Download Preview the material

Etiology And Clinical
Manifestations Of
Inflammatory Bowel Disease
JASSIN M. JOURIA, MD
DR. JASSIN M. JOURIA IS A MEDICAL DOCTOR,
PROFESSOR OF ACADEMIC MEDICINE, AND MEDICAL
AUTHOR. HE GRADUATED FROM ROSS UNIVERSITY
SCHOOL OF MEDICINE AND HAS COMPLETED HIS
CLINICAL CLERKSHIP TRAINING IN VARIOUS TEACHING
HOSPITALS THROUGHOUT NEW YORK, INCLUDING
KING’S COUNTY HOSPITAL CENTER AND BROOKDALE
MEDICAL CENTER, AMONG OTHERS. DR. JOURIA HAS PASSED ALL USMLE MEDICAL BOARD EXAMS,
AND HAS SERVED AS A TEST PREP TUTOR AND INSTRUCTOR FOR KAPLAN. HE HAS DEVELOPED
SEVERAL MEDICAL COURSES AND CURRICULA FOR A VARIETY OF EDUCATIONAL INSTITUTIONS. DR.
JOURIA HAS ALSO SERVED ON MULTIPLE LEVELS IN THE ACADEMIC FIELD INCLUDING FACULTY
MEMBER AND DEPARTMENT CHAIR. DR. JOURIA CONTINUES TO SERVES AS A SUBJECT MATTER
EXPERT FOR SEVERAL CONTINUING EDUCATION ORGANIZATIONS COVERING MULTIPLE BASIC
MEDICAL SCIENCES. HE HAS ALSO DEVELOPED SEVERAL CONTINUING MEDICAL EDUCATION
COURSES COVERING VARIOUS TOPICS IN CLINICAL MEDICINE. RECENTLY, DR. JOURIA HAS BEEN
CONTRACTED BY THE UNIVERSITY OF MIAMI/JACKSON MEMORIAL HOSPITAL’S DEPARTMENT OF
SURGERY TO DEVELOP AN E-MODULE TRAINING SERIES FOR TRAUMA PATIENT MANAGEMENT. DR.
JOURIA IS CURRENTLY AUTHORING AN ACADEMIC TEXTBOOK ON HUMAN ANATOMY & PHYSIOLOGY.
Abstract
Although no singular known cause for inflammatory bowel disease exists,
medical research has led to new treatments and a reduction in mortality
rates associated with the disease. Inflammatory bowel disease includes a
variety of gastrointestinal disorders that cause similar symptoms and impact
a patient's quality of life. There is no cure, but symptomatic relief can be
found with a variety of treatments, including medical, surgical, and
nutritional. As with many diseases, a multifaceted approach is commonly the
best for successful treatment of inflammatory bowel disease.
1
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Policy Statement
This activity has been planned and implemented in accordance with the
policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's Commission on
Accreditation for registered nurses. It is the policy of NurseCe4Less.com to
ensure objectivity, transparency, and best practice in clinical education for
all continuing nursing education (CNE) activities.
Continuing Education Credit Designation
This educational activity is credited for 4 hours. Nurses may only claim credit
commensurate with the credit awarded for completion of this course activity.
Statement of Learning Need
Health clinicians need to be able to differentiate between Ulcerative Colitis
and Crohn's Disease, as well as be able to describe the clinical
manifestations and potential effects of each on the gastrointestinal tract.
Understanding the common causes and symptoms of inflammatory bowel
disease, including the role that genetics may play and complications of the
disease is essential for a clear understanding of the four types of medical
and surgical techniques commonly used during treatment. Clinicians
supporting nutritional therapies and other health or group support resources
for patients and family members can be used during the treatment of
inflammatory bowel disease.
2
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Course Purpose
To provide health clinicians with knowledge of the potential causes of
inflammatory bowel disease to improve the chances that this illness can be
successfully treated or prevented.
Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses and
Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,
Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Please take time to complete a self-assessment of knowledge, on page 4,
sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge learned will be
provided at the end of the course.
3
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
1.
The exact reason why some people develop intestinal
inflammation and tissue damage associated with inflammatory
bowel disease (IBD) is
a.
b.
c.
d.
2.
increased levels of microorganisms in the gut.
genetic; i.e., a patient will get IBD if an ancestor had it.
not exactly known.
always due to poor diet.
True or False: Dysbiosis is an imbalance in the number of
beneficial and aggressive bacteria normally found in the
intestinal tract.
a. True
b. False
3.
The gastrointestinal tract contains trillions of bacteria that are
said to
a.
b.
c.
d.
4.
Two of the most common forms include those from the
________________________________ phyla.
a.
b.
c.
d.
5.
interfere with metabolites.
be beneficial to sustaining normal intestinal functioning.
generally encourage harmful bacteria.
interfere with equilibrium in the gut.
Firmicutes and the Bacteroidetes
Eubacterium and Lactobacillus
Escherichia coli and Mycobacterium avium
Enterobacteriaceae and Listeria monocytogenes
Normally, the amounts of gut microbiota vary until age ___, and
microorganism levels remain stable until approximately age 70.
a.
b.
c.
d.
3
12
21
30
4
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Introduction
Despite some of the differences in clinical manifestations and histology
between the different forms of inflammatory bowel disease (IBD), there has
yet to be confirmation of the exact reason why some people develop the
intestinal inflammation and tissue damage associated with this illness. There
are various theories on the potential causes of IBD. Although many patients
have symptoms that are similar, not everyone demonstrates the same
disease manifestations and the patterns of remission and disease
exacerbations differ among patients. Research investigations have focused
on several contributing factors of gut inflammation with promising outcomes
identifying the reason why some people develop IBD. However, despite
thorough research and extensive results in this area, questions still remain.
Possible causes include changes in the levels of microorganisms (both
aggressive and beneficial) in the gut, genetic factors, predisposition to the
disease, and the significance of family history; additionally, important
considerations include the role of diet, comparison between the diet of
Western industrialized countries and those of developing countries, and the
pathophysiological effects of a break in the protective mucosal barrier of the
intestinal tract. Understanding the potential causes of inflammatory bowel
disease improves the chances that this illness can be successfully treated or
may someday be prevented from developing at all.
Microbiota And The Development Of IBD
Several studies have shown that intestinal microbiota play a role in the
development of inflammatory bowel disease, including its continued
presence in the gastrointestinal tract and the type of symptoms produced.
Altered levels of intestinal microbiota, because of their important functions,
have been associated with a number of chronic diseases affecting the
gastrointestinal tract in addition to IBD, including irritable bowel syndrome,
5
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
dyspepsia, and nonalcoholic
steatohepatitis, as well as some
chronic illnesses that are considered
to be systemic diseases, including
diabetes and obesity.1,2
Normally, the gastrointestinal tract
contains trillions of bacteria that are
said to be beneficial to sustaining
normal intestinal functioning. Among
some of the routine functions of these
microorganisms are production of
certain metabolites, metabolism of
some dietary carbohydrates, drug
metabolism, immune regulation
through prevention of harmful bacteria, and homeostasis through
preservation of the intestinal mucosal lining.1,2 There are various species of
bacteria existing in the intestinal tract; however, two of the most common
forms include those from the Firmicutes and the Bacteroidetes phyla.3 These
microorganisms are referred to as gut microbiota and the majority of
organisms found in the intestinal tract at any one time are not considered
harmful to the host, rather, they live within the host and are responsible for
a number of protective mechanisms. The numbers of microbiota present can
fluctuate somewhat throughout the lifespan. With intestinal disease, the
numbers of gut microbiota may increase, although changes have also been
related to various other factors, including advancing age, diet, and ethnicity.
The large intestine contains approximately 70 percent of all microbiota in the
human body.2 Typically, when discussing microbiota, particularly that which
6
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
impacts inflammation and ulcerations associated with IBD, it is related to the
microorganisms found in the colon. There are various other factors that can
affect the amounts of gut microbiota, some of which are non-modifiable
factors. Age is related to the number of microbes found in the gut; the
intestinal tracts of newborn infants are colonized at birth, while children and
adolescents may have varying proportions of microorganisms, followed by
stability of microorganism levels by the age of 30 and remaining so until
approximately age 70.2 As people age, the fluctuations in numbers of
bacteria increase, demonstrating alterations in proportions of Firmicutes and
Bacterioidetes in older adulthood. When changes in the balance of some of
these microorganisms are significant, the affected adult is at greater risk of
frailty and illness.4
A condition known as intestinal dysbiosis occurs when there is an imbalance
of beneficial and harmful bacteria or organisms. Other elements that can
impact levels of gut microbiota include diet, use of antibiotics, ethnicity, and
even socioeconomic status.
Gut microbiota consist of various forms of bacteria, but also of many other
types of microorganisms as well, including certain viruses, fungi, and
protozoa. Although there is a large variety in the actual number of species
present in the gut at any one time, there are actually only a few divisions
that make up the majority of bacteria. Among these, the exact numbers
vary between people, with each individual having more of some and less of
others when compared to another person. Consequently, the types and
amounts of microbiota that are considered normal can actually differ
between persons.1-3 The healthcare community now recognizes that gut
microbiota plays a significant role in health of the host (the person whose
body the microorganisms inhabit). Alternatively, there are many diseases
7
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
that are thought as being related to alterations in the levels of normal gut
microbiota.
In cases of inflammatory bowel disease, there is evidence that alterations in
levels of gut microbiota play a role in the development of inflammation that
occurs with the disease; however, the specific bacteria that are responsible
for triggering inflammatory processes have not yet been isolated. Certain
types of bacteria in the intestinal tract have been linked to the development
of IBD and its associated inflammation, including strains of Escherichia coli
and Mycobacterium avium species. Some other types of bacteria that have
been linked specifically with Crohn’s disease include Yersinia
enterocolitica and Listeria monocytogenes.3
According to Sartor, et al., in the American Journal of Gastroenterology36,
there are four mechanisms that describe the relationship between IBD and
gut microbiota: dysbiosis, which is an imbalance in the number of beneficial
and aggressive bacteria normally found in the intestinal tract; the
development of inflammation in the gut in combination with aberrations in
the normal microbial flora; genetic defects of the host that involve an
inability to retain normal amounts of gut microbiota, and faulty immune
regulation. As mentioned, with the development of inflammation as part of
the immune response, the T cells release cytokines and regulate some of the
immune response. With any of the described mechanisms associated with
IBD and gut microbiota, when aggressive microorganisms multiply within the
gastrointestinal tract, the T cells will be exposed to more antigens because
of the numbers present. Additionally, the affected person’s immunity may be
below average in that he/she is unable to respond appropriately to foreign
antigens and then further develops inflammation.1-3
8
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Although there are some bacteria in the intestinal tract that are considered
beneficial and some that are antagonistic to a person’s health, there is no
specific bacterial species that has been found to have all of the same effects
in every person. Instead, an imbalance in the numbers of some types of
bacteria alters their impact on health and an increase in some other kinds
may be detrimental to overall health, all of which may vary between
people.1,2 As previously mentioned, this imbalance is known as intestinal
dysbiosis.
