.
of a person's abdomen • Explain the
(belly). procedure.
• Assist ability to hold
Abdominal breath.
X-ray (AXR) • Instruct to remove
metal objects.
• Provide gown to
change into.
Imaging
• Provide comfort.
An X-ray exam that can Before the Procedure:
detect changes or • Explain the
abnormalities in the large procedure and
intestine (colon). A contrast what to expect
Barium
(barium) solution is delivered after.
Enema
into the rectum via the anus • Advise patient to
to provide a clear follow a low-residue
visualization of the area. diet around 1-3
days before,
195

followed by a clear
liquid diet and
laxative the night
before the test.
Then, take nothing
by mouth post-
midnight before the
test.
• Provide gown and
remove all metal
objects.

• Assist with
positioning.
• Advise to hold
breath while x-ray
images are taken.
• Tell patient that
mild abdominal
cramping or
discomfort may be
felt.

• Advise patient to
take a laxative to
eliminate the
barium solution.
196

• Encourage
intake.
• Tell patient that
stool may be
colored white for 2-
3 days, and that
constipation may
be experienced.
A CT scan uses computers Before the Procedure:
and rotating X-ray machines • Obtain informed
to create cross-sectional consent.
images of the body. These • Explain the
images provide more procedure and
detailed information than what to expect
typical X-ray images. They after.
can show the soft tissues, • Assess if patient is
blood vessels, and bones in allergic to the dye
Computed various parts of the body. A or contrast media
Tomography contrast dye may be used in (if used).
(CT) Scan patients with IBD. • Ask the patient if he
has any implanted
metal devices or
prostheses, such
as vascular clips,
shrapnel,
pacemakers, joint
implants, filters,
and intrauterine
devices.
197

avoid
eating/drinking 4-6
hours beforehand.
remove all metal
objects.

• Tell the patient that
normal or usual
activities may be
resumed.
• Provide comfort
measures and pain
medication as
needed and
ordered because of
prolonged
positioning the
scanner.
• Encourage
intake to excrete
the dye.
• Monitor the patient
for the adverse
reaction to the
contrast medium
(flushing, nausea,
198

urticaria, and
sneezing).
An MRI machine uses a Before the Procedure:
magnet and radio waves to • Obtain informed
create pictures of the interior consent.
of the body. • Explain the
procedure and
what to expect
after, especially if
patient is
claustrophobic.
• Assess if patient is
allergic to the dye
or contrast media
Magnetic
(if used).
Resonance
• Ask the patient if he
Imaging
has any implanted
(MRI)
metal devices or
prostheses, such
as vascular clips,
shrapnel,
pacemakers, joint
implants, filters,
and intrauterine
devices.
avoid
eating/drinking 4-6
hours beforehand.
199

remove all metal
objects.

• Monitor the cardiac
function for signs of
ischemia. If
necessary, monitor
the patient’s
oxygen saturation,
cardiac rhythm, and
respiratory status
during the test.

• Tell the patient that
normal or usual
activities may be
resumed.
• Provide comfort
measures and pain
medication as
needed and
ordered because of
prolonged
positioning the
scanner.
• Encourage
200

intake to excrete
the dye.
• Monitor the patient
for the adverse
reaction to the
contrast medium
(flushing, nausea,
urticaria, and
sneezing).
A procedure that allows Before the Procedure:
visualization of the • Explain the
gastrointestinal (GI) tract procedure.
and detection of • Instruct to follow
abnormalities. diet instructions by
the doctor.
However, it is
common to have
the patient take
Intestinal nothing by mouth at
Ultrasound least 8-12 hours
(IUS) before the test.
remove metal
objects.

• Tell patient normal
diet and activity
may be resumed as
prescribed.
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b. PHARMACOLOGICAL MANAGEMENT
Anti-Inflammatory Drugs
• Aminosalicylates such as sulfasalazine (Azulfidine) are often effective for mild or
moderate inflammation and are used to prevent or reduce recurrences in long-term
maintenance regimens. Sulfa-free aminosalicylates (e.g., mesalamine [Asacol,
Pentasa]) are effective in preventing and treating recurrence of inflammation.
Antibiotics (e.g., metronidazole [Flagyl]) are used for complications such as
abscesses or fistula formation.
• Corticosteroids are used to treat severe and fulminant disease and can be given
orally (e.g., prednisone) in outpatient treatment or parenterally (e.g.,
hydrocortisone [Solu-Cortef]) in hospitalized patients. Topical (i.e., rectal
administration) corticosteroids (e.g., budesonide [Entocort]) are also widely used
in the treatment of distal colon disease. When the dosage of corticosteroids is
reduced or stopped, the symptoms of disease may return. If corticosteroids are
continued, numerous adverse sequelae may ensue.
Generic Name: Sulfasalazine

Brand Name: Apo-Sulfasalazine, Azulfidine, Sulfazine
Drug Aminosalicylates, Anti-inflammatory
Classification:
Pregnancy B
Category:
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Mode of Action: Inhibits prostaglandin synthesis by interfering with secretions
in the colon and causing local anti-inflammatory action.
Dosage: Ulcerative Colitis
PO: ADULTS, ELDERLY: Initially, 1 g 3–4
times/day in divided doses q4–6h. Maximum:
6 g/day. Maintenance: 2 g/day in divided doses at intervals
less than or equal to q8h. CHILDREN 6 YRS AND OLDER:
Initially, 40– 60 mg/kg/day in 4–6 divided doses.
Maximum: Initial dose: 4 g/day. Maintenance: 30 mg/kg/day in
4 divided doses at
intervals less than or equal to q8h. Maximum: Maintenance
Dose: 2 g/day
Indications: Treatment of mild to moderate colitis, adjunctive therapy in
severe ulcerative colitis, rheumatoid arthritis (RA), juvenile
rheumatoid arthritis
Contraindications: Hypersensitivity to sulfasalazine, sulfa, salicylates;;
porphyria;; GI or GU obstruction
Side Effects: Anorexia, nausea, vomiting, headache, oligospermia,
Hypersensitivity reaction (rash, urticaria, pruritus, fever,
anemia)
Adverse Effects: Anaphylaxis, Stevens-Johnson syndrome, hematologic toxicity
(leukopenia, agranulocytosis), hepatotoxicity, nephrotoxicity
Drug Interactions: Drug-drug:
Digoxin, folic acid: reduced absorption of these drugs
Drug-diagnostic tests:
Bilirubin, BUN, creatinine, eosinophils, transaminases:
increased levels
Granulocytes, hemoglobin, platelets, WBC: decreased levels
Urine glucose test: false-positive result
Drug-food:
Folic acid: decreased folic acid absorption
203

Drug-herbs:
Dong quai, St. John’s wort: increased risk of photosensitivity
Drug-behaviors:
Sun exposure: increased risk of photosensitivity
Nursing ● Monitor I&O, urinalysis, renal function tests
Responsibilities: R: To know if there is no any edema in the body and to assess
normal function of kidney
● Ensure adequate hydration (minimum output 1,500
ml/24 hrs)
R: to prevent nephrotoxicity.
● Assess skin for rash
R: discontinue drug, notify physician at first sign.
● Monitor daily pattern of bowel activity, stool
consistency.
R: Dosage increase may be needed if diarrhea continues,
recurs.
● Assess for and report immediately any hematologic
effects (bleeding, ecchymoses, fever, pharyngitis,
pallor, weakness, purpura).
R: To make physician warned and do plan of care
● Monitor LFT;; observe for jaundice. R: Help diagnose
liver diseases
● Educate that drug may cause orange- yellow
discoloration of urine, skin
R: To ensure patient it is normal and nothing to panicked
about
● Tell patient to take on regular schedule as prescribed,
along with a full glass of water. Instruct him/her to drink
plenty of fluids to minimize crystal formation in urine
● Urge patient to complete full course of treatment, even
if he feels better after a few days.
204

● Instruct patient to watch for and immediately report
signs and symptoms of hypersensitivity reaction,
especially rash.
● Tell patient drug can cause blood disorders, GI, and
liver problems, serious skin reactions, and other
infections. Describe key warning signs and symptoms
(easy bruising or bleeding, severe diarrhea, yellowing
of eyes, sore throat, rash, mouth sores). Instruct
patient to report these right away.
● Advise patient to promptly report scant or bloody urine
or inability to urinate.

Generic Name: Mesalamine

Brand Name: Apriso, Asacol
Drug Classification: GI anti-inflammatory drug
Pregnancy B
Category:
Mode of Action: Unknown. Thought to act in colon, where it blocks
cyclooxygenase and inhibits prostaglandin synthesis
Dosage: Active Ulcerative Colitis
Adults: 800 mg (P.O.) t.i.d. For 6 weeks
Proctosigmoiditis or proctitis
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Adults: 4-g enema (Rowasa 60 ml) P.R. daily at bedtime,
retained for 8 hours. Continue for 3 to 6 weeks
Active ulcerative colitis
Adults: 500 mg (P.R.) b.i.d., increased to t.i.d. If response
inadequate after 2 weeks. Or 1,000 mg (P.R.) at bedtime.
Continued for 3 to 6 weeks
Indications: Active ulcerative colitis, to induce remission in mildly to
moderately active ulcerative colitis, proctosigmoiditis,
proctitis, Active ulcerative proctitis
Contraindications: Hypersensitivity to drug, its components, or salicylates
Side Effects: Abdominal pain, abdominal discomfort, headache flatulence,
nausea, fatigue, general feeling of discomfort and weakness
Adverse Effects: CNS: headache, dizziness, fever, fatigue, malaise, asthenia,
insomnia, pain, vertigo, syncope, anxiety.
CV: chest pain, peripheral edema, HTN.
EENT: nasopharyngitis, pharyngitis, rhinitis, sinusitis
GI: abdominal pain, cramps, discomfort, flatulence, diarrhea,
rectal pain, bloating, nausea, pancolitis, vomiting, constipation,
eructation, hemorrhage
GU: interstitial nephritis, nephropathy, nephrotoxicity.
MUSCULOSKELETAL: Arthralgia, myalgia, back pain,
hypertonia
RESPI: bronchitis, cough, dyspnea
SKIN: itching, rash, acne, urticaria, hair loss
Antacids: increased risk of dissolution of coating of Apriso
granules
Azathioprine, 6-mercaptopurine: increased potential for blood
disorders
Nephrotoxic drugs (including NSAIDs): increased risk of
renal adverse reactions
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Nursing ● Monitor periodic renal function studies and blood cell
Responsibilities: counts in patients on long-term therapy.
● Because the mesalamine rectal suspension contains
potassium metabisulfite, it may cause hypersensitivity
reactions in patients who are sensitive to sulfites.
● Absorption of drug may be nephrotoxic.
● Drug may be associated with an acute intolerance
syndrome in which signs and symptoms (abdominal
pain, cramping, bloody diarrhea, headache, fever,
rash) may be similar to an ulcerative colitis
exacerbation. If acute intolerance syndrome is
suspected, discontinue drug.
● Apriso contains phenylalanine.
● Look alike-sound alike: don’t confuse Asacol with Os-
Cal;; mesalamine with mecamylamine, megestrol,
memantine, metaxolone, or methenamine;; or Apriso
with Apri or Lialda with Aldara.
● Instruct patient to carefully follow instructions supplied
with drug and to swallow tablets whole without
crushing or chewing.
● Tell patient not to take drug with antacids.
● Advice patient to report all adverse reactions and to
stop drug if fever or rush occurs. Patient intolerant of
sulfasalazine may also be hypersensitive to
mesalamine.
● Tell patient to remove foil wrapper from suppositories
before inserting into rectum.
● Teach patient about proper use of retention enema.

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Generic Name: Metronidazole
Brand Name: Apo-Metronidazole, Flagyl
Drug Antibacterial
Classification:
Pregnancy B
Category:
Mode of Action: They work by decreasing the colonic concentration of
ammoniagenic bacteria in hepatic encephalopathy. This
medication diffuses into the organism, inhibits protein
synthesis by interacting with DNA and causing a loss of helical
DNA structure and strand breakage. Therefore, it causes
cell death in susceptible organisms
Dosage: Dosage in Renal impairment
For mild to moderate impairment
• No adjustments
For severe impairment
Creatinine clearance less than 10 ml/min: administer 50% of

dose or q12h
Indications: Treatment of the following anaerobic infections:
Intra-abdominal infections
Contraindications: Hypersensitivity to metronidazole. Pregnancy (first trimester
with trichomoniasis), use of disulfiram within 2 weeks, use of
alcohol during therapy or within 3 days of discontinuing
Metronidazole
Side Effects: • Frequent: Systemic: Anorexia, nausea, dry mouth,
metallic taste.
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• Vaginal: Symptomatic cervicitis/vaginitis, abdominal
cramps, uterine pain.
• Occasional: Systemic: Diarrhea, constipation,
vomiting, dizziness, erythematous rash, urticaria,
reddish-brown urine.
• Topical: Transient erythema, mild dryness, burning,
irritation, stinging, tearing when applied too close to
eyes.
• Vaginal: Vaginal, perineal, vulvar itching;; vulvar
swelling.
• Rare: Mild, transient leukopenia;; thrombophlebitis with
IV therapy.
Adverse Effects: • CNS: SEIZURES, dizziness, headache.
• EENT: tearing (topical only).
• GI: abdominal pain, anorexia, nausea, diarrhea, dry
mouth, furry tongue, glossitis, unpleasant taste,
vomiting.
• Derm: rashes, urticaria: topical only— burning, mild
dryness, skin irritation, transient redness. Hemat:
leukopenia. Local: phlebitis at IV site.
• Neuro: peripheral neuropathy.
• Misc: superinfection, disulfiram-type reaction with
alcohol.
Drug Interactions: • Beta blockers (e.g., labetalol, metoprolol),
anticholinesterase inhibitors (e.g., donepezil,
rivastigmine) may increase effect/toxicity.
• Lab values: may increase serum amylase, lipase, ALT,
AST
Nursing ● Educate the patient that their urine may be red-brown or
Responsibilities: dark
● Advise patient to take drug with food if it causes GI upset
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● Watch for seizures;; notify physician immediately if
patient develops or increases seizure activity
● Be alert for confusion, agitation, headache, or other
alterations in mental status. Notify the physician
promptly if these symptoms develop
● Do not drink alcohol (beverages or preparations
containing alcohol, cough syrups);; severe reactions
may occur.
● You may experience these side effects: Dry mouth with
strange metallic taste (frequent mouth care, sucking
sugarless candies may help);; nausea, vomiting,
diarrhea (eat frequent small meals).
● Inform the patient that this medication may cause
dizziness or lightheadedness. Caution the patietn or
other activities requiring alertness until response to
medication is known
● For patients who have difficulty in swallowing, tablets
may be crushed
● Discontinue therapy immediately if symptoms of CNS
toxicity occur.
● Lab tests: obtain total and differential WBC counts
before, during
● and after therapy, especially if a second course is
necessary.

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Generic Name: Prednisone

Brand Name: Apo-Prednisone, Winpred
Drug Corticosteroid
Classification:
Pregnancy C
Category:
Mode of Action: Decreases inflammation by reversing increased cell capillary
permeability and inhibiting migration of polymorphonuclear
leukocytes. Suppresses immune system, by reducing lymphatic
activity
Dosage: Severe inflammation
Dosage individualized based on diagnosis, severity of
condition, and response. Usual dosage is 5 to 60 mg P.O.
daily as a single dose or in divided dose.
Indications: Arthritis, Rheumatic carditis, acute or chronic adrenal
insufficiency, congenital adrenal hyperplasia, bronchial asthma,
skin diseases, etc.
Contraindications: Hypersensitivity to drug, other corticosteroid, alcohol, bisulfate,
or tartrazine (with some products), systemic fungal infections,
Live-virus vaccines, active untreated infections
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Side Effects: Frequent: insomnia, heartburn, nervousness, abdominal
distention, diaphoresis, acne, mood swings, increased
appetite, facial flushing, delayed wound healing, increased
susceptibility to infection, diarrhea, constipation.
Occasional: headache, edema, change in skin color, frequent
urination
Rare: tachycardia, allergic reaction, psychological changes,
hallucinations, depression
Adverse Effects: Long-term therapy: muscle wasting, osteoporosis,
spontaneous fractures, amenorrhea, cataracts, glaucoma,
peptic ulcer, HF.
Abrupt withdrawal following long-term therapy: anorexia,
nausea, fever, headache, rebound inflammation, fatigue,
weakness, lethargy, dizziness, orthostatic hypotension,
sudden discontinuance may be fatal.
CYP3A4 inducers: may decrease effects Live virus vaccines:
may increase vaccine side effects, potentiate virus replication,
decrease patient’s antibody response to vaccine, may increase
effect of warfarin.
Drug-herbs:
St. John’s wort: may decrease concentration
Cat’s claw, echinacea: may have immunostimulant
properties
Drug-laboratory values:
Serum glucose, lipids, sodium, uric acid: increased values
Serum calcium, potassium, WBC, hypothalamic pituitary
adrenal axis function: decreased values
Nursing ● Assess for fatigue, weakness, joint pain, fever, appetite
Responsibilities: loss, shortness of breath, dizziness, syncope.
Rationale: This are early signs of adrenal insufficiency.
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● Monitor potassium, blood glucose, urine glucose while
on long-term therapy.
Rationale: Hypokalemia and hyperglycemia may occur
● Assess for increased temp, WBC even after withdrawal
of medication;; product masks infection symptoms.
Rationale: This could indicate infection
● Assess for paresthesias, fatigue, nausea, vomiting,
depression, polyuria, dysrhythmias, weakness, edema,
hypertension, cardiac symptoms.
Rationale: This could indicate potassium depletion
● Assess for affect, mood, behavioral changes,
aggression.
Rationale: Prednisone could affect the mental status of
a client
● Caution patient not to stop drug suddenly.
Rationale: Abruptly discontinuing could result in adrenal
crisis
● Caution patient not to take herbs or over-the-counter
drugs during therapy;; unless directed by the physician.
Rationale: Some drugs could alter the effects of
prednisone
● Teach patient to recognize symptoms of adrenal
insufficiency.
Rationale: To immediately report the sign and
symptoms of adrenal insufficiency
● Instruct patient to avoid vaccinations during therapy.
Rationale: Live virus vaccines are contraindicated

Immunomodulating Drugs
• Immunomodulators (e.g., azathioprine [Imuran], mercaptopurine [6- MP],
methotrexate [MTX], cyclosporine [Neoral]) have been used to alter the immune
213

response. They are used in patients with severe disease who have not responded
favorably to other therapies. These medications are useful in maintenance
regimens to prevent relapses.

Generic Name: Azathioprine
Brand Name: Azasan, Imuran
Drug Immunosuppressant
Classification:
Pregnancy D
Category:
Mode of Action: Antagonizes purine metabolism, inhibits DNA, protein, and
RNA synthesis. Therapeutic Effect: Suppresses cell-mediated
hypersensitivities;; alters antibody production, immune
response in transplant recipients. Reduces symptoms of
arthritis severity.
For people with UC, the typical dosage of azathioprine is
1.5–2.5 milligrams per kilograms of body weight (mg/kg).
Imuran is only available as a 50-mg tablet.
Indications: Adjunct in prevention of rejection in kidney transplantation.
Treatment of rheumatoid arthritis (RA) in pts unresponsive to
conventional therapy.
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Contraindications: Hypersensitivity to azathioprine. Pregnant women with RA, pts
previously treated for RA with alkylating agents
(cyclophosphamide, chlorambucil, melphalan) may have a
prohibitive risk of malignancy with azathioprine.
Side Effects: Frequent: Nausea, vomiting, anorexia (particularly during
early treatment and with large doses).
Occasional: Rash.
Rare: Severe nausea/vomiting with diarrhea, abdominal pain,
hypersensitivity reaction.
Adverse Effects: GI: pancreatitis.
Hematologic: leukopenia, myelosuppression, pancytopenia,
thrombocytopenia, immunosuppression.
Hepatic: hepatotoxicity.
Musculoskeletal: myalgia.
Other: infections, increased risk of neoplasia.
Drug Interactions: DRUG-DRUG: Allopurinol, sulfamethoxazole/trimethoprim may
increase activity, toxicity. Bone marrow depressants may
increase myelosuppression. Other immunosuppressants may
increase risk of infection or development of neoplasms. May
increase effects of live virus vaccines.
DRUG-HERBAL: Avoid cat’s claw, echinacea
(immunostimulant properties).
DRUG-LAB VALUES: May decrease Hgb, serum albumin,
uric acid, leukocytes, platelet count. May increase serum ALT,
AST, alkaline phosphatase, amylase, bilirubin.
Nursing ● Monitor CBC and platelet counts weekly for 1 month,
Responsibilities: twice monthly for 2 months, then monthly unless more
frequent monitoring is clinically indicated. Also monitor
counts at dosage changes. Notify prescriber if counts
drop suddenly or become dangerously low. Drug may
need to be temporarily withheld.
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● Watch for early signs and symptoms of hepatotoxicity
(such as clay-colored stools, dark urine, pruritus, and
yellow skin and sclera).
● Monitor patient periodically for increased alkaline
phosphatase, bilirubin, AST, and ALT levels.
● Monitor patient for bacterial, viral, fungal, protozoal,
and opportunistic infections, including reactivation of
latent infections such as TB.
● Warn patient to report even mild infections (colds,
fever, sore throat, malaise), because drug is a potent
immunosuppressant.
● Warn patient that some hair thinning is possible.
● Advise patient to report unusual bleeding or bruising.
● Tell patient that drug may be taken with food to
decrease nausea.
● Advise patient to use soft toothbrush and perform oral
care cautiously.

Biologic Agents
• Newer biologic therapies incorporate monoclonal antibodies, including infliximab
and adalimumab for treating ulcerative colitis. Clinical outcomes for the biologic
therapies are promising, although adverse effects may seriously limit their
usefulness.
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Generic Name: Infliximab

Brand Name: Remicabe
Drug Tumor necrosis factor (TNF) blocker
Classification:
Pregnancy B
Category:
Mode of Action: Binds to tumor necrosis factor (TNF), inhibiting functional
activity of TNF (induction of proinflammatory cytokines,
enhanced leukocytic migration, activation of
neutrophils/eosinophils).
IV Infusion: ADULTS, ELDERLY, CHILDREN 6 YRS AND

OLDER: 5 mg/kg followed by additional doses at 2 and 6 wks
after first infusion, then q8wks thereafter.
Indications: • Used to reduce the symptoms of moderate-to-severely
active Crohn's disease and ulcerative colitis in adults
and children who have been previously treated with
other medicines but did not work well.
• Used alone or together with other medicines (eg,
methotrexate) to reduce the symptoms and prevent the
progression of moderate-to-severely active rheumatoid
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arthritis, psoriatic arthritis, and active ankylosing
spondylitis.
• Used to treat chronic severe (extensive or disabling)
plaque psoriasis, which is a skin disease with red
patches and white scales that do not go away. It is used
in patients who cannot be treated with other medicines.
Contraindications: Hypersensitivity to inFLIXimab. Moderate to severe HF (doses
greater than 5 mg/kg should be avoided). Sensitivity to murine
proteins, sepsis, serious active infection.
Side Effects: Frequent (22%–10%): Headache, nausea, fatigue, fever.
Occasional (9%– 5%): Fever/chills during infusion,
pharyngitis, vomiting, pain, dizziness, bronchitis, rash, rhinitis,
cough, pruritus, sinusitis, myalgia, back pain.
Rare (4%–1%): Hypotension or hypertension, paresthesia,
anxiety, depression, insomnia, diarrhea, UTI.
Adverse Effects: Serious infections, including sepsis, occur rarely. Potential for
hypersensitivity reaction, lupus-like syndrome, severe hepatic
reaction, HF.
Drug Interactions: DRUG-DRUG: Anakinra, abatacept may increase risk of
infection. Immunosuppressants may reduce frequency of
infusion reactions, antibodies to inFLIXimab. Live virus
vaccines may decrease immune response (do not give
concurrently).
DRUG-HERBAL: Echinacea may decrease effects.
DRUG- LAB VALUES: May increase serum alkaline
phosphatase, ALT, AST, bilirubin.
Nursing ● Monitor daily pattern of bowel activity, stool
Responsibilities: consistency.
● Monitor patients for signs and symptoms of
hypersensitivity reactions (urticaria, dyspnea,
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hypotension), which may occur during or within 2 hours
of infusion and may be severe. Discontinue drug for
severe reactions and treat appropriately.
● Tell patient about infusion-reaction symptoms and
adverse effects and the need to report them promptly.
● Advise patient to report all adverse reactions and to
seek immediate medical attention for signs and
symptoms of infection (persistent fever, cough,
shortness of breath, fatigue, unusual bleeding or
bruising.
● Educate that treatment may depress your immune
system and reduce your ability to fight infection.
● Instruct to report symptoms of infection such as body
aches, chills, cough, fatigue, fever. Avoid those with
active infection.
● Instruct to not receive live vaccines.
● Inform that frequent tuberculosis screening is
expected.
● Instruct to report travel plans to possible endemic
areas.