Because of this imbalance, it can be difficult to pinpoint the direct role that
gut microbiota have on the development of Crohn’s disease and ulcerative
colitis. However, as stated, there are some bacteria that are known to be
harmful when found in the intestinal tract and elevated numbers of some of
these organisms have been seen in people with IBD. These bacteria may be
related to the actual cause of IBD or their numbers may have grown as a
result of inflammation from the disease.
Certain bacteria are considered harmful in the intestinal tract and can
contribute to intestinal inflammation in different methods. For example, C.
difficile, when present in the gastrointestinal tract, secretes small amounts
of toxins A and B, which can destroy intestinal cells. Toxin B, in particular,
changes the shape of epithelial cells on the intestinal surface and causes the
breakdown of actin (protein) molecules; the cells then can separate from the
wall and ulcers can form.5,6 E. coli contribute to inflammation by adhering to
epithelial cells in the mucosa and secreting tumor necrosis factor.
Some other studies have also linked specific bacteria associated with
development of inflammatory bowel disease. Mycobacterium is one type of
microorganism that has been associated with IBD development. It is
9
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
normally related to the growth of diseases such as tuberculosis and leprosy;
however, it may also be associated with infection in adults with Crohn’s
disease. Ongoing research is considering the effects of mycobacterium
avium infection, which is similar to an intestinal infection that can develop in
cattle, as a type of infection that could lead to Crohn’s symptoms if a person
with genetic susceptibility consumes meat or dairy products from animals
that contain this microorganism.1-3
Klebsiella, an anaerobic form of bacteria that has often been associated with
respiratory infections as well as post-surgical sepsis in some patients, may
also be related to development of some cases of IBD, particularly Crohn’s
disease. Rashid, et al., in the International Journal of Rheumatology discuss
the potential role of Klebsiella in the pathological damage of Crohn’s disease
in the gastrointestinal tract, as well as its potential for causing inflammatory
extra-intestinal symptoms of Crohn’s disease, including muscle and joint
inflammation.82
There are many other studies that have focused on specific organisms as the
cause of IBD inflammation and the research is still ongoing. Other types of
bacteria that are being explored as having direct correlations with IBD
development include the Proteus species, as well as previously noted
virulent E. coli strains, and uncontrolled C. difficile infection.
Because alterations in gut microbiota may be associated with inflammation
of IBD and low levels of normal gut flora may prevent the body from
protecting itself from certain antigens or foreign substances, using treatment
that may further upset the balance of gut microbiota may cause additional
complications. For example, certain immunomodulators such as TNF-
blockers may increase the risk of developing systemic infections with
10
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
opportunistic pathogens, which obviously perpetuates the problem of
inflammation, rather than promoting healing of the gut. Therefore, it is
important to keep the normal balance of microorganisms of the gut in mind
when providing treatment for IBD, knowing that an imbalance may hinder
relief from symptoms.7-9
In addition to the presence of increased levels of certain bacteria that
contribute to inflammation with IBD, people with inflammatory bowel
disease have also been shown to have reduced levels of certain types of
microbiota in the intestinal tract, especially those that are considered
beneficial bacteria, including Eubacterium and Lactobacillus.3 These bacteria
play an important role in transforming dietary fiber into short-chain fatty
acids. They also act as protective microorganisms against some other
aggressive microorganisms that would normally contribute to disease.
Consequently, a decrease in their numbers may more likely lead to
inflammation.
According to a clinical report in the Journal of Pediatric Gastroenterology and
Nutrition, alterations in gut microbiota can also play a role in the
development of infectious complications that often occur with IBD. Other
studies also confirm the role of intestinal flora with IBD disease progression
that may include intestinal abscesses and fistulas.9,10 Abscesses, as
described, are pockets of infection that can occur anywhere along the
gastrointestinal tract as a result of IBD. When there is an imbalance between
aggressive microbiota and beneficial bacteria in the intestinal tract, an area
of infection can develop if the immune system is unable to control the
multiplication of infectious organisms and an abscess can form. Similarly,
fistulae form because severe inflammation causes tissue breakdown and
necrosis, leading to a channel between two tissue areas or two organs. An
11
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
imbalance of microorganisms in the intestinal tract may be unable to prevent
such tissue breakdown and the tunneling that occurs as a result.9,10
Probiotics may play a role in preventing
development of inflammatory bowel
disease as well. Probiotics are foods
that are designed to populate the
intestinal tract with beneficial bacteria
when they are consumed. If
inflammatory bowel disease is related
to abnormalities in gut microbiota, then
consumption of probiotics could
possibly improve the balance of friendly
versus aggressive bacteria by causing a
shift toward healthy and beneficial
microorganisms in the gut.
An imbalance in T-helper (Th) cells of Th2 levels greater than Th1 levels can
lead to an autoimmune disease and an inflammatory bowel disease.
Research studies continue to investigate modulation of the gut immune
responses, such as probiotic use to prevent inflammatory gut symptoms.
The triggers associated with IBD flares may also be related to an imbalance
in gut bacteria. For example, an illness unrelated to IBD may act as a trigger
for a disease flare; acute and chronic illnesses can be related to an
imbalance in the normal flora of the gut.9-13 Based on some of these causes
and triggers, probiotic use could be a method of controlling bacterial levels
to maintain intestinal homeostasis and to prevent disease flares associated
with IBD.
12
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Based on the theory of intestinal dysbiosis being related to the development
of inflammatory bowel disease, it stands to reason that probiotics should
play a key role in the treatment and prevention of intestinal inflammation.
However, studies have shown that this is still being researched and there is
not one clear-cut method of introducing probiotics into the diet to control
inflammatory bowel disease symptoms. Systematic reviews have indicated
that while there is evidence to support the role of gut microbiota in the
development of IBD symptoms and that probiotics could potentially alter this
role in a favorable manner, further research is still needed to support the
use of probiotics as prevention of ulcerative colitis, and no evidence supports
the use of probiotics for Crohn’s disease.9,10,14
Although probiotics are very popular supplements on the market and some
patients with IBD may use them to control their symptoms, they are not
necessarily included as part of normal treatment. It is safe to say that
alterations in gut microbiota play an important role in IBD and that certain
microorganisms can interact favorably with the intestinal mucosa or they can
cause harm and contribute to inflammation. Isolating an exact causative
mechanism in this area still warrants further study.
Breach of Intestinal Barrier
The gastrointestinal tract repeatedly encounters various entities that can
contribute to disease or harm to the body, but the intestinal wall is designed
to act as a barrier to prevent certain substances from reaching circulation
and potentially causing harm. The linings of both the small and large
intestines are made up of epithelial cells that act as a physical barrier
because of their closely packed structures and prevent microorganisms from
invading the areas of the body outside of the gastrointestinal system.
13
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
In addition, the two mucosal layers of the intestinal tract — the mucosa and
the submucosa — usually provide sufficient protection against microbes and
harmful microorganisms that may cause illness and disease. As discussed,
the goblet cells in the intestinal tract secrete mucus, which acts as a
protective mechanism; goblet cells are also responsible for producing
mucins, which are a type of protein that further work to maintain the
intestinal barrier.
Within the small intestine, protection is also provided by the presence of
some goblet cells that secrete mucus; the small intestine also contains
multitudes of villi that are responsible for nutrient absorption. In addition to
goblet cells that secrete mucus, there are two other types of cells in the
epithelial lining of the intestinal tract that provide protection. Paneth cells,
named after the physiologist Joseph Paneth, are specific types of cells found
in the epithelium of the small intestine, most often at the base of the crypts.
They are necessary for providing some protection and defense against
microbes. Paneth cells play a role in maintaining the barrier of the
gastrointestinal barrier by secreting antimicrobial molecules known as
defensins into the crypts of the intestinal tract in response to antigen
presentation. Enteroendocrine cells secrete hormones that not only regulate
some metabolic functions, they are also responsible for tissue repair.15
The intestinal barrier is specifically designed to allow the body to carry out
some functions while simultaneously protecting it from some other entities.
The small and large intestines are involved with nutrient and fluid absorption
and the balance of electrolytes, all carried out with the assistance of the cells
in the intestinal barrier. At the same time, these cells prevent other
elements found in the digestive tract from entering circulation through a
highly selective process.
14
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Another role of gut microbiota in the protective mechanisms of the intestinal
tract is to prevent overgrowth of harmful bacteria by stimulating defense
mechanisms by the host. Some of the species of gut microbiota activate
dendritic cells, which are antigen-presenting cells of the immune system and
are responsible for presenting invading antigens to T cells. In response to
activation of these cells, plasma cells in the mucosal layer of the intestine
secrete secretory immunoglobulin A (IgA), an antibody that supports
immune function and that is produced by the B lymphocytes. The release of
IgA in turn provides protection for the mucosal barrier against invading
pathogens.14,15
Low levels of secretory immunoglobulin A has been associated with IBD as
well as with a number of gastrointestinal diseases, including celiac disease,
chronic Candida infection, and bacterial overgrowth of the small intestine.
However, a specific balance in the amount of secretory IgA must be present,
as elevated levels of this immunoglobulin have also been associated with
development of Crohn’s disease and ulcerative colitis, in addition to some
viral infections, including infection with Epstein-Barr virus and
cytomegalovirus. It is therefore important to consider the role of secretory
IgA in the context of IBD development and its ability or lack of ability to
protect the intestinal barrier. Deficiency in secretory IgA is not only related
to the activity of gut microbiota and their ability to stimulate dendritic cells,
but also to environmental and lifestyle factors, such as stress, poor diet, and
infection, which are further highlighted below.6,14-18
Gut associated lymphoid tissues (GALT) are one of the largest components
of the immune system within the body and are found in the gastrointestinal
tract. GALT is a component of the immune system in the gastrointestinal
tract that contains B and T lymphocytes. These tissues play an important
15
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
role in protecting the body from infection and inflammation at the level of
the intestinal barrier. Normally, the numbers of microbiota present within
the gastrointestinal tract affect the composition of GALT. When there is an
alteration in intestinal permeability and microorganisms are able to
penetrate the mucosal lining, the GALT produces an inflammatory response.
Further, antigens in the intestinal tract can actually adhere to the epithelial
lining of the intestinal barrier, which increases the immune response, since
the body seems to understand that a breach in this barrier can lead to
systemic complications.
In order to provide adequate protection, the intestinal lining must maintain a
particular balance between cell growth and destruction. Old cells are
eventually broken down and are replaced by new cells that continue the
process of protection and providing a barrier. When there is a break in
maintaining this balance, there is a risk of penetration of the intestinal
barrier, which can lead to disease development and a breach in protective
mechanisms.