Sedatives, Antidiarrheal, Anti-peristaltic medications
• Used to minimize peristalsis in order to rest the inflamed bowel. They are continued
until the patient’s stools approach normal frequency and consistency. One such
anti-diarrheal medication is loperamide [Imodium].
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Generic Name: Loperamide

Brand Name: Imodium
Drug Anti-Diarrheal
Classification:
Pregnancy B
Category:
Mode of Action: Slows intestinal motility, prolongs transit time of intestinal
contents by reducing fecal volume, diminishing loss of fluid,
electrolytes, increasing viscosity, bulk of stool. Increases tone
of anal sphincter.
Dosage: ADULTS, ELDERLY: Initially, 4 mg, then 2 mg after each
unformed stool.
CHILDREN 9–12 YRS, WEIGHING MORE THAN 30 KG:

Initially, 2 mg 3 times a day for 24 hrs.
CHILDREN 6–8 YRS, WEIGHING 20–30 KG: Initially, 2 mg

twice a day for 24 hrs.
CHILDREN 2–5 YRS, WEIGHING 13–20 KG: Initially, 1 mg 3

times a day for 24 hrs.
Indications: Acute diarrhea, Chronic diarrhea, Traveler’s diarrhea
Contraindications: Abdominal pain without diarrhea, Paralytic ileus, high fever,
stool with blood
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Side Effects: Dry mouth, drowsiness, abdominal discomfort, allergic
reaction (rash, pruritus), dizziness, tiredness
Adverse Effects: Toxicity results in constipation, GI irritation (nausea, vomiting),
CNS depression. Activated charcoal is used to treat
loperamide toxicity.
Drug Interactions: Ritonavir may increase concentration, side effects.
DRUG-HERBAL: None significant.
DRUG-FOOD: None known. LAB VALUES: None significant
Nursing ● Monitor therapeutic effectiveness. If improvement does
Responsibilities: not occur within this time, it is unlikely that symptoms
will be controlled by further administration.
● Assess bowel sounds for peristalsis because
hyperactive bowel sound indicates for a diarrhea
● Monitor daily pattern of bowel activity, stool
consistency to assess the condition of the patient if it is
improving
● Monitor Intake and Output to monitor for any kind of
dehydration
● Stay alert for CNS effects, especially in children
● Instruct patient not take alcohol and other CNS
depressants concomitantly unless otherwise advised
by physician;; may enhance drowsiness.
● Instruct patient to report fever, mucus in stool, or
history of hepatic disease before using drug.
● Instruct measures to relieve dry mouth;; rinse mouth
frequently with water, suck hard candy.
● Withhold drug, notify physician promptly if the patient
with ulcerative colitis develops abdominal distention or
other GI symptoms.
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● Discontinue if there is no improvement after 48 h of
therapy for acute diarrhea.
F. SURGICAL MANAGEMENT
Surgery Definition Rationale
Total Surgical removal of the This surgery is done to
Colectomy entire colon. remove diseased
Surgical removal of part of portions of the large
the colon, either the intestine to decrease
ascending colon (attached incidences of flare-ups
to the small intestine on the and complications. This
Partial or right side of the abdomen) may also be done
Colectomy Subtotal or descending colon because of severe rectal
Colectomy (attached to the rectum on bleeding or when the
the left side). After, the body ineffectively
surgeon reconnects the responds to the
non-diseased portions of medications.
the colon together.
Surgical removal of the left
Hemicolectomy
or right portion of the colon.
In addition to colectomy, an An ileostomy is done to
ileostomy is also performed either temporarily or
after, which involves permanently stop
creating an opening digestive waste passing
(stoma) in the abdominal through the full length of
Colectomy with Ileostomy
wall. The stool comes out the small intestine or
from the ileostomy and colon, as well as relieve
empties into a pouch that is inflammation of the colon
attached to the skin around in ulcerative colitis.
the stoma.
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Continent Ileostomy is a The K-pouch is used in
different type of ileostomy, cases of ulcerative colitis
wherein a pouch that when the large intestine
collects waste is made from and rectum need to be
part of the small intestine. removed because of
This pouch stays inside the disease and the anal
Colectomy with Continent
body, and it connects to the sphincter muscles are
ileostomy (Kock-pouch)
stoma through a valve weak, or because a J- or
created by the surgeon. S-pouch cannot or
The valve prevents the should not be made.
stool from constantly
draining out, so a pouch is
usually not worn.
A procedure that does not The ileoanal procedure
need to create a permanent cures ulcerative colitis by
opening in the abdomen removing all the tissue
(stoma) for passing bowel that the disease could
movements after a return to.
proctocolectomy. The lining
of the rectum is removed,
and the lower end of the
Colectomy with Ileoanal
small intestine (the ileum)
Anastomosis (J-pouch)
is attached to the opening
of the anus. The surgeon
makes a pouch from the
ileum to hold fecal material
(stool). The lower end of
the pouch is attached to the
anus. The muscles around
the rectum are left in place.
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This allows for fairly normal
bowel movements.
Surgical removal of the More commonly
large intestine and rectum, considered as the last
leaving the lower end of the option for surgery, this
small intestine (the ileum). procedure permanently
The doctor sews the anus cures ulcerative colitis,
closed and performs an restores life expectancy
ostomy, where a small to normal, and
Proctocolectomy with opening called a stoma is eliminates the risk of
Ileostomy made in the skin of the colon cancer. However,
lower abdomen. An inflammation develops in
ileostomy is also performed the small intestine in
to create an opening to the about 25% of people
intestine to eliminate after surgery even
wastes. though their small
intestine was not
previously affected.
G. NURSING MANAGEMENT
Nursing Diagnosis Goals Nursing Interventions
Diarrhea related to Within 8 hours of • Record number, amount,
inflammatory changes of nursing care, the characteristics, and
the bowel as evidenced patient will be able to: consistency of stools per
by loose, liquid stools, a. lessen day.
more than 3 times in 24 frequency of R: Documentation of
hours bowel output provides a baseline
elimination to 1- and helps direct
Rationale: 3 times a day;; replacement fluid therapy.
Diarrhea is an increase and
in the frequency of
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bowel movements, as b. report a more • Promote bedrest provide
well as the water normal stool bedside
content and volume of consistency commode/bedpan.
the waste. It may arise (firm, solid). R: Rest decreases
from a variety of factors, intestinal motility and
including inflammatory reduces the metabolic
bowel diseases. Due to rate when infection or
ulcerative colitis, hemorrhage is a
inflammation is present complication. Urge to
in the large intestine and defecate may occur
rectum, causing without warning and be
diarrhea and making the uncontrollable, increasing
colon empty itself. risk of incontinence or
falls if facilities are not
close at hand.
• Empty the bedpan and
commode promptly.
R: To remove source of
odor and decrease the
patient’s anxiety about
incontinence.
• Administer anti-diarrheal
medications as ordered.
R: Most anti-diarrheal
drugs
suppress
gastrointestinal motility,
thus allowing
for more fluid
absorption.
Supplements
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of beneficial
bacteria
(“probiotics”)
or yogurt
may reduce
symptoms by
reestablishing normal flora
in the intestine.
• Identify and restrict foods
and fluids that precipitate
diarrhea (vegetables and
fruits, whole-grain cereals,
condiments, carbonated
drinks, milk products).
R: Avoiding intestinal
irritants promote intestinal
rest and reduce intestinal
workload.
Acute pain related to GI Within 1 hour of • Administer analgesics as
inflammation as nursing care, the prescribed.
evidenced by pain scale patient will be able to: R: To promote pain relief
of 8/10 and abdominal a. report pain scale and comfort.
cramping of 1-3 out of 10;; • Encourage patient to
b. demonstrate assume position of
Rationale: absence of comfort (knees flexed).
Ulcerative colitis is guarding R: reduced abdominal
characterized by a behavior;; and tension and promotes
chronic, long-term c. demonstrate sense of control.
inflammation in the large absence of facial • Provide comfort measures
intestine and rectum that expression of (repositioning, back rub)
can also lead to open pain. and diversional activities.
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sores (ulcers). This R: To promote relaxation
inflammation is the and refocus attention and
common cause of enhance coping abilities.
abdominal pain or • Encourage to do deep
cramping. breathing exercises.
R: To reduce restlessness
and promote relaxation.
Deficient fluid volume Within 8 hours of • Record color and amount
related to diarrhea as nursing care, the of urine, and report urine
evidenced by dry patient will be able to: output less than 30 cc/hr.
mucous membranes, a. demonstrate for two consecutive hours.
poor skin turgor, and moist mucous R: Normal urine output is
decreased urine output membranes;; not less than 30 cc/hr.
b. demonstrate Concentrated urine
Rationale: good skin turgor;; denotes fluid deficit.
Ulcerative colitis causes and • Weigh patient daily and
inflammation of the large c. increase urine record.
intestine, preventing it output to 30-60 R: An accurate daily
from absorbing fluid. cc/hr. weight is an important
Thus, the extra water indicator of fluid balance
exits the body in watery in the body.
bowel movements • Monitor and record intake
(diarrhea). This can lead and output.
to fluid output increasing R: Monitoring ensures
more than fluid intake. correct fluid replacement
therapy.
• Provide parenteral
replacement of fluids,
electrolytes, and vitamins
as prescribed.
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R: To maintain hydration
status.
• Provide measures to
prevent excessive
electrolyte loss (e.g.,
resting the GI tract,
administering anti-
diarrheal medications as
ordered by the physician).
R: Fluid losses from
diarrhea should be
concomitantly treated with
antidiarrheal medications,
as prescribed.
Imbalanced nutrition: Within 8 hours of • Weigh patient as indicated
less than body nursing care, the and record.
requirements related to patient will be able to: R: An accurate weight can
loss of appetite as a. verbalize provide additional
evidenced by insufficient understanding of information about the
interest in food important of nutritional needs of the
sufficient dietary patient.
Rationale: intake and • Promote undisturbed rest
Ulcerative colitis causes regaining periods, especially before
inflammation and sores healthy weight;; meals.
in the intestines, which b. verbalize R: Proper rest can help
is where the body awareness of reduce metabolic
absorbs most of its what foods to demands and conserve
nutrients from food. avoid;; and energy.
During flares, there’s c. demonstrate • Encourage proper oral
more inflammation in the behavior on hygiene, especially before
colon, leading to severe following the meals.
228

symptoms such as prescribed R: To prevent
diarrhea and decreased dietary intake. bleeding/sore gums and
appetite. bad breath, and enhance
taste of food.
• Encourage patient to eat
all meals and explain its
importance in regaining
healthy weight.
R: Improved nutrition and
having a healthy weight
are important for recovery
and helps prevent severe
malnutrition. Gaining a
healthy weight can also
help increase muscle
tone.
• Avoid or limit foods such
as milk products, foods
high in fiber or fat, alcohol,
caffeinated beverages,
chocolate, peppermint,
tomatoes, orange juice.
R: These foods may
cause or exacerbate
abdominal cramping and
flatulence.
Deficient Knowledge Within 1 hour of • Recognize awareness of
related to inadequate nursing care, the the patient’s concerns.
information regarding patient will be able to: R: Acknowledgment of the
disease process and its a. verbalize patient’s feelings validates
management as understanding of the feelings and
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evidenced by the disease communicates
questioning members of process and acceptance of those
the health care team possible feelings.
complications of • Inform about the disease
Rationale: ulcerative colitis;; process and effects of
Knowledge about b. verbalize ulcerative eclampsia on
certain diseases or understanding of the body and its
conditions play an adhering to the management.
important role in a prescribed R: An informed patient
diseased person’s life treatment and family are more likely
and recovery and can regimen;; and to adhere to the
promote health. c. participate in prescribed therapy and
treatment participate in the
Although ulcerative regimen. therapeutic regimen.
colitis is a common • Explain the importance in
disease, it is not a complying with the
typical household name. treatment regimen,
As such, there may be particularly the
people who hold medications.
misconceptions about it, R: A relapse may occur
especially for those who from an abrupt withdrawal
experience the disease of medications, causing
for the first time. inflammation and
symptoms to return.
Proper education may
help promote involvement
and participation
regarding the treatment
regimen
• Discuss the significance
of maintaining good
230

general health, (adequate
diet, rest, moderate
exercise, and avoidance
of exhaustion, alcohol,
caffeine, and stimulant
drugs).
R: Healthy lifestyle
changes promote health.
Smoking, in particular,
should be ceased
because it can increase
intestinal motility,
aggravating symptoms.
• Emphasize need for long-
term follow-up and
periodic reevaluation.
R: Patients with IBD are at
increased risk for colon or
rectal cancer, and regular
diagnostic evaluations
may be required.
H. RELATED LITERATURE
Title: A Challenging Colectomy for Acute Severe Ulcerative Colitis Complicated by
COVID-19
This article discussed how COVID-19 affected the management of patients with
inflammatory bowel disease, especially ulcerative colitis, by presenting a case wherein a
patient had to undergo a colectomy while diagnosed with the virus.
According to the article, a 60-year old female was admitted with a severe disease
flare and exhibited bloody diarrhea, up to 10 bowel movements per day, abdominal pain,
and fatigue. Although, she had already received treatment a week earlier that included:
intravenous (IV) corticosteroid therapy with anti-thrombotic prophylaxis and total
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parenteral nutrition (TPN). Nevertheless, her condition showed no improvement, and her
drug therapy of infliximab and cyclosporine was ineffective. Thus, a colectomy was the
next option.
However, the patient was diagnosed with COVID-19, prompting the surgery to be
delayed due to their nutritional status and postoperative respiratory failure. Over time, her
condition improved after being treated with medications and oxygen. A CT scan result
then showed a significant regression of pneumonia. Thus, a laparoscopic colectomy with
terminal ileostomy was done with the health care team following a COVID-19 surgical
care pathway as nasopharyngeal swabs still test positive. Results showed no
complications, and eventually, the patient was discharged after finally testing negative for
the virus.
The article concluded that the World Health Organization (WHO) and the
International Organization for the Study of Inflammatory Bowel Disease (IOIBD) recently
published recommendations to avoid routine corticosteroids and cancel or delay surgery.
However, the patient in the case presentation needed her surgery to be delayed due to
infection complications, logistical difficulties, and a lack of COVID-19 case studies to refer
to. As such, the authors stated that further studies are needed to evaluate the timing of
surgical intervention in similar situations.

Title: Eltrombopag and its beneficial role in management of ulcerative Colitis
associated with ITP as an upfront therapy case report
This article discussed how eltrombopag could be used as a medication in treating
ulcerative colitis (UC) and immune thrombocytopenic purpura (ITP) by presenting a case
wherein a patient was diagnosed and treated with those conditions.
According to the article, Eltrombopag (EPAG) was defined as a thrombopoietin
agonist that is administered orally to increase platelet production;; hence, it is appropriate
to treat ITP. ITP is very rarely associated with UC, so only a few cases are show this
relation, including the case in the article that showed a 21-year old male exhibiting
diarrhea and up to 12 bowel movements daily. He underwent sigmoidoscopy showing
features consistent with UC. Also, his initial blood count showed thrombocytopenia and
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high calprotectin. He was then treated with EPAG, as well as Mesalazine and
Mesalamine.
The article stated that standard treatment for UC includes mesalamine, steroids,
and immunosuppressive medications. However, it concluded that EPAG could also be
safely used as the patient showed marked improvement in the platelets and regression
of UC. Although no case studies or clear data are reporting the relationship between
EPAG and the deterioration of UC and/or ITP, the former’s effects were shown to be
effective as a management of the latter.

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HEMORRHOIDS

Introduction
Gastrointestinal diseases are among the most common problems in tropical
countries and commonly manifest as diarrhea, abdominal pain, abdominal distention,
gastrointestinal bleeding, intestinal obstruction, malabsorption, or malnutrition. One
example condition with problems under gastro is hemorrhoids. They affect millions of
people around the world and represent a major medical and socioeconomic problem. It
has a social impact, as it is inter-linked to lifestyles, such as interpersonal, and impacted
by food and hygienic and sexual habits, and has an economic burden on health systems
indirect costs and working days lost. The hemorrhoidal disease creates physical and
psychological discomfort and significantly affects the quality of life of the patients due to
its sensitive symptoms such as anal bleeding, pain, and itching sensation. Besides,
hemorrhoids hinder patients’ ability to live normally and work efficiently even after
management due to its frequent recurrence, incomplete elimination of discomfort, and
postoperative pain.
Defining hemorrhoids are clusters of vascular tissues, smooth muscles, and
connective tissues that lie along the anal canal in three columns—left lateral, right
anterior, and right posterior positions. Because some do not contain muscular walls, these
clusters may be considered sinusoids instead of arteries or veins. Hemorrhoids are
present universally in healthy individuals as cushions surrounding the anastomoses
between the superior rectal artery and the superior, middle, and inferior rectal veins these
hemorrhoidal venous cushions are normal structures of the anorectum and are
anatomically present unless a previous intervention has taken place. Because of their rich
vascular supply, highly sensitive location, and tendency to engorge and prolapse,
hemorrhoidal venous cushions are common causes of anal pathology. Nonetheless, the
term “hemorrhoid” is commonly invoked to characterize the pathologic process of
symptomatic hemorrhoid disease instead of the normal anatomic structure. Classification
of hemorrhoid corresponds to its position relative to the dentate line. External
hemorrhoids are located below the dentate line and develop from ectoderm
embryonically. They are covered with anoderm, composed of squamous epithelium, and
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are innervated by somatic nerves supplying the perianal skin and thus producing pain.
Vascular outflows of external hemorrhoids are via the inferior rectal veins into the
pudendal vessels and then into the internal iliac veins. In contrast, internal hemorrhoids
lie above the dentate line and are derived from the endoderm. They are covered by
columnar epithelium, innervated by visceral nerve fibers, and thus cannot cause pain.
Vascular outflows of internal hemorrhoids include the middle and superior rectal veins,
which subsequently drain into the internal iliac vessels. While no taxonomy of external
hemorrhoids is used clinically, internal hemorrhoids are further stratified by the severity
of prolapse. First-degree internal hemorrhoids do not prolapse out of the canal but are
characterized by prominent vascularity. Second-degree hemorrhoids prolapse outside of
the canal during bowel movements or straining but reduce spontaneously. Third-degree
hemorrhoids prolapse out of the canal and require manual reduction. Fourth-degree
hemorrhoids are irreducible even with manipulation. Patients with hemorrhoids are
usually asymptomatic but the common symptoms are bleeding with or without defecation,
swelling, mild discomfort or irritation, and pruritus. Though some patients need to undergo
surgery, many hemorrhoid patients can successfully be treated with conservative
medication and ointments.
According to a study conducted by Kibret et al. 2021 in the United States,
hemorrhoid disease is the fourth leading outpatient gastrointestinal diagnosis, accounting
for 3.3 million ambulatory care visits. The estimated worldwide prevalence of hemorrhoids
in the general population is to be 4.4%. Globally, various studies were conducted to
assess the prevalence and associated factors of hemorrhoids. The prevalence of
hemorrhoids is higher in Australia (38.93%) which is followed by Israel (16%) and Korea
(14.4%). Very few attempts have been made to assess the prevalence of hemorrhoids in
Africa. The prevalence of hemorrhoids among Egyptian patients subjected to
colonoscopy was 18%. In the Philippines, many Filipinos are going through nightmares
of hemorrhoids or piles (almoranas, almuranas in Tagalog). It is not just a Filipino matter
as it is a universal issue. Studies show that around 75% of adults would bump into this
problem at some point in their adult lives. Shockingly, even young adults nowadays tend
to deal with the same medical condition

235

I. Objectives
At the end of the virtual seminar conducted by the BSN 4D Group 1, the BSN
participants will be able to gain a better synthesis of information and knowledge that can
grasp the understanding about hemorrhoids and create a new frontier to enhance the
nursing practice, research, and education.
a. Present an introduction composing a brief overview of the disease and relevant
statistics;;
b. compose objectives that are specific, measurable, attainable, realistic, and time-
bounded;;
c. define hemorrhoids;;
d. discuss the etiologic factor that leads to the development of the disease;;
e. identify the symptomatology of the disease;;
f. trace the pathophysiology of the disease through a schematic diagram;;
g. list the possible medical, surgical, and nursing management, its indication relating
to hemorrhoids including diagnostic, laboratory examinations, and possible
medications;;
h. present a summary on related literature published not earlier than 5 years;; and
i. arrange an alphabetical list of references used in the study using APA format.

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A. Definition
§ Hemorrhoids (HEM-uh-roids), also called piles, are swollen veins in your
anus and lower rectum, like varicose veins. Hemorrhoids can develop inside
the rectum (internal hemorrhoids) or under the skin around the anus
(external hemorrhoids). Nearly three out of four adults will have
hemorrhoids from time to time. Hemorrhoids have several causes, but often
the cause is unknown. Fortunately, effective options are available to treat
hemorrhoids. Many people get relief with home treatments and lifestyle
changes.
§ An abnormal mass of dilated and engorged blood vessels in swollen tissue
that occurs internally in the anal canal or externally around the anus, that
may be marked by bleeding, pain, or itching, and that when occurring
internally often protrude through the outer sphincter of the anus and when
occurring externally may lead to thrombosis —usually used in plural
(Meriam Webster, 1828).
§ A form of varicose vein, hemorrhoid may develop from anal infection or from
an increase in intra-abdominal pressure, such as occurs during pregnancy,
while lifting a heavy object, or while straining at stool. It may be a
complication of chronic liver disease or tumors. The weakness in the vessel
wall that permits the defect to develop may be inherited (Britannica).

B. Statistics
According to a study conducted by Kibret et al. 2021 in the United States,
hemorrhoid disease is the fourth leading outpatient gastrointestinal diagnosis, accounting
for 3.3 million ambulatory care visits. The estimated worldwide prevalence of hemorrhoids
in the general population is to be 4.4%. Globally, various studies were conducted to
assess the prevalence and associated factors of hemorrhoids. The prevalence of
hemorrhoids is higher in Australia (38.93%) which is followed by Israel (16%) and Korea
(14.4%). Very few attempts have been made to assess the prevalence of hemorrhoids in
Africa. The prevalence of hemorrhoids among Egyptian patients subjected to
colonoscopy was 18%. In the Philippines, many Filipinos are going through nightmares
237

of hemorrhoids or piles (almoranas, almuranas in Tagalog). It is not just a Filipino matter
as it is a universal issue. Studies show that around 75% of adults would bump into this
problem at some point in their adult lives. Shockingly, even young adults nowadays tend
to deal with the same medical condition.

II. Anatomy and Physiology
Hemorrhoids are not varicosities;; they are clusters of vascular tissue (eg,
arterioles, venules, arteriolar-venular connections), smooth muscle, and connective
tissue lined by the normal epithelium of the anal canal. Hemorrhoids are present in utero
and persist through normal adult life.

Figure 1. Anatomy of the anal canal and vasculature of hemorrhoids.
Classification of hemorrhoid corresponds to its position relative to the dentate line.
External hemorrhoids are located below the dentate line and develop from ectoderm
embryonically. They are covered with anoderm, composed of squamous epithelium, and
are innervated by somatic nerves supplying the perianal skin and thus producing pain.
Vascular outflows of external hemorrhoids are via the inferior rectal veins into the
pudendal vessels and then into the internal iliac veins. In contrast, internal hemorrhoids
lie above the dentate line and are derived from the endoderm. They are covered by
238

columnar epithelium, innervated by visceral nerve fibers, and thus cannot cause pain.
Vascular outflows of internal hemorrhoids include the middle and superior rectal veins,
which subsequently drain into the internal iliac vessels.