It is thought that weaknesses in the protective barrier of the intestinal lining
can contribute to IBD development. Antoni, et al., in the World Journal of
Gastroenterology, state that there are various factors that can contribute to
a breakdown in intestinal barrier function, including defects in the mucus
layer and mucus-producing cells of the epithelium, increased intestinal
permeability, variations in the production of antimicrobial peptides normally
produced by some of the epithelial cells, and increases in cell autophagy,
which is a process of cell destruction.90 As a consequence of all of these
factors, an imbalance develops between the gut microbes and the body’s
defense mechanisms, and the immune system is disproportionately
16
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
triggered, leading to an exaggerated immune response and chronic
inflammation.
While some specific types of bacteria have been identified as being
associated with development of inflammation related to IBD, there is not one
particular pathogen that is distinctive to all cases. Due to the large numbers
of microorganisms that may be present in the intestinal tract, a breach in
the intestinal barrier can lead to one or more mechanisms of harmful
microbes entering circulation and stimulating the immune response.
Some professionals use the term “leaky gut” to describe the intestinal
permeability that could be responsible for some symptoms of IBD as well as
other intestinal illnesses. The concept of a leaky gut is that the epithelial
cells normally form a tight barrier that allows certain elements to pass,
namely nutrients, electrolytes, and fluids, but that prevents other
substances from breaking through. When a person supposedly has a leaky
gut, there is a breakdown in the barrier, the epithelial cells do not maintain a
tight wall with which to provide protection, and harmful elements are able to
get by. Leaky gut syndrome has been associated with a number of
gastrointestinal conditions, including IBD as well as many other systemic
disorders (asthma, allergies, type 1 diabetes, rheumatoid arthritis, and
psoriasis).
The concept of a leaky gut is relatively the same as the concept of a breach
in the intestinal barrier leading to an exaggerated inflammatory response.
The mechanisms of how a breach develops are important considerations to
take into account. The breach in the intestinal barrier may occur as a result
of such factors as disease or environmental stressors, and in a manner
similar to those triggers that prompt an inflammatory bowel disease flare.
17
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
The reason why some people are susceptible to IBD and develop the disease
is partially explained by the idea of a leaky gut or breach in the intestinal
barrier. Researchers at Emory University School of Medicine found that a
person who is genetically susceptible to developing IBD and who has a
chronically leaky gut is likely to develop IBD symptoms when there are
defects in the immune system. This requires a multifactorial process that
comes together to result in inflammation; such as genetic susceptibility,
impairment of the immune system, and triggers that contribute to a breach
in the intestinal barrier.
Consequently, there is general agreement about the notion that the
existence of a break in the lining of the intestinal tract allowing certain
microorganisms to get through and cause inflammation does not adequately
explain the cause of IBD in all cases. Instead, the concept of a leaky gut is
typically combined with various other factors that all lead to increased
inflammation and damage to the intestinal tissues that occurs with IBD.
Diet And Inflammatory Bowel Disease
The idea that diet contributes as a cause of inflammatory bowel disease
comes from the fact that the incidences of diagnosed cases of IBD are on the
rise, particularly within the U.S. and Europe. The increase in cases of IBD is
occurring at the same time as an increase in several other disorders that
also may be related to dietary intake, including type 2 diabetes and obesity.
The diets of Westerners and Europeans differ from diets of those in
developing countries where IBD is less prominent. The combinations of
increased food intake due to large portions, as well as increased intake of
items that could potentially harm the gastrointestinal tract or upset the
balance of healthy gut microbiota could play a role in development of excess
inflammation associated with IBD, as discussed here.10,17,18
18
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Gut microbiota are able to function in relation to diet. Many microorganisms
found in normal gut flora obtain nutrients from the host’s diet, meaning that
dietary factors and a person’s intake of food and nutrients can impact the
work of normal gut microbiota. A significant amount of nutrients for gut
microbiota come from digestion of dietary carbohydrates; i.e., the digestion
and fermentation of some types of carbohydrates and fiber produce shortchain fatty acids, which are associated with the control of cell proliferation
and serve anti-inflammatory purposes.
Some elements of gut microbiota play a role in lipid metabolism as well.
Adipocytes normally inhibit some of the activity of lipoprotein lipase, an
enzyme that breaks down triglycerides to be used by the body for energy.
Gut microbiota have been shown to restrain this inhibition in some
instances, leading to weight changes. Inflammatory bowel disease shares
some characteristics of chronic inflammation with obesity; people who are
obese have increased levels of inflammatory cytokines that have been seen
in people with Crohn’s disease and ulcerative colitis. A murine study by Paik,
et al., in the Journal of Nutrition found that genetically susceptible mice that
were given a high-fat diet had increased levels of mesenteric and
gastrointestinal inflammation.95 Some of the mice in the study did not
develop such inflammation, despite administration of the same high-fat diet;
however, these mice had a different genetic background, which suggests
that diet, when combined with genetic susceptibility toward inflammatory
bowel disease, can play a role in IBD development.
Gut microbiota mediate the synthesis of bile acids, which are important for
lipid transport. The production of certain types of bile acids are associated
with an increased risk of colorectal cancer, as well as some other types of
gastrointestinal diseases. Gut bacteria can also produce lipopolysaccharides,
19
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
which make up part of the cell wall in some forms of pro-inflammatory
bacteria. Lipopolysaccharides can have an impact on the immune system;
they are associated with increased inflammation and may contribute to the
development of some forms of inflammatory conditions as well.
The gut microbiota are responsible for metabolizing some amounts of
polyphenols taken in through the diet. Polyphenols are micronutrients in the
diet that are said to play a role in the prevention of certain chronic diseases,
such as cardiovascular disease and certain types of cancer. These
polyphenols are often bound to dietary sugars such as glucose, galactose,
and ribulose. The microbiota in the intestinal tract transform polyphenols,
where they can then be sent to other areas of the body via circulation. Some
examples of polyphenols that exist in the diet include tannins, which are
found in raspberries, strawberries, and grapes, and that are broken down by
Butyrivibrio species in the gut. Polyphenols also include flavonoids. Flavanols
are primarily found in onions, capers, and broccoli and are degraded by such
microorganisms as Bacteroides distasonis, Enterococcus casseliflavus, and
Bacteroides uniformis in the gut. Isoflavones found in soy, beans, and
lentils, are degraded by Lactobacillus and Bifidobacterium in the intestinal
tract. Flavonoids known as anthocyanidins are found in most types of red
and blue berries; they are broken down by Lactobacillus plantarum, L. casei,
L. acidophilus, and Bifidobacterium longum in the intestinal tract.
While there is not one specific food or fluid that causes symptoms of
inflammatory bowel disease, some foods can act as triggers for disease
flares. The types and amounts of foods that lead to symptom flares vary
between people but persons with IBD should be aware of possible
connections. Some people have success with keeping a food diary to
chronicle meals and snacks and to determine if there is a correlation
20
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
between certain foods and symptoms. Some foods that cause flares in
certain individuals also contain necessary nutrients for the body. Individuals
who eliminate these foods from their diet in order to control IBD symptoms
run the risk of suffering from nutrient deficiency. For example, fibrous foods
can cause diarrhea in some people, yet fiber is an important component of
the diet to promote normal stool excretion and to maintain normal
cholesterol. Instead of completely eliminating foods with fiber, the person
affected by these foods can try preparing them in a different manner, such
as by cooking them to soften the foods, or through a process of trial and
error to find alternative foods that are just as nutritious but that do not
cause disease symptoms.
Overall, the Western-style diet may be associated with an increased risk of
developing chronic illnesses such as inflammatory bowel disease. The
combination of factors, including high fat and calories, large amounts of
refined carbohydrates, increased amounts of sugar and high-fructose corn
syrup, and poor quality nutrients can all have negative consequences.
Additionally, a Western-style diet often lacks important nutrients that are
essential for gut health, including many vitamins, fiber, antioxidants,
polyphenols, and minerals. The role of diet in the overall health of an
individual should not be underestimated and diet as a proponent of
inflammatory conditions such as IBD continues to be examined as a specific
cause.
Genetics And Inflammatory Bowel Disease
The study of genetics and its relationship to development of IBD is ongoing
through various research projects and investigations. It is well known that
many patients with inflammatory bowel disease have a family history of
some type of IBD. A family member’s disease may not necessarily be the
21
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
same or similar to a current patient’s
diagnosis but the presence of some
type of IBD in an ancestor’s medical
history may mean that the current
patient was predisposed to the
diagnosis. The study of genetics
describes how heredity affects the
expression of certain traits within
people. In examining how genetics
causes IBD, clinicians are attempting to
isolate specific genes to determine their
contribution toward the disease
process, as well as study the effects of
bacterial genes that are specific to gut
microbiota. This section provides an overview of the role of genetics in
inflammatory bowel disease.1,2,28,43,47,95,96
Metagenomics of the Human Intestinal Tract (MetaHIT) is a project operating
in eight different countries in Europe and is designed specifically to
determine how genes associated with certain bacteria in the intestinal tract
affect human disease. Through the many studies conducted by MetaHIT, the
organization has speculated that there are more than 10 million different
types of genes in the human body. Based on continued research into the
connection between genetics and inflammatory bowel disease, studies
continue to suggest that genetic abnormalities that affect the immune
system may predispose some people to developing IBD.
Genes play a role in the types of microbiota present in the intestinal tract,
which can further influence health and the possibility of developing intestinal
22
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
disease. There has been some evidence of greater propensity for disease
development in people who have low gene counts in the intestinal tract;
defined as lower than average of the normal microbial genes in the gut.
People who are considered to have lower numbers of microbial genes are
more likely to have higher counts of pro-inflammatory bacteria in the
intestinal tract, which may contribute to inflammatory bowel disease.
Variations in the NOD2/CARD15 gene have been associated with the
development of Crohn’s disease. Studies suggest that when these variations
are present in some people, they are genetically predisposed to developing
Crohn’s disease. The NOD2 gene codes for the creation of particular proteins
that support immune system functioning. Certain cells in the gastrointestinal
system express the NOD2 gene, including Paneth cells and monocytes of the
immune system. The NOD2 gene plays a significant role in defending the
body against foreign antigens, so when there are variations in the gene, the
body may be more susceptible to certain diseases, and Crohn’s disease is
one condition that is specifically involved when disparities exist.
The NOD2/CARD15 gene has also been shown to impact the response to
antibiotic therapy for some patients with perianal Crohn’s disease. Persons
with Crohn’s disease affecting the perianal area may respond more favorably
to antibiotic treatment when the NOD2/CARD15 wild type gene is present.
Some studies have also found correlations with other genes when variations
are present along with increased incidences of IBD. A variant in the ATG16L1
gene has also been associated with development of Crohn’s disease. There
are some genetic polymorphisms of ATG16L1 that alter the immune
system’s functioning and actually stimulate cell destruction of normal tissue.