Figure 2. Types of Hemorrhoids.

Figure 3. Diagram of common sites of major anal and internal hemorrhoids. A: Diagram
of common sites of major anal cushions;; B: Common sites of internal hemorrhoids.
The theory of sliding anal canal lining is widely accepted which proposes that
hemorrhoids develop when the supporting tissues of the anal cushions disintegrate or
deteriorate. Hemorrhoids are therefore the pathological term to describe the abnormal
downward displacement of the anal cushions causing venous dilatation. There are
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typically three major anal cushions, located in the right anterior, right posterior, and left
lateral aspect of the anal canal, and various numbers of minor cushions lying between
them. They are further categorized — and treated — according to their degree of
prolapse. Patients may experience painless bleeding with any grade:
• Grade I hemorrhoids bleed but do not prolapse;; on colonoscopy, they are

seen as small bulges into the lumen.
• Grade II hemorrhoids prolapse outside the anal canal but reduce

spontaneously.
• Grade III hemorrhoids protrude outside the anal canal and usually require
manual reduction.
• Grade IV hemorrhoids are irreducible and constantly prolapsed. Acutely

thrombosed hemorrhoids and those involving rectal mucosal prolapse are
also graded as IV.
Figure 4. Different degrees of hemorrhoids.

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III. Pathophysiology
A. Etiology
B. PREDISPOSING FACTOR
Familial tendency Abnormal hemorrhoids tend to be
hereditary. You're more likely to get them
if your parents had them.
Colon malignancy Hemorrhoids and cancer are very different
conditions that can cause some of the
same symptoms including rectal bleeding,
anal itching, and lump in anal opening.
Portal Hypertension Portal hypertension has often been
mentioned in conjunction with
hemorrhoids. However, hemorrhoidal
symptoms do not occur more frequently in
patients with portal hypertension than in
those without it, and massive bleeding
from hemorrhoids in these patients is
unusual. Bleeding is very often
complicated by coagulopathy.
Age over 50 Hemorrhoids are most common among
adults over age 50 yearsTrusted Source.
However, young people and children can
also get them.
Spinal cord Injury hemorrhoids are extremely common in
people with SCI, and the longer you have
been injured, the more likely you are to get
them. Clinicians I spoke with say that in
people with SCI, the main cause seems to
be chronic minor irritation or trauma that
happens during a bowel program

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C. PRECIPITATING FACTOR
Anal Intercourse Since hemorrhoids are natural parts of
your anatomy, the short answer is no, anal
sex should not cause new hemorrhoids to
pop up. However, the penetration could
theoretically irritate hemorrhoids you
already have, leading to symptoms like
bleeding and tenderness.
Pregnancy As unborn baby grows, your uterus gets
bigger and begins to press against your
pelvis. This growth puts a lot of pressure
on the veins near your anus and rectum,
and these veins may become swollen and
painful as a result.
The increase in the
hormone progesterone during pregnancy
can also contribute to the development of
hemorrhoids, as it relaxes the walls of your
veins, making them more prone to
swelling. An increase in blood volume,
which enlarges veins, can also contribute
to hemorrhoids during pregnancy.

Heavy lifting Lifting with hemorrhoids will only prolong
the healing process, and can make those
bothersome hemorrhoids worse.
However, other exercise such as walking,
stretching, or even a yoga class may even
relieve some of the symptoms.
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Obesity Haemorrhoids are highly common in
obese individuals as a result of having
excess weight body weight or pressure
that constricts the blood vessels
surrounding the anus and rectum. Excess
weight, especially around the abdominal
regions, create a higher risk for developing
haemorrhoids
Low fiber diet Hemorrhoids are rare in cultures with high-
fiber, unrefined diets. Low-fiber diet leads
to strain during BMs because of smaller,
harder stools. Straining increases
abdominal pressure, obstructing venous
return, increasing pelvic congestion, and
weakening veins.
Severe straining/constipation When you’re constipated, you’re more
likely to push hard to try to go. That can
make the veins around your rectum and
anus swell. These swollen veins are called
hemorrhoids, or piles. They’re like
varicose veins around your anus. They
can be external, which means they’re
under the skin around the anus, or
internal, which means they’re in the lining
of your anus or rectum.

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D. Symptomatology
Signs and symptoms of hemorrhoids usually depend on the type of hemorrhoid.
INTERNAL HEMMORHOIDS
Internal hemorrhoids often happen in clusters around the wall of the anal canal. They are
often painless. But they may prolapse (protrude out of the anus) due to straining or
pressure from hard stool. After the bowel movement is over, they may then reduce (go
back inside the body). Internal hemorrhoids often bleed. They can also discharge mucus.
The most common hemorrhoids symptom
is painless bleeding. A hemorrhoid
Painless bleeding sufferer may notice bright red blood on the
outside of the stools, on the toilet paper, or
dripping into the toilet.
The bleeding usually resolves itself
without treatment. Nevertheless, rectal
bleeding with a bowel movement is never
normal and should prompt a visit to a
health care professional.

Irritation and pain (prolapsed) internal hemorrhoid can become
prolapsed if it pushes down from the
rectum and bulges out from the anus.
There are several possible causes and
risk factors for this weakening of the
connective tissue. Straining during bowel
movements is one possible cause, as the
straining can put extra pressure on the
hemorrhoid.

EXTERNAL HEMMORHOIDS
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External hemorrhoids are located at the anal opening, just beneath the skin. These
tissues rarely cause problems unless they thrombose (form a blood clot). When this
happens, a hard, bluish lump may appear. A thrombosed hemorrhoid also causes
sudden, severe pain. In time, the clot may go away on its own. This sometimes leaves a
“skin tag” of tissue stretched by the clot.
Itching/Irritation External hemorrhoids cause painful
burning, and can also itch. But when
patients report severe itching, we usually
expect to see a prolapsing internal
hemorrhoid. When a hemorrhoid slips
through the anus, it brings with it mucus
that can irritate the sensitive skin around
the anus. This irritation can cause the kind
of activity-limiting itching many of our
patients describe.
When the hemorrhoid remains prolapsed,
the anal mucosa continues to produce
mucus and the irritation continues. In
addition, stool can mix with the mucus and
leak out of the anus. This coats the skin
around the anal opening, causing even
more irritation.

Pain and Discomfort External hemorrhoids can be painful. They
are usually most painful immediately
following a bowel movement or after
straining or lifting. They may be especially
painful if they develop a blood clot, which
is known as a thrombosed hemorrhoid.
Swelling around anal area During bowel movements, hemorrhoids
swell with blood and become slightly
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larger. This swelling helps protect and
cushion the anal canal as stool passes
from the body. Once the stool has passed,
the tissues stop swelling and go back to
normal. Abnormal swelling can cause by
many factors including constipation and
heavy lifting. Pressure due to straining or
other factors can cause hemorrhoid
tissues to stay swollen. When this
happens to the hemorrhoid tissues in the
anal canal, they’re called internal
hemorrhoids. Swollen tissues around the
anal opening are called external
hemorrhoids. Depending on the location,
your symptoms can differ.

Bleeding Bleeding hemorrhoids usually occur after
a bowel movement. A person may see
traces or streaks of blood on the tissue
after wiping. Sometimes, small amounts of
blood may be visible in the toilet bowl, or
in the stool itself. The blood from bleeding
hemorrhoids is usually bright red
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E. Schematic Diagram

PREDISPOSING PRECIPITATIING FACTORS

FACTORS - Anal Intercourse
- Familial Tendency - Pregnancy
- Colon Malignancy - Heavy Lifting
ETIOLOGY
- Portal Hypertension - Obesity
- Age over 50 - Low Fiber Diet
- Spinal Cord Injury - Severe straining /
constipation

Normal Hemorrhoids

Increased Abdominal S/Sx: Passing fewer than three
stools a week, Dry hard stool,
Pressure
Painful passing of stools

Dilation in anal vein

Supporting tissue Constipation
weakens

Abdominal Pressure

Further anal vein dilation continues to increase

HEMORRHOIDS
A
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A

External Hemorrhoids

Vascular cushions engorge B

Inflammation of vascular
wall and connective

tissue

S/Sx: Thrombosis,
Prothrombotic state
Swelling

Activation of somatic
S/Sx: Pain nerve receptors

A
Internal Hemorrhoids
Dilation of hemorrhoidal

B venous plexus C
Increase in compression
S/Sx: Painless rectal

Damage in epithelium
bleeding
248

249

B

Increase in mucus
secretion

Fecal soiling of
prolapsing hemorrhoids

S/Sx: Itching, Sebaceous gland
perianal irritation increases secretion

IF TREATED IF NOT TREATED

Presence of hemorrhoids Prolapsing of
will be eliminated hemorrhoids continues

Severe bleeding with

severe pain
Infection related to the

GOOD PROGNOSIS disease

BAD PROGNOSIS
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F. Narrative
Internal hemorrhoids cannot cause cutaneous pain, because they are above the dentate
line and are not innervated by cutaneous nerves. However, they can bleed, prolapse,
and, as a result of the deposition of an irritant onto the sensitive perianal skin, cause
perianal itching and irritation. Internal hemorrhoids can produce perianal pain by
prolapsing and causing spasm of the sphincter complex around the hemorrhoids. This
spasm results in discomfort while the prolapsed hemorrhoids are exposed. This muscle
discomfort is relieved with reduction.
Internal hemorrhoids can also cause acute pain when incarcerated and strangulated.
Again, the pain is related to the sphincter complex spasm. Strangulation with necrosis
may cause more deep discomfort. When these catastrophic events occur, the sphincter
spasm often causes concomitant external thrombosis. External thrombosis causes acute
cutaneous pain. This constellation of symptoms is referred to as acute hemorrhoidal crisis
and usually requires emergent treatment.
Internal hemorrhoids most commonly cause painless bleeding with bowel movements.
The covering epithelium is damaged by the hard bowel movement, and the underlying
veins bleed. With spasm of the sphincter complex elevating pressure, the internal
hemorrhoidal veins can spurt.
Internal hemorrhoids can deposit mucus onto the perianal tissue with prolapse. This
mucus with microscopic stool contents can cause a localized dermatitis, which is called
pruritus ani. Generally, hemorrhoids are merely the vehicle by which the offending
elements reach the perianal tissue. Hemorrhoids are not the primary offenders.
Each hemorrhoids are graded based on their appearance and progression. Grade 1
hemorrhoids are internal hemorrhoids which do not prolapse, or protrude out of the anus.
For Grade 1 hemorrhoids doctors will most likely recommend a hemorrhoid treatment
regimen of adding fiber to your diet and trying one of many new over-the-counter
hemorrhoid treatments. Preparation H is a very popular over-the-counter hemorrhoid
treatment in the United States. Proctofoam, Tucks hydrocortisone ointment, and
Analpram are all over-the-counter hydrocortisone creams for hemorrhoid treatment.
These hemorrhoid treatment creams decrease inflammation, swelling, and itching from
hemorrhoid irritation.
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Grade 2 - Hemorrhoid protrudes through the anus during straining or evacuation but
returns spontaneously.
Grade 2 hemorrhoids are internal hemorrhoids which prolapse, but then go back inside
the anus spontaneously without interference. For Grade 2 hemorrhoids, doctors will often
try conservative hemorrhoid treatment therapies, starting with treatment for Grade 1
hemorrhoids and moving to painless in-office hemorrhoid treatment procedures as
needed. Such painless hemorrhoid treatment therapies include rubber band ligation,
injection sclerotherapy, or infrared coagulation. It is very important to note that all of these
hemorrhoid treatments are performed on internal prolapsed hemorrhoids only, not
external hemorrhoids. These procedures can require multiple applications and these
hemorrhoid treatment options do not address the source of the problem hemorrhoid, so
they are not curative. While these treatments for Grade 2 hemorrhoids usually only last
six months to a year before they need to be repeated, results have shown that they can
be effective on many patients. The obvious advantages of these in-office hemorrhoid
treatment procedures are that they are done without anesthesia and cause minimal
discomfort.
Grade 3 hemorrhoids are internal hemorrhoids which prolapse, but do not go back inside
the anus until the patient pushes them back in. Grade 4 hemorrhoids are prolapsed
internal hemorrhoids which will not go back inside the anus. For treatment of Grade 3
hemorrhoids and Grade 4 hemorrhoids, doctors will often refer patients to surgeons for
more serious hemorrhoid treatment procedures. The most common surgical hemorrhoid
treatments are surgical hemorrhoid excision or a surgical hemorrhoid stapling procedure.
Grade 3 An excisional hemorrhoidectomy is the most common surgical hemorrhoid
treatment and generally has the best results. Unfortunately, the procedure is very painful
so the patient’s recovery is quite difficult. Most patients require a full two weeks to recover.
Due to the amount of pain after an excisional hemorrhoidectomy, a new hemorrhoid
treatment technique was created to be minimally invasive

External hemorrhoids cause symptoms in two ways. First, acute thrombosis of the
underlying external hemorrhoidal vein can occur. Acute thrombosis is usually related to a
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specific event, such as physical exertion, straining with constipation, a bout of diarrhea,
or a change in diet. These are acute, painful events.