When the immune system is stimulated to this destruction, known as
23
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
autophagy, the process affects how antigens are exhibited and the immune
response may not be activated at the appropriate times. In other words,
when autophagy occurs, the body may be destroying healthy cells but failing
to recognize the presentation of antigens that it should be fighting off
instead.
Specifically, the T300A variant of the ATG16L1 gene is one of the best
known factors involved with development of Crohn’s disease. Some studies
have examined the effects of reducing the chemical complex of T300A on
inflammation associated with IBD. A study by Murthy, et al., in the journal
Nature showed that starvation induced metabolic stress in macrophages (the
cells of the immune system responsible for phagocytosis) increased the
breakdown of T300A variants in the ATG16L1 gene, resulting in diminished
autophagy.38 Further studies in mice have shown that maintaining another
variant of ATG16L1 gene, the T316A variant, may result in problems with
eliminating certain types of harmful bacteria in the gut, specifically Yersinia
enterocolitica, an organism often responsible for gastrointestinal
inflammation and diarrhea.
The Paneth cells, as previously described, are also related to inflammation
development when genetic variations exist. Paneth cells express the NOD2
genes but may also be related to irregularities with the ATG16L1 gene as
well. Some studies with mice have shown that abnormalities of the ATG16L1
gene is sometimes correlated with abnormal Paneth cells when the norovirus
species is present; the mouse norovirus studies were similar in structure to
some noroviruses that infect humans to cause gastroenteritis. The studies
about the specific relationship between Paneth cells and alterations in
ATG16L1 are still ongoing but there is evidence that a connection exists
24
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
between these two factors when viral antigens are also present, which can
affect the maintenance of the mucosal lining of the intestinal tract.
The study of genetics and its relationship to development of inflammatory
bowel disease is widespread and extensive. Because of the many differences
in genetic variations and their effects on the gastrointestinal system,
research in this area is ongoing and evolving. It is reasonable to say that
people with genetic susceptibility to IBD have a greater chance of developing
symptoms, particularly when other factors are present, such as diet and
lifestyle factors or other triggering influences. The specific genes involved
that cause a person to become susceptible are still being investigated.
Inflammatory Bowel Disease Symptoms
Disease symptoms are the manifestations of how inflammatory bowel
disease presents itself in the affected patient. Symptoms of IBD may be
obvious, prompting a patient to seek help and treatment. Symptoms may
also be subtle and nonspecific, in which they are difficult to distinguish from
other illnesses. Inflammatory bowel disease typically causes periods where
symptoms fluctuate. During flares, symptoms can be debilitating and painful,
while at other times symptoms may be mild to non-existent. Depending on
the extent of the disease, the symptoms of IBD may be considered mild,
moderate, or serious, and any combination of severity may be present when
symptoms develop.
Most symptoms of IBD affect the gastrointestinal tract, often causing pain
and disability when present. Other symptoms unrelated to the intestine also
can occur, known as extra-intestinal symptoms; these often develop
because of the effects of inflammation, pain, and bleeding associated with
25
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
IBD and they are frequently related to the systemic influences of the
disease, which are covered below.1,4-6,25-29,48-55,60-65,93-102
Anemia
One of the most common manifestations of inflammatory bowel disease that
is not specifically associated with bowel function is anemia, which is known
as an extra-intestinal manifestation of IBD. Historically, anemia has been so
common among patients with IBD that it has often been considered an
unfortunate consequence of the disease and one that is simply to be
expected. According to Rogler, et al., in the journal Frontiers in Medicine,
approximately 27 percent of persons with Crohn’s disease and 21 percent of
persons with ulcerative colitis suffer from anemia, with iron deficiency
anemia being present in 57 percent of these cases.47 The presence and
severity of anemia as an extra-intestinal symptom of IBD does not
necessarily correlate with the areas or locations of tissue involved.
The most common type of anemia associated with Crohn’s disease and
ulcerative colitis is iron deficiency anemia. Iron deficiency anemia occurs
when there are too few red blood cells in the body due to a lack of iron.
Unfortunately, iron deficiency anemia is also frequently underdiagnosed
among patients with IBD, despite its prevalence. The main reasons why
individuals with IBD develop anemia are due to blood loss through frequent
diarrhea and rectal bleeding. Diarrhea causes significant fluid loss, and for
some people undigested food is found in the stool as well. If food is not
absorbed in the intestinal tract and instead passes through the system
quickly to be expelled as diarrhea, the body is not taking in enough nutrients
from the food. In addition to iron malabsorption, there may be limited
absorption of many other nutrients because of frequent diarrhea, including
protein and fat.
26
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
The body needs iron to be able to maintain normal circulation and to
produce enough blood cells. Most iron in the body is found in the blood and
in the muscle tissues. Normally, the red blood cells carry oxygen to the
body’s tissues when oxygen molecules attach to hemoglobin in the
erythrocytes. Iron is needed to create hemoglobin, a protein that is made up
of iron atoms bound to heme, which is the non-protein component.
Decreased iron in the body, whether through inadequate iron stores, poor
dietary intake, malabsorption, or through blood loss can impact
erythropoiesis and results in poor oxygen delivery through diminished
production of hemoglobin.
When iron is absorbed by the small intestine, it is shifted to transferrin,
which is created in the liver. This transferrin can then move iron to
erythrocytes where it is needed for erythropoiesis. Extra iron that is not used
in this manner is stored as hemosiderin or as ferritin. Iron is also recycled in
the body and can be taken from old erythrocytes or from storage to be used
as needed when iron absorption from food is poor. Hepcidin, a hormone that
is secreted by the liver, is involved with iron regulation by controlling how
iron enters circulation. It binds to a cellular iron transporter known as
ferroportin, causing it to breakdown and thereby preventing iron absorbed
from the duodenum to enter circulation.
The synthesis of hepcidin and its effects on dietary iron absorption was first
discovered in 2000. When iron deficiency develops, hepcidin production is
suppressed. Alternatively, when plasma iron stores are elevated, hepcidin
synthesis is increased. This prevents additional iron absorption from the
intestine, which would otherwise further contribute to iron excess in the
body. Hepcidin, therefore, is important for maintaining a normal balance of
iron in the body and preventing iron deficiency as well as iron overload.
27
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Hepcidin levels seem to play a role in inflammatory bowel diseases,
particularly in relation to its effects on iron and erythropoiesis. Elevated
levels of hepcidin have been found in the urine of people suffering from
active Crohn’s disease and elevated levels were correlated with increased Creactive protein and interleukin-6 in these cases. A review in the journal
Advances in Clinical and Experimental Medicine also noted that hepcidin
levels are often lower in patients with inflammatory bowel disease when
compared to people with normal bowel function. The methods of regulating
hepcidin levels in the body to control iron stores are still being studied, but
people with IBD who have lower hepcidin levels can be at higher risk of
problems with iron regulation, further leading to iron deficiency anemia.
Iron depletion may develop initially, which is a condition that is a precursor
to iron deficiency anemia and is usually much more common than actual
anemia. Iron depletion describes a condition in which there are reduced
amounts of iron stores in the body. The condition does not cause anemia
unless iron levels are low enough that the body is unable to make enough
red blood cells and hemoglobin levels drop. An individual with inflammatory
bowel disease may initially develop iron depletion because of frequent
diarrhea and malabsorption; however, it can often be asymptomatic or may
cause mild symptoms that are not obvious right away, including fatigue and
lethargy. For some people, iron deficiency could cause stomatitis, sore
tongue, delayed wound healing, and hair loss.
Malabsorption of iron due to damaged intestinal tissue is another cause of
iron deficiency anemia. This condition is seen more commonly in patients
with Crohn’s disease who have involvement of the small intestine. Iron
absorption is impaired when inflammation impacts the small intestine,
primarily the duodenum or the jejunum, the main sites of iron absorption in
28
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
the gastrointestinal tract. The human body loses some iron from stores
through the sloughing of skin cells, but it does not actually excrete much
iron from stores through the urinary or gastrointestinal systems. As a result,
iron deficiency and anemia develop not when too much iron is excreted, but
rather as a lack of appropriate iron absorption.
As with iron depletion, iron deficiency anemia as a result of IBD causes
symptoms of fatigue, poor concentration, lethargy, and poor stamina. The
individual may also exhibit pallor or muscular weakness, or may be short of
breath. Severe symptoms of iron deficiency anemia include changes in the
shape of the nails, causing them to become brittle and spoon-shaped, as
well as glossitis and cheilosis in the mouth, pruritis, dizziness, and
irritability; some individuals also develop pica, in which they crave non-food
items.
Treatment of iron deficiency anemia requires supplemental iron in doses
given once or twice a day. A standard, adult dose of iron is approximately 60
mg; only a certain amount of iron is absorbed with oral intake, so too large
of a dose will not increase the chances of correcting a deficiency all at once.
The excess will not be absorbed or used. Iron supplements should be taken
on an empty stomach, as some foods can decrease absorption; however,
vitamin C has been shown to improve iron absorption, so taking the
supplement with a source of vitamin C, such as with a glass of orange juice,
could improve its uptake.
Dietary iron intake can also alleviate some of the negative effects of iron
deficiency anemia. Dietary iron is available to the body in two different
forms: heme iron and non-heme iron. Heme iron is found in foods that are
meat based, including beef, chicken, turkey, and pork and is absorbed more
29
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
easily by the body when compared to non-heme iron, which requires certain
gastric secretions to break it down to the ferrous state before it can be
absorbed. Some other items, including tannins found in tea, polyphenols,
and some antibiotics, can also limit absorption of non-heme iron. Sources of
non-heme iron in foods include enriched breakfast cereals, beans, tofu, dried
fruits, and seeds.
A health clinician can determine that a patient with iron deficiency anemia is
responding to iron supplementation by checking hemoglobin levels. Serum
hemoglobin should rise slowly with iron supplementation and the patient will
eventually suffer from fewer symptoms of iron depletion. However,
treatment of the underlying IBD is essential for correcting iron deficiency, as
no amount of supplementation will correct the loss that occurs from bleeding
or intestinal damage due to inflammatory disease.
People with IBD can be at risk of other types of anemia in addition to iron
deficiency. The malabsorption of nutrients due to inflammation and intestinal
damage can lead to nutrient deficiencies that are harmful to normal body
processes. Vitamin B12 deficiency anemia may develop in some patients
with Crohn’s disease because of malabsorption of the vitamin. This type of
deficiency also causes a decrease in red blood cells, as vitamin B12 is
needed for erythropoiesis. When vitamin B12 deficiency anemia occurs as a
result of a lack of intrinsic factor in the stomach, which is needed to absorb
vitamin B12, the condition is known as pernicious anemia. However, among
other people, such as those with IBD, vitamin B12 anemia may develop
when the areas of the intestinal tract that normally absorb vitamin B12 are
damaged by the disease, such as in Crohn’s disease. The use of certain
types of drugs for treatment of IBD, including methotrexate and
30
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
sulfasalazine, or when patients with IBD have had surgery to remove part of
the small intestine, may further impair vitamin absorption.