Pain results from rapid distention of innervated skin by the clot and surrounding edema.
The pain lasts 7-14 days and resolves with resolution of the thrombosis. With this
resolution, the stretched anoderm persists as excess skin or skin tags. External
thromboses occasionally erode the overlying skin and cause bleeding. Recurrence occurs
approximately 40-50% of the time, at the same site (because the underlying damaged
vein remains there). Simply removing the blood clot and leaving the weakened vein in
place, rather than excising the offending vein with the clot, will predispose the patient to
recurrence.
External hemorrhoids can also cause hygiene difficulties, with the excess, redundant skin
left after an acute thrombosis (skin tags) being accountable for these problems. External
hemorrhoidal veins found under the perianal skin obviously cannot cause hygiene
problems;; however, excess skin in the perianal area can mechanically interfere with
cleansing.

Prognosis
The prognosis is generally excellent for persons with hemorrhoids, because many
symptomatic episodes of hemorrhoids resolve with conservative measures. If further
intervention is required, the prognosis remains very good, although recurrent symptoms
may occur. Early in the clinical course of hemorrhoidal disease, prolapse reduces
spontaneously. Later, the prolapse may require manual reduction and may cause mucus
discharge, which can cause pruritus ani. Pain usually is not a symptom of internal
hemorrhoids unless prolapse occurs. Pain may be associated with thrombosed external
hemorrhoids. Death from hemorrhoidal bleeding is rare.

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IV. Management (medical, surgical, nursing)

DIAGNOSTIC TEST

DIAGNOSTIC TEST RATIONALE NURSING RESPONSIBILITIES
Digital Rectal Exam A digital rectal exam (DRE) Before Procedure:
is a test that examines a 1. Ensure the physician’s order.
person's lower rectum, 2. Obtain informed consent
pelvis, and lower belly. This properly signed.
test can help your doctor 3. Introduce yourself including
check for cancer and other your role within the patient’s
health problems, including: care.
Prostate cancer in men. An 4. Explain the procedure to the
abnormal mass in the anus client the reason and nature
or rectum. of the technique of rectal
examination.
5. Reassure the patient that the
examination may be
uncomfortable, but it should
not be painful.
6. Collect and prepare the
equipment needed.
7. Put the patient in a hospital
gown.
8. A private area for the patient
to undress from the waist
down should be available
and a cover for the patient
provided.

During Procedure:
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1. Patient should be asked to lie
in the lateral position, close to
the edge of the bed with the
hips and knees flexed.
Expose only as much as
necessary.
2. A blanket should be draped
across the patient to
minimize exposure and
reduce the level of the
patient’s vulnerability.
3. Have a clean tray containing
K-Y jelly and tissues.
4. Assist the doctor by giving a
pair of disposable gloves and
K-Y jelly to lubricate the
gloved index finger.
5. Look for hemorrhoids,
rashes, fissures, and warts.
After Procedure:
1. Place the patient in a
comfortable position.
2. Document all the necessary
findings/information.
3. Do aftercare.
Anoscopy An anoscopy is a Before Procedure:
procedure that uses a small 1. Ensure the physician’s order.
tube called an anoscope to 2. Obtain informed consent
view the lining of your anus properly signed.
and rectum. A related
procedure called high
255

resolution anoscopy uses a 3. Introduce yourself including
special magnifying device your role within the patient’s
called a colposcope along care
with an anoscope to view 4. Explain the procedure to the
these areas client.
5. Put the patient in a hospital
gown and remove
underwear.
6. Empty the bladder and/or
have a bowel movement
before the test or administer
an enema in the morning.
7. The doctor will also inform
both of you if there are any
special instructions to follow.
During Procedure:
1. Put the patient in a left side-
lying position. Cover the
open part of the patient for
privacy.
2. Assist the physician in
applying a lubricant to the
anoscope.
After Procedure:
comfortable position and
provide privacy.
2. Monitor for complications.
findings during the
procedure.
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4. Do aftercare.
Rigid Proctosigmoidoscopy A proctoscopy (rigid Before Procedure:

sigmoidoscopy) is a 1. Ensure the physician’s order.
procedure to examine the 2. Obtain informed consent
insides of the rectum and properly signed.
the anus. A proctoscope is 3. Introduce yourself including
a hollow tube, usually with your role within the patient’s
a tiny light at the end, that care
can also be used to take 4. Explain the procedure to the
tissue samples for biopsies client.
as a cancer screening tool. 5. Put the patient in a hospital
The procedure also helps gown and remove
your gastroenterologist find underwear.
other causes of rectal and 6. Empty the bladder and/or
anal bleeding, such as have a bowel movement
hemorrhoids. before the test or administer
an enema in the morning.
7. The doctor will also inform
both of you if there are any
special instructions to follow.
During Procedure:
1. Put the patient in a left side-
lying position. Cover the
open part of the patient for
privacy.
2. Assist the physician in
applying a lubricant to the
anoscope.
After Procedure:
257

comfortable position and
provide privacy.
2. Monitor for complications.
findings during the
procedure.
4. Do aftercare.

MEDICATIONS
Generic Name:

Hydrocortisone Acetate
Brand Name: Cortizan
Classification: Antiinflammatory Corticosteroids;;

Steroids and steroid derivatives
Mode of Action: An adrenocortical steroid that inhibits accumulation of inflammatory cells
at inflammation sites, phagocytosis, lysosomal enzyme release and
synthesis, and release of mediators of inflammation
Route and Dosage: Adult: As hydrocortisone acetate supp: Insert 1 supp (25 mg) bid. Dosage
and treatment duration may vary according to the severity of the condition
and patient response.
Indication: Hydrocortisone rectal is used to treat itching or swelling caused by
hemorrhoids or other inflammatory conditions of the rectum or anus.
Hydrocortisone rectal is also used together with other medications to treat
258

ulcerative colitis, proctitis, and other inflammatory conditions of the lower
intestines and rectal area.
Contraindication: Systemic infections (unless treated with specific anti-infective), cerebral

malaria;; untreated oral infection (buccal tab). Parenteral: Idiopathic
thrombocytopenic purpura (IM);; infected joint or surrounding tissues;; inj
directly into the tendons, spinal or other non-diarthrodial joints (intra-
articular/local inj). Rectal: Systemic fungal infections, ileocolostomy during
the immediate or postoperative period (enema);; abscess, obstruction,
perforation, peritonitis, fresh intestinal anastomoses, extensive fistulas
and sinus tracts (foam). Ophthalmic: Herpes simplex or other viral
diseases of conjunctiva and cornea;; ocular tuberculosis, purulent
infections and fungal diseases of the eye, undiagnosed red eye, increased
intraocular pressure. Topical: Untreated fungal, bacterial, or viral
infections;; tubercular or syphilitic lesions, acne vulgaris, peri-oral
dermatitis, rosacea;; use in widespread plaque psoriasis (as
hydrocortisone butyrate). Concomitant use with live or live-attenuated
vaccines (immunosuppressive doses).
Side Effects: Stinging, burning, irritation, dryness, or redness at the application site may
occur. Acne, excessive hair growth, "hair bumps" (folliculitis), skin
thinning/discoloration, or stretch marks may also occur. If any of these
effects persist or worsen, notify your doctor or pharmacist promptly.
Adverse Effects: Adrenal suppression (e.g. hypercortisolism, suppression of hypothalamic-
pituitary-adrenal [HPA] axis), immunosuppression (prolonged use),
Kaposi sarcoma (prolonged use), acute myopathy, myocardial rupture,
osteoporosis, growth retardation (in infancy, childhood, and adolescence),
visual disturbances (e.g. blurred vision, increased intraocular pressure,
glaucoma, posterior subscapular cataract, central serous
chorioretinopathy, corneal perforation), scleroderma renal crisis,
psychiatric disturbances (e.g. insomnia, euphoria, mood swings,
personality changes, severe depression, psychotic manifestations),
259

seizures;; venous thromboembolism, epidural lipomatosis (high dose,
prolonged use);; dermal or subdermal skin depression at inj site. Topical:
Allergic contact dermatitis, local sensitisation (e.g. irritation, redness),
systemic effects (e.g. Cushing’s syndrome, glucosuria, hyperglycaemia).
Rarely, anaphylactoid reactions.
Drug Interaction: Increased risk of hypokalaemia with digoxin, K-depleting agents (e.g.
diuretics, amphotericin B, theophylline, carbenoxolone, salbutamol). May
cause severe weakness with anticholinesterase agents in myasthenia
gravis patients. Increased risk of gastrointestinal bleeding and ulceration
with aspirin, NSAIDs. May enhance the metabolism and reduce the
therapeutic effects with enzyme inducers (e.g. barbiturates, rifampicin,
rifabutin, carbamazepine, primidone, aminoglutethimide). May antagonise
the effects of oral hypoglycaemics, insulin, antihypertensive agents.
Plasma levels and risk of side effects may be increased by CYP3A4
inhibitors (e.g. erythromycin, ketoconazole, cimetidine) and cobicistat-
containing agents. May enhance the efficacy of coumarin anticoagulants.
Increased plasma concentrations with estrogens and other oral
contraceptives. Plasma levels of hydrocortisone acetate may be
increased by ritonavir. May cause convulsions with ciclosporin. Increased
risk of haematologic toxicity with methotrexate.
Nursing 1. You should not use hydrocortisone rectal if you are allergic to
Responsibilities hydrocortisone or palm oil.
2. Tell your doctor if you have a fever or any type of infection.
3. Tell your doctor if you are pregnant.
4. You should not breastfeed while using hydrocortisone rectal.
5. Do not give this medicine to a child without medical advice.

260

Generic Name:

Lidocaine
Brand Name: Lidocaine 4%
Classification: local anesthetics.
Mode of Action: The principal mechanism of action of lidocaine as a local anaesthetic is
through blockade of voltage-gated sodium channels (VGSCs) leading to
a reversible block of action potential propagation.
Route and Dosage: Hemorrhoids, Perianal pain and itching
Adult: Apply topically or using applicator insert rectally, up to 6 times daily.
Child: ≥12 yr. Apply topically or using applicator insert rectally, up to 6
times daily.
Indication: This combination medication is used to treat minor pain, itching, swelling,
and discomfort caused by hemorrhoids and other problems of the anal
area (such as anal fissures, itching
Contraindication: Hypovolemia, complete heart block, Adam-Stokes syndrome, Wolff-
Parkinson-White syndrome. Must not be applied to inflamed or injured
skin.
Side Effects: • Blistering, crusting, irritation, itching, or reddening of the skin
• cough
• cracked, dry, or scaly skin
• fast heartbeat
• fever
• hives or welts, itching, skin rash
261

• hoarseness
• irritation
• joint pain, stiffness, or swelling
• large, hive-like swelling on the face, eyelids, lips, tongue, throat,
hands, legs, feet, or genitals
• noisy breathing
• swelling of the eyelids, face, lips, hands, or feet
• tightness in the chest
• trouble breathing or swallowing
Adverse Effects: Arrhythmia, bradycardia, arterial spasms, CV collapse, oedema, flushing,
hert block, hypotension, sinus node suppression, agitation, anxiety, coma,
confusion, drowsiness, hallucinations, euphoria, headache,
hyperaesthesia, hypoaesthesia, lightheadedness, lethargy, nervousness,
psychosis, seizure, slurred speech, unconsciousness, somnolence,
nausea, vomiting, metallic taste, tinnitus, disorientation, dizziness,
paraesthesia, resp depression and convulsions. Patch: Bruising,
depigmentation, petechiae, irritation. Ophth: Conjunctival hyperaemia,
corneal epithelial changes, diplopia,visual changes.
Drug Interaction: May increase serum levels w/ cimetidine and propranolol. Increased risk
of cardiac depression w/ β-blockers and other antiarrhythmics. Additive
cardiac effects w/ IV phenytoin. Hypokalaemia caused by acetazolamide,
loop diuretics and thiazides may antagonise effect of lidocaine. Dose
requirements may be increased w/ long-term use of phenytoin and other
enzyme-inducers.
Nursing 1. Check BP and cardiac monitor prior to administration of lidocaine.
Responsibilities 2. For stable patients, doses should be given slow IV push at 25
mg/minute.
3. Monitor blood pressure and cardiac monitor during therapy with
lidocaine.
262

4. Assess neurological and respiratory status frequently for signs of
toxicity.
5. When treating a patient for ventricular dysrhythmias with lidocaine,
an IV infusion (drip) must be started soon after the bolus or serum
level will drop below therapeutic range and ventricular
dysrhythmias will return.
6. If patient appears upset or agitated, consider lidocaine toxicity. If
toxicity is evident, simply discontinue IV infusion–serum levels drop
in 10-20 minutes.