The symptoms of vitamin B12 deficiency can vary between persons; some
symptoms are similar to those of iron deficiency anemia, while others are
clearly different. Common symptoms of vitamin B12 deficiency anemia
include numbness and tingling in the hands and feet, muscular weakness,
ataxia, glossitis, fatigue, anorexia, nausea, diarrhea, and tachycardia.
Vitamin B12 deficiency is a type of megaloblastic anemia that is often seen
with folate deficiency. At times, both types of anemia may be present. A
patient can best manage this type of anemia by increasing dietary intake of
foods that contain B12 and folate, as well as taking vitamin B12
supplements. As with iron deficiency anemia, supplements and dietary
changes may help to relieve some symptoms of anemia but unless
malabsorption due to IBD (such as Crohn’s disease) is managed, the
problem will continue.
The long-term state of inflammation associated with inflammatory bowel
disease can lead to a type of anemia known as anemia of chronic disease.
This describes a condition in which there is decreased erythropoiesis and a
shortened lifespan of the red blood cells because of the chronic damage from
inflammation to the intestinal tract. Anemia of chronic disease is also
associated with various other types of long-term illnesses, including chronic
viral infections and cancer. Next to iron deficiency, anemia of chronic disease
is the second most common type of anemia.
Anemia of chronic disease is characterized by red blood cells that become
microcytic over time, causing poor hemoglobin synthesis and deficiency in
erythropoiesis. There is an increased production of certain types of
31
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
cytokines, including interleukin-1 and tumor necrosis factor, which also
contribute to poor production of erythropoietin and consequent limited
erythropoiesis. The red blood cells have shorter lifespans with this type of
anemia; there is also a decrease in red blood cell production when the bone
marrow is unresponsive to erythropoietin stimulation. When red blood cells
age, they are termed senescent red blood cells, meaning they are nearing
the end of their life spans. Normally, the body removes extra iron from
senescent red blood cells and puts it into storage. This iron is unable to be
used for hemoglobin synthesis, so if red blood cells have shorter life spans,
the body cannot recycle the iron to create more hemoglobin. Consequently,
anemia develops because of a decrease in red blood cells and a drop in
hemoglobin.
Anemia of chronic disease often develops slowly, and the symptoms may not
be noticeable when compared to the actual underlying disease process. For
example, an individual struggling with frequent diarrhea, abdominal pain,
and bloody stools related to ulcerative colitis may be less likely to notice an
increase in fatigue that comes on slowly because of anemia of chronic
disease. Laboratory findings may show an indication that something is
wrong; transferrin saturation levels are often low and there may be
alterations in reticulocyte hemoglobin content and mean corpuscular volume.
Symptoms are often mild overall, and the anemia may be difficult to identify
and pinpoint as the cause of the person’s symptoms. It usually responds well
to treatment with erythropoietin.
The most important form of treatment for anemia of chronic disease is
management of the underlying condition contributing to the anemia; in this
case, the anemia of chronic disease can develop from uncontrolled
inflammatory bowel disease, so proper management of inflammation, severe
32
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
diarrhea, and bleeding is paramount for controlling anemia. Erythropoietin, a
growth factor that can be administered as an injection, stimulates the bone
marrow to produce more red blood cells and is another standard form of
treatment for this type of anemia, often when combined with chronic disease
treatment.
Treatment of anemia is usually successful with supplementation of the
missing nutrient, typically with iron, vitamin B12, or folate. This type of
treatment actually may provide greater benefits than treatment with
medication to control inflammation of IBD. However, administration of
supplements, including oral iron therapy, is often not well tolerated by
people with inflammation of the bowel. When oral therapy is poorly tolerated
and the effects of anemia are significant, including evidence of hemoglobin
levels < 10 g/dL, intravenous iron therapy should be initiated, which has
shown to be well tolerated and more effective than oral iron
supplementation. While medical therapies for IBD can reduce inflammation
and may eliminate bleeding from ulcers that can cause anemia, many
patients have more success with treating anemia when these drugs are
combined with nutrient supplements as specific treatment for the anemia.
People with a history of anemia and IBD that is in remission should continue
to have laboratory values checked on a routine basis, whether the effects of
inflammation are present or not. Alves, et al., in the Sao Paulo Medical
Journal recommend routine surveillance every 6 to 12 months for patients
with remissive Crohn’s disease or ulcerative colitis, including testing of
complete blood count, serum iron and ferritin levels, transferrin
concentration and saturation, lactate dehydrogenase, and reticulocyte count,
as well as B12 and folic acid levels in those at risk.7 The numbers of people
who are suffering from anemia as a result of IBD is slowly decreasing as
33
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
health clinicians become more aware of this potential complication of the
disease and seek to identify it and provide treatment during the early
stages. Still, there are many cases that continue to be overlooked and are
not treated until symptoms are severe and debilitating.
Abdominal Pain
Abdominal pain describes any type of pain that develops in the region below
the chest and above the groin. It can be dispersed throughout the entire
region or localized to one specific area. Abdominal pain is also described in
various ways, and those with IBD may suffer from abdominal pain
predominantly during times of disease flares when the pain is constant and
occurring all the time, or intermittent, in which it comes and goes. Some
people refer to abdominal pain associated with IBD as “stomach pain” or a
“stomach ache,” although the pain is usually not associated with actual
stomach organ.
The pain that develops with inflammatory bowel disease is often related to
the type of IBD present and the area most affected. In cases of ulcerative
colitis, where the disease is located almost entirely in the colon and/or the
rectum, the patient is more likely to experience pain in the lower abdomen.
The pain associated with Crohn’s disease may be located in the areas
affected, and so may occur anywhere throughout the abdomen, depending
on whether the disease impacts more of the small intestine, the colon, or
both areas. Among patients with IBD, abdominal pain may be a common
symptom and one that many people tolerate; however, when abdominal
pain increases in intensity and severity, it may be a sign that treatment
methods need to be increased or modified.
34
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Abdominal pain most commonly develops during disease flares, when
symptoms of inflammation and ulceration are present and are at their worst.
A patient who is having an acute flare of ulcerative colitis may complain of
severe abdominal pain that is unrelieved by pain relievers or antispasmodic
medications designed to treat cramps and spasms in the gut. The pain may
or may not be relieved temporarily following a bowel movement. Treatment
administered to relieve inflammation and to control further disease flares
may help with some abdominal pain. Use of non-steroidal anti-inflammatory
agents (NSAIDs), while effective in managing a patient’s pain and
inflammation from extra-intestinal symptoms, are not usually warranted for
abdominal pain associated with IBD. These drugs can irritate the intestinal
lining and could contribute to further pain for the patient. While there is no
direct association between NSAID use and an increase in disease flares, the
side effects of these drugs often mean that there may be other medications
to use that are better options for pain control.
Other options that have been used as alternatives for pain relief include
opioid analgesics, antidepressants, and anticonvulsants. Some of these
drugs can be used in combination or as adjuvant therapies to provide more
relief. Medications prescribed solely for relief of abdominal pain are often not
effective in relieving all abdominal pain. Instead, a patient affected with IBD
may have more success with a combination of medication and
psychotherapy, or by managing the disease process itself to reduce
inflammation and ulceration associated with the illness. Medications should
be continued throughout remission and taken as prescribed to avoid further
flares of the disease and recurrent abdominal pain.
Abdominal pain can cause multiple other effects for a patient because it can
be painful enough to be debilitating. Many people suffering from acute
35
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
abdominal pain experience other symptoms as well, including nausea,
vomiting, and anorexia. At times, pain can be so intense as to cause nausea
for some people; if pain and nausea develop shortly after eating a meal,
they could lead to vomiting of recent food intake. Often, abdominal pain is
so intense that the affected person has little desire to eat. The pain may be
worsened with food intake and the individual may want to avoid any pain
exacerbation as much as possible. Frequent anorexia and missed meals
leads to weight loss over time when the affected person does not take in
enough calories or nutrients to meet daily recommendations and to sustain a
healthy weight.
Chronic abdominal pain can also cause psychological symptoms, particularly
if a patient has difficulty controlling the pain and it affects quality of life.
Unrelenting pain is linked with an increase in anxiety and depression for
many; modifying activities to accommodate the pain, knowing that there
have been many attempts at therapy or treatment to manage the pain but
that have been unsuccessful can cause a person to feel disheartened and
depressed. If abdominal pain worsens at certain times, such as following
food intake, the individual may develop anxiety over eating or because of
social situations, or have a fear of experiencing further pain.
Abdominal pain associated with IBD is often related to inflammation and
ulcerations in the gastrointestinal tract. The tissues of the small or large
intestine, when they become inflamed, may swell and press on nearby
nerves that serve the gastrointestinal system. This extra pressure may
stimulate these nerves to send pain messages to the brain that abnormal
activity is taking place in the gastrointestinal tract. While the abdominal pain
can alert the brain to the presence of abnormal activity, it is often
uncomfortable and not easily remedied. At times, abdominal pain may be
36
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
the only symptom a patient is experiencing or it may be the symptom that
leads the individual to seek help and a diagnosis. Ulcerations in the intestinal
tract cause tissue breakdown and stimulation of nerve receptors, which can
also lead to abdominal pain. The pain may be at the location of the ulcerated
areas in the gastrointestinal tract, or it may radiate to other parts of the
abdomen.
At times, abdominal pain is a sign of a complication of IBD. A person with
ulcerative colitis or Crohn’s disease may have successfully managed
symptoms during times of disease flares for a while, but a change in the
intensity or severity of abdominal pain may indicate that something else is
wrong. An abscess in the gut, caused by a pocket of infection due to chronic
inflammation and accumulation of microorganisms in a particular area can
cause significant pain for the affected individual. Intestinal strictures, in
which the lumen of the gastrointestinal tract becomes narrowed due to
scarring or thickening of the intestinal wall may also lead to abdominal pain,
particularly when digestion slows and there may be a buildup of gas in the
intestine. Other causes of pain in the intestinal tract that have developed,
often as a consequence of IBD, include gastritis, fistulas, fissures, adhesions,
or small bowel obstruction.
While IBD may be confused with irritable bowel syndrome, the two
conditions are not the same. However, there is mounting evidence of a
connection between inflammatory bowel disease and irritable bowel
syndrome (IBS). The American College of Gastroenterology revealed that
there is a potential overlap between the two disorders in that the
inflammation associated with IBD could lead to the development of IBS.
Further, there may be inflammation present even when the disease appears
to be in remission, which can cause symptoms of IBS. Irritable bowel
37
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
syndrome is a chronic functional bowel disorder that causes symptoms of
abdominal pain and diarrhea that are similar to those of IBD. The condition
can also cause chronic constipation and abdominal bloating, although testing
and diagnostic procedures typically are unable to pinpoint an exact cause of
the discomfort and there are no changes in laboratory findings or testing
results.
The American College of Gastroenterology also showed that some
antidepressants, which are often used for the treatment of IBS, have been
used with some success in treatment of inflammatory bowel diseases.
Tricyclic antidepressants (TCAs) are some of the more commonly prescribed
drugs for treatment of IBS. When administered to patients with
inflammatory bowel diseases, TCAs may be beneficial in managing some
abdominal pain and diarrhea associated with IBD.
A patient that presents with consistent abdominal pain needs further
investigation and diagnostic procedures to identify the cause. If the patient
has already been diagnosed with IBD and the pain is unrelated to a disease
flare or it differs significantly from discomfort normally experienced during a
flare, it should be investigated further to determine the cause, as the pain
could be related to a complication of the disease. Diagnostic testing may
involve laboratory testing and a physical examination. A complete blood
count may indicate changes in leukocyte counts or may reveal infection or
inflammation due to elevated white blood cell levels. A C-reactive protein
level and erythrocyte sedimentation rate, if elevated, can indicate an
increase in inflammation. A patient who is suffering from anemia may exhibit
low albumin levels and when present, can help the health clinician to
determine whether protein loss is ongoing.
38
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
The physical examination may reveal signs of pathology, including
abdominal bloating or specific areas of tenderness. If laboratory evidence is
lacking and the physical exam does not reveal an obvious, external source of
the abdominal pain, the patient may need endoscopy or other imaging
procedures to rule out complications. Depending on the location of the pain,
a colonoscopy may be performed to examine the large intestine, the sigmoid
colon, and the rectum, while an upper endoscopy may be needed to examine
the esophagus, the stomach, and the duodenum of the small intestine.
Unfortunately, abdominal pain seems to be very common and widespread
among patients with IBD and it is often consistent, even after thorough
assessment. According to Docherty, et al., in the Journal of Gastroenterology
and Hepatology, approximately 20 percent of patients with IBD continue to
have pain despite verification of inflammatory bowel disease remission.53
Regular abdominal pain, while a common element of disease flares
associated with IBD, should be managed and treated to the fullest extent
possible and not simply accepted as a symptom that a patient must learn to
live with.
Vomiting
Vomiting describes the forceful expelling of stomach contents, whether it is
voluntary or uncontrolled, through the contraction of the muscles in the
stomach and the abdomen. Vomiting is often associated with nausea, a
feeling of queasiness in the stomach that may also include the sensation of a
headache or dizziness. For some patients with IBD, vomiting is a symptom
that commonly develops during disease flares because of the pain and
inflammation occurring in the intestinal tract.
39
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Nausea is controlled by the brain stem, near the regulatory centers of
various other bodily functions. The area of the brainstem that controls
emesis is actually known as the vomiting center. There are various
mechanisms that can stimulate the vomiting center and that can cause a
person to experience nausea and/or vomiting. The chemoreceptor trigger
zone, also called the area postrema, is an area in the vomiting center that
contains receptors for various neurotransmitters, including dopamine,
serotonin, and substance P. Stimulation of these receptors or the nearby
regulatory centers, including the vestibular center or the vagus nerve, can
also stimulate vomiting.
People with inflammatory bowel disease flares who have developed
symptoms may be more likely to experience vomiting if some of their
symptoms stimulate the receptors found in the chemoreceptor trigger zone
of the vomiting center. For example, some people who have severe,
unremitting pain develop nausea as a result. When IBD causes debilitating
abdominal pain, the area postrema in the brain may eventually be
stimulated, which activates the sympathetic and parasympathetic nervous
systems to induce vomiting. Ongoing stress may also cause someone to
experience vomiting because of activation of the dopamine receptors in the
chemoreceptor trigger zone, which leads to the similar effects of emesis.
Not all patients with inflammatory bowel disease experience vomiting as part
of their symptoms of disease flares. For some people, vomiting may be a
sign of a complication of the disease, particularly if it is not normally
associated with flare symptoms. Vomiting may be a sign that a stricture has
developed in the intestinal tract, a potential complication of IBD. When
strictures form, the passage of food and fluids through the intestinal tract is
slowed. Severe cases of strictures can lead to enough of an obstruction that
40
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
very little material is able to pass through the intestine. This is not only
painful for the patient but can also lead to slowed digestion and absorption,
as well as intestinal blockage, in which the patient experiences pain,
abdominal bloating, and nausea, as well as vomiting.
In some cases of gastroduodenal Crohn’s disease, vomiting occurs because
of the effects of the disease on the stomach lining. Because of chronic
inflammation of the stomach and duodenum, a patient with gastric Crohn’s
disease often experiences a feeling of fullness soon after eating, as well as
indigestion, nausea, and vomiting. Vomiting may also be a sign of
complications associated with gastroduodenal Crohn’s. Gastric outlet
obstruction is one of the more common complications of Crohn’s affecting
this area of the intestinal tract. When strictures close the opening of the
passage between the stomach and the duodenum, food remains in the
stomach and does not pass into the small intestine for further digestion. In
addition to pain and bloating, gastric outlet obstruction can cause vomiting,
early satiety, fullness in the abdomen, anorexia, nausea, indigestion, and
weight loss.
Another rare but significant complication of gastroduodenal Crohn’s disease
that can cause excessive vomiting is when a fistula develops between the
stomach and the colon. Known as gastrocolic fistula, this occurs as tunneling
between the stomach and usually the transverse section of the colon; this
complication most often develops when a patient has concomitant Crohn’s
lesions in both the stomach and the colon. The patient with this type of
fistula develops symptoms of abdominal pain, weight loss, diarrhea, and
rectal bleeding in addition to vomiting. The vomiting that occurs in this case
may contain stool, known as feculent vomiting. The patient may complain of
a bad taste in the mouth or there may be the smell of stool on the breath.
41
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
This condition requires surgical intervention to correct the fistula.
Fortunately, this type of vomiting is a rare complication of Crohn’s. Any
patient that develops severe vomiting that contains fecal matter requires
further evaluation for surgery.
Treatment of vomiting often depends on its cause. Vomiting that occurs as a
result of pain from inflammation or slowed motility (unrelated to gastric
outlet obstruction) could be managed with antiemetic medications. These
drugs work by blocking stimulation of the vomiting center in the brain. The
chemoreceptor trigger zone is actually outside of the blood-brain barrier,
which means that medications can reach it directly to control the sensations
of nausea and to stop vomiting. A patient with regular vomiting may also try
to eat smaller, more frequent meals and should continue to try to drink
fluids to avoid dehydration. When vomiting develops as a result of a
complication associated with IBD, such as an intestinal obstruction or fistula,
the condition must be treated as soon as possible, since vomiting in these
cases is almost always a sign that warrants further action.
Frequent vomiting has its consequences, as the continued loss of food and
fluid can result in weight loss and malnutrition. A patient who suffers from
frequent vomiting associated with IBD is at risk of dehydration due to loss of
fluids and electrolytes. It may be difficult to take in enough food or fluids,
particularly if nausea is also present. The effects of stomach acid when it
comes into contact with the lining of the esophagus during emesis can be
harmful to the delicate tissues at the back of the throat and can erode
enamel off of the teeth. While vomiting is a consequence of inflammatory
bowel disease for some, like some other symptoms that are associated with
Crohn’s disease or ulcerative colitis, vomiting is not a symptom to be ignored
in hopes that it will go away. A patient who experiences ongoing vomiting as
42
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
part of disease flares should be given treatment and monitored for further
problems related to this symptom.
Diarrhea
Diarrhea is a common clinical manifestation of inflammatory bowel disease.
Diarrhea occurs as an increased urge to defecate with loose, watery stools
as a result. The inflammation of the gastrointestinal tract causes destruction
of the mucosal lining of the intestine, which increases the urge to have a
bowel movement. For people with ulcerative colitis and Crohn’s disease that
affects the colon, inflammation in the lining of the colon prevents the large
intestine from adequately absorbing water from fecal material that passes
through. Consequently, the material contains more water when it is expelled
from the body, leading to the watery stool of diarrhea.
Ulcerative colitis and Crohn’s disease cause frequent diarrhea; the stool is
often bloody due to tissue breakdown and sloughing from the ulcers. The
affected individual may have more than 10 loose stools per day in severe
cases of the disease. Sometimes, the diarrhea contains both blood and pus,
particularly if small pockets of infection are present or ulcerated areas
contain excess microorganisms. A patient often suffers from increased
urgency to have a bowel movement in addition to increased frequency,
which is usually stimulated from the chronic inflammation in the intestinal
tract. There is often considerable pain with defecation and release of gas.
Diarrhea increases the risk of dehydration, so any patient who is struggling
with ongoing diarrhea due to IBD should be evaluated for fluid loss and signs
of dehydration. Patients should be encouraged to increase their oral intakes
of fluids, particularly through fluids that do not contain caffeine or excess
sugar, in order to replace some of the fluids lost through diarrhea. Liquid
43
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
electrolyte supplements, such as sports drinks may also be needed.
Intravenous fluid support is necessary in severe cases of dehydration as a
result of chronic diarrhea, which provides not only the needed fluid for the
body’s tissues, but the electrolytes lost through frequent diarrhea. The main
electrolytes lost through frequent diarrhea include sodium, potassium,
phosphorus, and magnesium, all of which can cause serious side effects of
weakness, fatigue, and nausea.
Diarrhea is most common when an individual is experiencing a disease flare,
but during periods of remission, the diarrhea is often limited. The affected
individual may still experience diarrhea on occasion during remission, a
period that can last months or even years, but the majority of diarrhea that
develops with IBD occurs during active symptoms associated with flares.
Fulminant colitis, a severe form of ulcerative colitis, may occur in certain
patients and can be the cause of significant complications, including toxic
megacolon and bowel perforation. The term fulminant describes a condition
that develops very suddenly and severely. People with fulminant ulcerative
colitis tend to have significant diarrhea, evidenced by over 10 loose stools
each day, as well as continuous rectal bleeding. The diarrhea associated with
fulminant ulcerative colitis is often sudden and explosive, leading to loss of
large volumes of stool and fluid. In addition to severe diarrhea, other
symptoms associated with fulminant colitis include abdominal pain and
bloating, anorexia, and fever. The condition is also sometimes called toxic
colitis.