Generic Name:

phenylephrine
Brand Name: Preparation H
Classification: sympathomimetic amines.
Mode of Action: The mechanisms of sympathomimetic drugs can be direct-acting (direct
interaction between drug and receptor), such as α-adrenergic agonists, β-
adrenergic agonists, and dopaminergic agonists;; or indirect-acting
263

Route and Dosage: Rectal dosage (suppository)
Adults
1 suppository/dose rectally up to 4 times daily, usually in the morning,
evening, or after each bowel movement
Children and Adolescents 12 to 17 years
1 suppository/dose rectally up to 4 times daily, usually in the morning,
evening, or after each bowel movement.
Indication: This medication is used to temporarily relieve swelling, burning, pain, and
itching caused by hemorrhoids. It contains phenylephrine, which belongs
to a class of drugs known as sympathomimetic amines. It works by
temporarily narrowing the blood vessels in the area.
Contraindication: Severe hypertension, ventricular tachycardia, severe hyperthyroidism.
Ophthalmic (10% solution): Close-angle glaucoma. Children and elderly.
Cold preparations should not be used in children <2 years. Concomitant
or within 14 days of MAOI use (oral).
Side Effects: 1. allergic reactions like skin rash, itching or hives, swelling of the
face, lips, or tongue
2. bleeding from the rectum
3. breathing problems
4. chest pain
5. fast, irregular heartbeat
6. feeling faint or lightheaded, falls
Adverse Effects: Significant: Reflex bradycardia, extravasation (IV);; rebound miosis
(ophthalmic);;
Cardiac disorders: Arrhythmia, ischemia, extrasystoles, palpitation,
tachycardia.
Eye disorders: Eye pain, irritation, stinging or burning sensation, blurred
vision, photophobia, mydriasis, vitreous opacity (transient).
Gastrointestinal disorders: Nausea, vomiting.
Nervous system disorders: Headache, paresthesia, tremor, weakness.
264

Psychiatric disorders: Anxiety, agitation, insomnia, nervousness,
excitability.
Renal and urinary disorders: Urinary retention (in males).
Respiratory, thoracic and mediastinal disorders: Dyspnoea, pulmonary
oedma.
Skin and subcutaneous tissue disorders: Blanching of skin, pallor,
piloerection.
Vascular disorders: Hypertension, hypertensive crisis.
Drug Interaction: Some products that may interact with this drug are: MAO inhibitors
(isocarboxazid, linezolid, metaxalone, methylene blue, moclobemide,
phenelzine, procarbazine, rasagiline, safinamide, selegiline,
tranylcypromine), drugs to treat high blood pressure (including
guanethidine, beta blockers such as metoprolol).

Nursing 1. This medicine is for rectal use only. Do not take by mouth.
Responsibilities 2. Wash hands before and after use
3. Identify if the patient is allergic to the medicine
4. Instruct patient not to take any milk or milk containing products
5. Make sure to monitor the side effects at home
6. Instruct patient to drink at leat 1-2 liters of water

TREATMENTS
Warm Sitz Bath Your doctor might suggest one if you have
hemorrhoids, an anal fissure, or if you've just had
a baby. You can easily draw one in your own
bathtub. Soak up to three times a day for 10 to 15
minutes. Depending on your condition, a doctor
may suggest more.

If you’re making a sitz bath in your tub:
265

Fill the bathtub with about 2 to 3 inches of warm
water.
Sit in the tub, making sure your private area is
covered.
Afterward, gently pat the area dry using a soft
towel. You can also dry off by using a hair dryer on
a cool or low, warm setting.
High Fiber Diet Your doctor may recommend that you eat more
foods that are high in fiber. Eating foods that are
high in fiber can make stools softer and easier to
pass and can help treat and prevent hemorrhoids.
Drinking water and other liquids, such as fruit
juices and clear soups, can help the fiber in your
diet work better. Ask your doctor about how much
you should drink each day based on your health
and activity level and where you live. If your
hemorrhoids are caused by chronic constipation,
try not to eat too many foods with little or no fiber,
such as cheese, chips, fast food, ice cream, meat,
prepared foods, such as some frozen and snack
foods, processed foods, such as hot dogs and
some microwavable dinners.

SURGICAL MANAGEMENT
Rubber band ligation Rubber band ligation is a procedure that doctors
use to treat bleeding or prolapsing internal
hemorrhoids. A doctor places a special rubber
band around the base of the hemorrhoid. The
band cuts off the blood supply. The banded part of
the hemorrhoid shrivels and falls off, most often
266

within a week. Scar tissue forms in the remaining
part of the hemorrhoid, often shrinking the
hemorrhoid. Only a doctor should perform this
procedure—you should never try this treatment
yourself.
Sclerotherapy The doctor injects a solution into an internal
hemorrhoid, which causes scar tissue to form. The
scar tissue cuts off the blood supply, often
shrinking the hemorrhoid. The most commonly
used chemicals include zinc chloride, quinine, and
polidocanol.
Infrared photocoagulation A doctor uses a tool that directs infrared light at an
internal hemorrhoid. Heat created by the infrared
light causes scar tissue to form, which cuts off the
blood supply, often shrinking the hemorrhoid.
Hemorrhoidectomy A doctor, most often a surgeon, may perform a
hemorrhoidectomy to remove large external
hemorrhoids and prolapsing internal hemorrhoids
that do not respond to other treatments.
Stapled hemorrhoidopexy A doctor, most often a surgeon, may use a special
stapling tool to remove internal hemorrhoid tissue
and pull a prolapsing internal hemorrhoid back into
the anus. Your doctor will give you anesthesia for
this treatment.

267

NURSING MANAGEMENT

NURSING RATIONALE GOALS INTERVENTIONS
DIAGNOSIS
Acute pain related to Hemorrhoids are After 2 hours of 1. Assess the patient
hemorrhoidal pain swollen veins in your nursing interventions, for complaints of
and GI bleeding as lower rectum. Internal the patient will report headaches, sore
evidenced by hemorrhoids are pain is controlled or throat, general
verbalization of pain usually painless, but eliminated as malaise or body
scale of 8 over 10, tend to bleed. External evidenced by weakness, muscle
facial grimace, and hemorrhoids may decreased pain scale aches, and pain.
rectal bleeding. cause pain. of 8 over 10 to 4 over 2. Assess VS for
Hemorrhoids (HEM- 10. changes from
uh-roids), also called baselines
piles, are swollen 3. Administer
veins in your anus and analgesics as
lower rectum, similar ordered.
to varicose veins. 4. Provide restful, quiet
environment.
5. Provide warm baths
or heating pad to
aching muscles.
6. Provide cool
compress to head
prn.
7. Provide backrubs
prn.
8. Encourage gargling
with warm water;;
provide throat
268

lozenges as
necessary.
9. Instruct patient or
SO in deep
breathing, relaxation
techniques, guided
imagery, massage
and other
nonpharmacologic
aids.
10. Instruct patient or
SO regarding use of
acetaminophen and
to avoid the use of
aspirin.

Impaired Tissue Visible damage to After 8 hours of 1. Assess patient for
Integrity related to tissues is common in- nursing interventions, the presence of
Hemorrhoidal patient post-surgery. A the patient will have hemorrhoids,
surgery and break in tissue intact skin with no discomfort or pain
procedures integrity is usually signs or symptoms of associated with
repaired by the body rectal prolapse such hemorrhoids, diet,
very well. However, as pain and discomfort fluid intake, and
there are felt deep within the presence of
circumstances that it lower abdomen, constipation.
doesn’t repair it at all difficulties passing a 2. Administer topical
and replaces the bowel motion and medication as
damaged tissue with protrusion of the ordered.
connective tissue. rectum through the 3. Provide “donut
When tissue integrity anus. cushion” for the
is left untreated, it
269

could cause local or patient to sit on if
systemic infection and needed.
ultimately lead to 4. Administer stool
necrosis softeners as
ordered.
5. Assist with
procedures for the
treatment of
hemorrhoids.
6. Instruct patient
and/or family
regarding causes of
hemorrhoids,
methods of avoiding
hemorrhoids, and
treatments that can
be performed.
7. Instruct patient
and/or family
regarding all
procedures required.
8. Instruct patient
and/or family in
dietary
management.
9. Instruct patient
and/or family
regarding the use of
bulk producing
agents, such as
psyllium husk.
270

10. Instruct patient
and/or family in
comfort measures to
use with the
presence of
hemorrhoids.

Constipation related When you're After 8 hours of 1. Determine the

to low residue diet constipated, you may nursing interventions, patient’s bowel
and hemorrhoidal find yourself straining the patient will have a habits, lifestyle,
medications. to pass stool. Straining normal elimination ability to sense an
during bowel pattern re-established urge to defecate,
movements can cause and maintained as painful hemorrhoids,
the veins in your anus evidenced by 2-3 and history of
and lower rectum to bowel elimination per constipation.
swell. These swollen day. 2. Assess patient’s
veins are known as stool frequency,
hemorrhoids or piles. characteristics,
On the other hhand, presence of
Pain medications, flatulence,
called “opioids” (such abdominal
as morphine, discomfort or
hydromorphone, distension, and
oxycodone and straining at stool.
Tylenol #3,) may 3. Auscultate bowel
cause constipation. sounds of presence
Opioids slow down the and quality.
movement of stool 4. Monitor diet and fluid
through your bowel intake.
271

(intestines). This gives 5. Monitor for
your bowel more time complaints of
to take the water out of abdominal pain and
your stool, making it abdominal
hard, dry and difficult distention.
to pass. 6. Monitor patient’s
mental status,
syncope, chest pain,
or any transient
ischemic attacks.
Notify the physician
if these symptoms
occur.
7. Assess for rectal
bleeding.
8. Provide bulk, stool
softeners, laxatives,
suppositories, or
enemas as
warranted.
9. Provide a high-fiber
diet, whole grain
cereals, bread, and
fresh fruits.
10. Monitor medications
that may predispose
patient to
constipation.
11. Instruct patient in
activity or exercise
programs within
272

limits of the disease
process.