The treatment of diarrhea depends on the extent to which the patient is
passing loose stools, as well as whether there is pain, blood loss, or pus
present in the stool. Some people find relief by using antidiarrheal
44
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
medications, which can be purchased without a prescription. These drugs are
useful in slowing intestinal motility so that the bowel has more time to
absorb fluid and electrolytes as fecal material passes through. They may also
relieve some of the cramping that often occurs with diarrhea. However,
patients who take antidiarrheal medications should know that they are only
for symptomatic use and they do not cure IBD, nor do they relieve
inflammation. The source of the diarrhea is still present, even when taking
antidiarrheals. Other medications used to treat Crohn’s disease and
ulcerative colitis may help to relieve some of the inflammation in the
intestinal tract that is contributing to diarrhea. These drugs are also not a
cure for IBD, but they can help to minimize many of the symptoms that
develop during flares, such as diarrhea. Treatment with corticosteroids and
anti-inflammatory agents can reduce some of the inflammation and
ulcerations in the intestinal tract and can promote remission, during which
time the affected individual will be less likely to experience diarrhea.
Even without a diagnosis of a complication due to Crohn’s or ulcerative
colitis, there are instances when diarrhea is so persistent or unrelenting that
it warrants medical attention. A patient with IBD should seek medical
attention when diarrhea is more than the usual amount noted with flares or
when it becomes very heavy and is unrelieved by any measures. Some
people pass a small amount of pus or blood with diarrhea, which is not
unusual, but larger amounts of pus, accompanied by fever or severe
abdominal pain, as well as large blood clots in diarrhea warrant medical
attention.
Rectal Bleeding
Blood loss from the rectum may occur as a relatively common symptom
associated with Crohn’s disease or ulcerative colitis. Rectal bleeding is often
45
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
associated with diarrhea, in which the patient passes loose stools that
contain blood. Mucus and discharge may also be combined with blood
through diarrhea. Although rectal bleeding and diarrhea commonly occur
together, rectal bleeding may also develop on its own, aside from diarrhea.
There are many potential causes of rectal bleeding. Consequently, if a
patient has not already been diagnosed with IBD, rectal bleeding and blood
with a bowel movement is a cause for further testing. A patient who does
have a diagnosis of IBD may become accustomed to some amount of rectal
bleeding when disease flares occur. The bleeding may be mild and may
consist of a few drops of blood seen on toilet paper; alternatively, rectal
bleeding can also be much more serious and may consist of larger amounts
of blood as well as blood clots. Frank, red blood indicates bleeding from near
the anus or in the rectum, while dark red blood or blood that is mixed with
stool is more likely to have passed through part of the intestine tract and
indicates bleeding from within the gastrointestinal system. It should be
noted, though, that bright red blood could come from higher in the
gastrointestinal tract and it is not always an indication of a superficial wound
or ulceration.
Some patients with inflammatory bowel disease that affects the anus and/or
the rectum are more likely to develop rectal bleeding when ulcerations cause
tissue breakdown that leads to leakage of blood from the anus. Fissures and
cracks in the skin of the anal opening can also lead to blood loss and are
sometimes quite painful; however, depending on their depth and severity,
fissures may not cause pain with defecation, even though they do often
bleed. Patients with perianal Crohn’s disease can have rectal bleeding from
various causes, as many of the lesions seen with this particular type of
Crohn’s affects the skin around the anus and the perineum.
46
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Fistulizing disease describes an inflammatory bowel condition where the
affected patient has developed fistulas or channels between areas of tissue.
Patients with Crohn’s disease, because of the transmural nature of the
disease, are often more likely to develop intestinal fistulas. A large
percentage of fistulas develop around the anus and an opening may develop
between the gastrointestinal tract and the outside of the body, such as
between the rectum and the skin or between the anus and the vagina.
Additionally, internal intestinal fistulas may also develop, which cannot be
seen from outside of the body, but may still cause pain and rectal bleeding.
In these cases, a small hole actually develops from part of the intestinal
tract as the fistula connects the portion of the intestine with a nearby organ
or another area of tissue. In some cases, rectal bleeding may be one of the
only indications that gastrointestinal complications have developed because
of inflammatory bowel disease.
Bleeding from the rectum, while somewhat common with IBD, is not a
normal process that should be considered simply part of the disease. When it
occurs, rectal bleeding must be investigated to rule out potential
complications and to prevent other consequences of the condition, such as
infection or anemia. Rectal bleeding often contributes to anemia through
blood loss, particularly when the bleeding is heavy and chronic. A patient
may develop other symptoms in addition to bleeding, such as itching around
the opening of the anus, pain with defecation, or unremitting leakage of
mucus or fluid from the rectum. Blood loss is often obvious when the
individual has a bowel movement or as noted on toilet paper when using the
bathroom. In some situations, however, a stool sample may be needed to
test for occult blood to determine if there are microscopic particles of blood
within the stool or whether bleeding is occurring outside of bowel
movements.
47
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
A patient experiencing rectal bleeding should have an examination to
determine the cause of the bleeding, even if he/she already has a diagnosis
of IBD. A stool sample or a sample of the blood can give an indication as to
the location of the bleeding and whether there are other factors present,
such as a potential infection. A rectal examination can identify the presence
of lesions, strictures, fissures, or abscesses that have developed around the
opening of the anus. Blood loss that appears dark and that may come from a
lesion higher in the intestinal tract typically requires examination and
diagnosis with endoscopy. Because rectal bleeding is also a potential sign of
colorectal cancer and persons with IBD are at increased risk of developing
this type of cancer, a biopsy should be performed to rule out potential
malignancy. The patient should be further assessed for complications of
blood loss in addition to anemia if the rectal bleeding is frequent or chronic,
skin color and overall appearance shows pallor, and vital signs of tachycardia
or drop in blood pressure occur, which is indicative of blood loss.
The management of rectal bleeding may range from application of
medication directly to the anus for minor lesions or fissures that are causing
bleeding to possible surgery if damage within the intestinal tract is severe.
Underlying sources of the bleeding are typically managed on a case-by-case
basis to prevent hemodynamic instability, excessive blood loss, and patient
discomfort from this symptom.
Abdominal Cramps
Cramping is a type of pain often felt in the abdomen that can be caused by a
number of sources. Abdominal cramps may vary in intensity and severity
and they may be intermittent or a constant source of pain for the patient.
Some people experience abdominal cramping shortly after eating a meal, as
the process of digestion and absorption affects the movement of food
48
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
through the intestinal tract. Cramping may also be associated with increased
gas in the bowel, causing intermittent abdominal pain; abdominal cramping
is often not serious but it can be quite painful.
Cramping often occurs with spasms of the muscles in and around the
intestinal tract. The smooth muscles of the intestines normally contract to
move food through the gastrointestinal tract during digestion. Smooth
muscles of the gut consist of two layers: one is circular and one is
longitudinal. These muscular layers work together to flex and contract to
promote peristalsis. Intestinal inflammation can cause abdominal cramping
when the smooth muscles of the intestines do not work properly, leading to
periods of dysmotility. The intestinal tract is a hollow organ that is squeezed
by these abnormal contractions, leading to pain because of muscle spasms.
The pain may be intermittent and is often irregular, corresponding to the
timing of the smooth muscle spasms.
The development of inflammation in the intestinal tract typically begins with
the mucosal layer of the intestinal wall. This inflammation causes changes in
the functions of the smooth muscles through activation of the immune
system, which changes the environment. The immune cells, namely
macrophages and cytokines, affect the contractility of the smooth muscle
cells because they can actually alter the form and morphology of the smooth
muscles.
Abdominal cramping is often associated with diarrhea, but it can also occur
on its own. One reason for abdominal cramping that develops with Crohn’s
disease is the malabsorption of fatty acids in the small intestine. The ileum
of the small intestine is responsible for fatty acid absorption. When damage
from Crohn’s disease affects how these acids are absorbed, they are instead
49
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
excreted into the colon and the fat-soluble vitamins contained within them
are not absorbed. Consequently, fatty acid secretion into the large intestine
leads to abdominal cramping and resultant diarrhea and fluid loss through
stool.
Abdominal cramping is often associated with disease severity; consequently,
a person with mild symptoms of IBD may have only mild, irregular
abdominal cramps, while someone with severe inflammation and frequent
diarrhea may be more likely to suffer from regular bouts of cramping and
pain. Treatment of abdominal cramps may best be achieved by managing
the underlying bowel disease through medical therapies designed to control
inflammation. When cramping precedes or is associated with diarrhea,
control of loose stools through antidiarrheal agents that improve motility
may also be helpful in relieving abdominal cramps. Pain relievers such as
acetaminophen and ibuprofen are generally not efficient in easing the pain of
abdominal cramps.
Antispasmodic medications such as hyocyamine and mebeverine may help to
control smooth muscle contractions in the intestinal tract that contribute to
abdominal cramps. They generally attach to certain receptor sites in the
intestinal tract or act as smooth muscle relaxants to relieve spasms and
abnormal contractions in the intestinal tract. It should be noted that use of
these drugs, as with some other preparations designed to treat symptoms of
IBD, do not completely stop the symptoms and only alleviate their severity.
Treating IBD and using medical therapies to help a patient achieve remission
is one of the only methods of truly eliminating the intestinal cramps that
often occur as symptoms of the disease.
50
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Weight Loss
Weight loss is a symptom that often occurs over time as the affected patient
develops malnutrition and has difficulty absorbing important nutrients.
Weight loss may develop in a patient with IBD for various reasons, whether
related to malnutrition due to poor nutrient absorption, because of social
factors related to eating, or because of loss of important nutrients through
frequent and excessive bowel movements and diarrhea.
One of the more common reasons for weight loss in patients with IBD is
because of malabsorption of nutrients in the gastrointestinal tract. The small
intestine is responsible for absorption of a significant amount of nutrients to
be used by the body for energy and to maintain overall health.
Carbohydrate, fat, and protein absorption, as well as absorption of important
vitamins and minerals takes place almost exclusively in the small intestine,
which allows the body to continue to maintain healthy organs and tissues.
When areas of intestinal absorption become damaged due to IBD, the
patient may take in fewer nutrients and more materials may be excreted,
unabsorbed in the stool. Over time, the frequent loss of nutrients that occurs
during disease flares can lead to electrolyte imbalances, anemia, and weight
loss when nutrients are not replenishing the body.
Loss of appetite is common with IBD. A person diagnosed with the disease
may have a general distaste for food and little desire to eat due to the
effects of eating, which sometimes causes rapid symptoms of abdominal
pain and diarrhea. A patient may avoid eating to prevent symptoms, further
contributing to weight loss. Other effects of symptoms, such as anemia and
fatigue, may make eating a chore and the individual may have too little
energy to consume much food. Depression because of having a chronic
51
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
illness, as well as anxiety over when symptoms may develop can also cause
a loss of interest in eating and in food overall, as well as contributing to
weight loss and a decrease in overall appearance and self-care.
Frequent diarrhea associated with IBD may be another factor that
contributes to weight loss. As with damage to the intestinal tract that causes
a lack of absorption of important nutrients, diarrhea also prevents nutrient
absorption when the transit time of food is greatly increased through the
intestinal tract. Instead of getting adequate nutrients from food, the body
uses what it has in storage, which can quickly deplete any reserves and can
lead to weight loss. A patient with IBD, particularly after a period of time
spent struggling with pain and other symptoms, often not only struggles
with weight loss, but also develops a general appearance of being unwell. In
addition to other symptoms, he/she may also suffer from fatigue, lethargy,
and malaise, as well as fever and complaints of joint and muscle pain, which
can significantly impact overall activity levels. Symptoms that are unrelated
to the gastrointestinal tract often occur during a flare when other
gastrointestinal symptoms are also present.