V. Review of Related Literature

Title: Prevalence and associated factors of hemorrhoids among adult patients visiting the
surgical outpatient department in the University of Gondar Comprehensive Specialized
Hospital, Northwest Ethiopia
Bibliography: Kibret, A. A., Oumer, M., &; Moges, A. M. (2021). Prevalence and
associated factors of hemorrhoids among adult patients visiting the surgical outpatient
department in the University of Gondar Comprehensive Specialized Hospital,
Northwest Ethiopia. PLOS ONE. Retrieved March 3, 2022, from
https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0249736
Summary:
The study was conducted to determine the prevalence of hemorrhoids in adult
patients visiting surgical OPD at the UOG Comprehensive Hospital, Ethiopia, and to
define associated risk factors. Constipation and being overweight were found to be
significantly associated with hemorrhoids.
In this study, the prevalence of hemorrhoids was found to be 13.1%. The result is
consistent with a study conducted in Israel 16% and Korea 14.4%. However, it is lower
than the study from Australia and Egypt which reported the prevalence to be 38.9% and
18% respectively. In Australia, participants were from colorectal cancer screening and the
investigation was conducted in a multi-centered area. In a way, hemorrhoids and
273

colorectal cancer have similar symptoms which may increase the prevalence in Austria
study. Similarly, a study conducted in Egypt included those patients who came for
colonoscopic examinations and patients with an anorectal disease which may contribute
to the rise of the prevalence of hemorrhoid. However, in their study, they considered
merely patients who visited surgical OPD.
In their study, study subjects with constipation were more likely to have
hemorrhoids as compared to their counterparts. Similarly, studies conducted elsewhere
supported the notion of the significant contribution of constipation to the induction of
hemorrhoids. This could be due to degeneration of the supportive tissue in the anal canal
and tear of elastic supportive tissue due to prolonged straining during defecation and hard
stool. Subsequently, causing a distal displacement of anal cushions and the development
of hemorrhoids. Passage of hard stool and increased intra-abdominal pressure could also
obstruct venous return, resulting in engorgement of the hemorrhoidal plexus and
arteriovenous anastomoses of the anorectal junction this leads to the development of
hemorrhoid.
The current study found that being overweight increased the odds of having
hemorrhoids. The notion of their study is supported by other studies done elsewhere. This
could be attributed to an increase in the intra-abdominal pressure due to the high body
weight and visceral fats which are thought to give rise to the venous congestion of the
distal rectum. Obesity will induce the release of inflammatory cytokines and acute-phase
proteins which will eventually activate the innate immune system and affect metabolic
homeostasis, which contributes to the formation of hemorrhoids.
This study helps us to know the burden and possible risk factors of the disease
and may allow us to easily identify individuals at risk of hemorrhoids and to provide early
diagnosis, prevention measures, and appropriate interventions. However, there are some
limitations of this study such as it could not establish a cause-effect relationship because
of the cross-sectional nature of the study design. In addition, this study was institution-
based, and the findings may not fully reflect the entire population, and possible that recall
bias may have been introduced. The study did not assess the frequency of fiber diet intake
based on the recommendations of WHO.
274

In conclusion, a hemorrhoid is found to be the common health problem among
surgical patients and its prevalence was higher in male subjects. Constipation and being
overweight were found to increase the odds of having hemorrhoids. Screening for early
identification and intervention of hemorrhoids, especially for risk groups is better to be
practiced by health professionals. We should recommend every individual to maintain
their normal body weight and avoid any risk that can cause constipation. Further, a
community-based study should be conducted on the burden of hemorrhoids in Ethiopia.

Title: The prevalence, characteristics, and treatment of hemorrhoidal disease: results of
an international web-based survey
Bibliography: Sheikh, P., Régni, C., Goron, F., &; Salmat, G. (2020). The
prevalence, characteristics, and treatment of hemorrhoidal disease: Results of an
international web-based survey. Journal of comparative effectiveness research.
Retrieved March 3, 2022, from https://pubmed.ncbi.nlm.nih.gov/33079605/
Summary:
In this online survey study, the prevalence of hemorrhoidal disease in adults was
11%, but most respondents had low severity episodic disease. Only about 40% of
respondents with hemorrhoidal disease sought help from a medical practitioner as the
first step in the treatment pathway, highlighting a pattern of underdiagnosis and
undertreatment, as well as the need for respondents to be able to access reliable and
accurate health information from other sources. Their findings highlight the need for
greater education of individuals with hemorrhoidal disease to seek medical advice for
early diagnosis and treatment, as well as education for family practitioners to thoroughly
investigate hemorrhoidal symptoms.
Patient education should include reducing the taboo around rectal conditions, so
that reluctance and embarrassment do not delay medical assessment. Any rectal
bleeding, which patients are likely to attribute to hemorrhoidal disease, needs to be
promptly investigated to exclude other more serious conditions, such as inflammatory
bowel disease or cancer. Therefore, prompt assessment of the first signs of hemorrhoidal
disease will not only provide early symptom relief for patients but may also assist in early
colorectal cancer detection. General practitioners should also receive education on
275

guideline-recommended treatments so that patients receive the most effective protocol
available rather than relying on empirical treatment with poorly effective therapies.
The strengths of this research study include the fact that it was conducted in a
large and representative sample of the general population and that it examined multiple
demographic and clinical characteristics relevant to hemorrhoidal disease across a range
of countries. They also used random sampling to limit the potential for responder/non-
responder bias. However, the researchers did not confirm the hemorrhoid diagnosis
against responders’ medical records, so there is a potential for overestimation of the
prevalence because patients are prone to attribute any anal symptoms to hemorrhoidal
disease. However, they consider this to be unlikely since the survey provided detailed
definitions of hemorrhoid severity, in terms of both specific symptoms and signs, including
the presence and reducibility of prolapse.
In addition, the fact that the prevalence of hemorrhoidal disease in their study, both
in the overall population and in each individual country, lies completely within the range
reported in the published literature suggests that overestimation, if present, was not
marked. However, another limitation is that, because they did not have access to the
patients’ medical records, they cannot determine whether the high incidence of pain was
related to coexisting painful conditions, such as anal fissure.

Title: Dietary Intake and Physical Activity in Patients After Invasive Treatment of
Hemorrhoidal Disease
Bibliography: Burmeister, G., Lieb, W., Franke, A., Schafmaye, C., Hinz, S., Hendricks,
A., Németh, C. G., Schniewind, B., Doniec, J. M., Bokelmann, F., Jongen, J., Peleikes,
H.-G., Kahlke, V., &; Ratjen, I. (2020, August 5). Dietary intake and physical activity
in patients after invasive treatment of hemorrhoidal disease. Home. Retrieved March 4,
2022, from https://www.researchsquare.com/article/rs-50755/v1
Summary:
In a Northern German cohort of patients with a history of the invasive treatment of
hemorrhoidal disease, the researchers observed the following main results. First,
whereas in males there were no statistically significant differences in food intake between
hemorrhoid patients and age- and sex-matched controls, female hemorrhoid patients had
276

a higher intake of potatoes, nuts, and animal fat than female controls. Additionally,
patients with a history of hemorrhoidal disease reported significantly more gardening
activities and less time watching TV when compared to matched controls. Second, within
the hemorrhoid patient cohort, individuals with higher hemorrhoid grades had greater
odds of higher fiber and lower alcohol intake than patients with grade I hemorrhoids.
In contrast, patients who have had surgery instead of rubber band ligation or
sclerotherapy were more likely to have a greater alcohol intake and more sleeping hours
at night. Patients that required another treatment after first hemorrhoid surgery revealed
higher odds of more sleeping hours a day, but also a higher amount of home repair
activities when compared to those without further therapy. The odds of an animal fat
intake above the cohort-specific median were significantly higher in patients who would
not be willing to undergo another surgery, if necessary, compared to those who would be
willing. Furthermore, patients with current afflictions at the anus had a higher probability
of eating more potatoes and of doing more home repair activities than the patient group
without anal afflictions.
277

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Assigned Topics:
PUD- John Daniel L. Arguelles & Jamie Stefanie G. Chiu
GERD- Joennielle Clark I. Colegado & Sachi Megan I. Cang
Gastroenteritis- Nicole Anne M. Alcober & Tristan Jay H. Amoroso
Crohn’s Disease- Kristine Joy V. Billiones & Justin Joshua C. Espinas
Ulcerative Colitis- Laetexia Ysabelle G. Dujon & Maria Ana Cecilia B. Arendain
Hemorrhoids- Viannah Eve A. Escobido & James Nathaniel G.Abedejos

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GASTROINTESTINAL

An esophageal ulcer is a breach in the mucosal border of the esophagus.

PREDISPOSING FACTORS RATIONALE

Blood Type (O) Helicobacter pylori, the most common

Family History Usually a significant number of people who

Genetic Factor Peptic ulcer disease is inherited as a

PRECIPITATING FACTORS RATIONALE

NSAIDs NSAIDs work by inhibiting enzymes

Excessive Alcohol Intake More gastric acid is produced when you

Smoking Cigarette smoking hastens gastric

Zollinger Edison Syndrome (ZES) Zollinger-­Ellison syndrome is an

Cirrhosis Peptic ulcers are more common in

Chronic Kidney Disease (CKD) Hemodialysis patients face a risk that is

SIGNS AND SYMPTOMS RATIONALE

Anemia Internal bleeding can occur if peptic ulcers

Fatigue As a result of the increased absence of

Syncope Syncope can occur when your blood

Melena Peptic ulcer disease, in which painful

Hematesis Hematemesis is the vomiting of blood,

Abdominal Distention Infection with H. pylori causes a lot of

Loss of Appetite Individuals with peptic ulcers may develop

Unexplained Weight Loss Weight loss is inevitable if patients with

Feeling of Fullness When the lining of your stomach is

Diagnostic Rationale Nursing responsibilities

To assess for pain, epigastric

A gastrointestinal endoscopy -­ Explain the procedure to

Serology tests employ enzyme -­ Define and explain the

A barium swallow is used to help -­ Explain the procedure

Action Mode of action Side effect/ Nursing intervention

Generic name cimetidine

Brand name Tagamet HB

Action classification H2 inhibitor

Mode of action Competitively inhibits histamine action at

Dose and route Active duodenal ulcer (short-­term

Indication -­ Active duodenal ulcer

contraindication -­ Hypersensitivity to drug

Side effects -­ pain when swallowing;;

Adverse effects -­ CNS: confusion, dizziness,

Nursing responsibilities -­ Monitor creatinine levels in

Generic name omeprazole

Brand name Prilosec

Action classification Proton pump inhibitor

Mode of action Reduces gastric acid secretion and

Dose and route Short-­term treatment of active duodenal

Indication -­ Short-­term treatment of active

contraindication hypersensitivity to drug or its component

Adverse effects -­ CNS: dizziness, headache,

Drug interactions Drug-­drug. Ampicillin, cyanocobalamin,

Nursing responsibilities -­ Assess vital signs.

Generic name lansoprazole

Brand name prevacid

Action classification Gastric acid pump inhibitor

Dose and route Active duodenal ulcer

Indication -­ Active duodenal ulcer

contraindication Hypersensitivity to drug or its components

Side effects -­ headaches.

Adverse effects -­ CNS: headache, confusion,

Drug interactions Drug-­drug.

Nursing responsibilities -­ Monitor for GI adverse reactions.

Generic name amoxicillin

Brand name Amoxil

Dose and route -­ PO (adults): 250-­500 mg q8 or 875

Indication To treat h.pylori in the digestive tract

contraindication history of severe hypersensitivity

Zollinger Edison Syndrome (ZES) Zollinger-Ellison syndrome is an

A gastrointestinal endoscopy - Explain the procedure to

Serology tests employ enzyme - Define and explain the

A barium swallow is used to help - Explain the procedure

Dose and route Active duodenal ulcer (short-term

Indication - Active duodenal ulcer

contraindication - Hypersensitivity to drug

Side effects - pain when swallowing;;

Adverse effects - CNS: confusion, dizziness,

Nursing responsibilities - Monitor creatinine levels in

Dose and route Short-term treatment of active duodenal

Indication - Short-term treatment of active

Adverse effects - CNS: dizziness, headache,

Drug interactions Drug-drug. Ampicillin, cyanocobalamin,

Nursing responsibilities - Assess vital signs.

Indication - Active duodenal ulcer

Side effects - headaches.

Adverse effects - CNS: headache, confusion,

Drug interactions Drug-drug.

Nursing responsibilities - Monitor for GI adverse reactions.

Dose and route - PO (adults): 250-500 mg q8 or 875

Adverse effects - CNS: agitation, anxiety, behavioral

Drug interactions - Allopurinol: increased risk of rash

- Avoid high fiber food

- Provide information on the side

- Tell client to refrigerate client to

contraindication - Prostaglandin hypersensitivity

Side effects - diarrhea;;

Drug interactions - DRUG: Antacids may increase

Nursing responsibilities - Instruct patient to take with food.

Drug Class Antiemetics / GIT Regulators, Antiflatulents & Anti-Inflammatories

Mode of Action Domperidone is a peripheral dopamine-receptor blocker. It

Period of flare-ups

Drug Classification: Anti-inflammatory