People with IBD may need to increase their calorie intake to avoid excess
weight loss. This is especially important during times of disease flares when
excess diarrhea, vomiting, or bloody stool is present. Patients should be
taught about the importance of continuing to eat and selecting the correct
foods that will minimize symptoms but still provide energy. An increase of
500 calories per day during times of active symptoms may be necessary for
some people with IBD to prevent consistent weight loss. Depending on a
patient’s general state of health and the associated symptoms of IBD, a diet
plan may be necessary to ensure that the patient is able to take in enough
calories to maintain a normal weight. A registered dietitian may be able to
52
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
guide the patient toward making appropriate food choices that will ensure
adequate nutrient intake. Additionally, the treatment of other symptoms
associated with IBD can prevent some weight loss by averting some of the
causes of malabsorption and diarrhea. By getting control of other symptoms,
resulting weight loss can be controlled and minimized.
Diagnosis Of Inflammatory Bowel Disease
Diagnosis of inflammatory bowel disease requires testing to specifically
identify the disease present and to rule out other forms of gastrointestinal
illness, such as diverticulitis, celiac disease, or irritable bowel syndrome. In
patients with ulcerative colitis and Crohn’s disease, there are no exact tests
that will definitively diagnose the conditions; instead, diagnosis is often one
of exclusion of other illnesses when the disease presents with characteristic
symptoms and diagnostic measures identify its typical manifestations.66-80,100
For some, diagnosis may take months or years to achieve, particularly when
symptoms are intermittent and occur only during flares. For example, in the
case of Behcet’s disease, an affected patient may have intermittent
abdominal pain, rectal bleeding, and diarrhea that occur over the course of
several months. Testing may confirm that the patient has an IBD, but it may
take months to actually determine that it is Behcet’s disease and not another
inflammatory condition. While it is helpful to know that an IBD is the cause
of a patient’s symptoms, certain illnesses may be treated in slightly different
ways, so it is important to also know which type of IBD is present to better
determine the course of treatment.
Some diagnostic tests are routine for anyone seeking help for IBD
symptoms. A patient may need initial laboratory testing, such as a complete
blood count and metabolic panel, to determine if underlying factors are
53
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
present, including anemia, infection, or electrolyte imbalances. C-reactive
protein (CRP) is often ordered initially to determine the presence of
inflammation; an erythrocyte sedimentation rate (ESR) may or may not be
included as part of an initial examination as well. Often, a stool sample is
necessary to check for occult blood, the presence of infection or pus, or
excess fat in stool and to determine consistency, such as in the cases of
chronic diarrhea. There is not one particular type of infectious organism
causing IBD that may be found in a stool sample, but there may be
indicators of infection or bleeding, including pus, mucus, and blood in the
stool.
Radiographic images, including abdominal x-rays, are normally not
performed as part of diagnostic testing, unless a patient is suffering from
such severe symptoms that performing endoscopic procedures would be
damaging and too invasive. Abdominal x-rays can be useful in detecting
some complications that have developed as a result of IBD, including toxic
megacolon or intestinal perforation, so these kinds of tests are often
employed when a patient presents with severe symptoms that indicate
complications, rather than as part of routine diagnosis of IBD.
Physical examination is of some benefit to determine if there are obvious
outward signs of IBD, as well as to assess for any extra-intestinal disease
manifestations. The health clinician should assess a patient’s history for
connections that could indicate a diagnosis of IBD, including assessment of
family history of the disease, as well as the frequency and severity of
diarrhea and other symptoms present, including their effects on overall
health and wellbeing. An examination of a patient’s abdomen usually does
not reveal IBD, but it could identify particular areas of tenderness and pain,
as well as any masses or bulges that are associated with another illness and
54
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
that would most likely rule out IBD. A visual inspection of the anus and the
perineum may be necessary if the patient complains of rectal bleeding or has
lesions and ulcerations on the anus. A digital rectal examination may be
needed in cases of perianal Crohn’s disease. Inspection of the perianal area
may show fissures, fistulas, or lesions on the skin and at the anal opening.
The digital examination can help the clinician to determine whether stenosis,
skin tags, or strictures are present in the anus, but the process should be
done very gently to avoid further tissue trauma.
When identifying and diagnosing IBD most measures involve inspection and
assessment of the intestinal tract to look for characteristic signs of
inflammation and ulcers. Diagnostic procedures often include an assessment
of stool to check for the presence of inflammation in the gut, visual
inspection of the intestinal tract through endoscopy, and evaluating tissue
samples through biopsy.
Inflammatory Markers in Stool
Markers of inflammation found in stool can identify the presence of
inflammatory disease. These biomarkers may also help to predict the course
of the disease and its severity. When inflammation is present in the
intestinal tract, biomarkers will be shed by the inflamed mucosa into the
stool; when a stool sample is checked and these markers are present, the
clinician can know that inflammation is occurring somewhere along the
intestinal tract. Biomarkers of inflammation may indicate the presence of
other inflammatory diseases of the gastrointestinal tract as well, so they are
not necessarily specific for IBD, but they do provide an initial indication of
inflammation.
55
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Calprotectin is one of the main inflammatory markers found in stool when
inflammation is present. It is a type of antimicrobial protein found within
several kinds of white blood cells. Lehmann, et al., in Therapeutic Advances
in Gastroenterology note that calprotectin is most often found in neutrophilic
granulocytes, the most abundant type of white blood cell, in which
calprotectin makes up almost 60 percent of the cytoplasm within its cells.100
Calprotectin is also found in other cells of the immune system, including
within macrophages and monocytes. When there is excess inflammation in
the intestinal tract, the inflammatory cells will release calprotectin in the
stool as evidence. While the presence of calprotectin does not specifically
provide a diagnosis of IBD, the biomarker is elevated in stool samples of
patients with ulcerative colitis and Crohn’s disease and its presence can
differentiate whether the patient has an inflammatory disease or some other
type of gastrointestinal disorder, such as irritable bowel syndrome.
Calprotectin, as a biomarker, can be found in other body fluids in addition to
stool, including in plasma, urine, synovial fluid, cerebrospinal fluid, and
saliva. It is also detected upon biopsy when a sample of tissue from the
affected area of the intestinal tract is obtained. However, the stool test for
calprotectin is simple and straightforward and is most often used for
detecting inflammatory bowel disease. A patient may provide a stool sample
for analysis. Because calprotectin is typically found throughout stool in a
homogenous pattern rather than settling in certain areas of the sample,
almost any test area of the stool can indicate the existence of calprotectin
when it is present. This method of testing is an inexpensive and
straightforward approach to initially identifying inflammation in a noninvasive manner.
56
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
A second type of inflammatory biomarker, lactoferrin, may also be detected
in stool in patients with inflammatory bowel disease. Lactoferrin is a
glycoprotein that is also released by neutrophils in the intestinal tract. When
inflammation develops in the intestine, neutrophils move from the
bloodstream into the mucosal wall to engulf antigens and protect the body
as part of the immune response. The lactoferrin released from these white
blood cells is then shed into the stool, the presence of which can be
assessed after a patient has a bowel movement and provides a stool sample.
As with calprotectin, fecal lactoferrin levels can differentiate between
inflammatory conditions such as IBD and other gastrointestinal disorders
that may have similar symptoms, including irritable bowel syndrome.
Studies have shown that elevated levels of lactoferrin in the stool are
indicative of inflammation caused by IBD, particularly in cases of moderateto-severe inflammatory disease. Lactoferrin is stable within a stool sample
and like calprotectin, it can be tested with relative ease and speed after
obtaining a stool sample from a patient. Lactoferrin is not specifically
diagnostic of IBD; however, it can be used as a screening process to
differentiate from IBS, it can assess the severity of flares in patients already
diagnosed with IBD, and it can determine whether a patient undergoing a
workup for potential IBD requires further testing through endoscopy.
In addition to testing inflammatory markers in stool, the health clinician may
need to check stool for occult blood and may perform a stool culture to
assess for infection within the gastrointestinal tract. Because some kinds of
intestinal infections, such as C. difficile infection, can cause similar
symptoms to IBD and may even demonstrate inflammatory biomarkers in
the stool, further confirmatory testing is often necessary. When
inflammatory markers are present in the stool, further testing through
57
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
endoscopy is typically required to support this evidence and to definitively
diagnose IBD.
Colonoscopy
The main test used for diagnosis of
IBD is colonoscopy, a visual
inspection of the components of the
large intestine. Colonoscopy is
considered the gold standard in
diagnosing IBD; the test determines
the presence of IBD, its extent and
severity, and it can differentiate
Crohn’s disease from ulcerative
colitis. Colonoscopy enables the
endoscopist to visualize the lining of
the gastrointestinal tract and to view
the condition of the tissues involved.
It also allows for tissue sampling for
biopsy, which can aid with the final
diagnosis of the type of IBD, as well as rule out other possible causes of the
patient’s symptoms, including cancer.
Colonoscopy is also valuable in that it can act as a guide for treatment.
Depending on the extent of damage present and the condition of the tissue
within the gastrointestinal tract, the clinician may have a better idea of the
most appropriate course to take for treatment, including administration of
specific types of medications or surgery as part of management of the
condition. Often, colonoscopy is performed early in the diagnostic process,
before implementing other measures. The European Crohn’s and Colitis
58
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
Organization (ECCO) recommends that an ileocolonoscopy should be
performed shortly after a patient is referred for diagnosis of IBD and possibly
before introducing any medical therapies. An ileocolonoscopy is an
endoscopic examination of the ileum of the small bowel and of the colon.
The American Society for Gastrointestinal Endoscopy (ASGE) has the same
recommendations for IBD diagnosis. This is because therapy through use of
medications may obscure some of the evidence of inflammation that might
normally be seen upon colonoscopy.
When Crohn’s disease that affects the colon or when ulcerative colitis of the
large intestine is suspected, standard colonoscopy, with or without
examination of the ileum, is warranted. Colonoscopy allows for inspection of
the mucosal lining of the large intestine, including that of the rectum, the
colon, and the terminal ileum. Based on the appearance of the affected
tissue, colonoscopy cannot only identify inflammatory bowel disease, but it
can often differentiate between ulcerative colitis and Crohn’s disease. This
type of examination is effective in distinguishing between the two conditions
in 90 percent of cases.
Patients with ulcerative colitis may begin with flexible sigmoidoscopy as part
of endoscopic diagnostic procedures. Flexible sigmoidoscopy allows the
healthcare provider to visualize and sample the tissue at the distal end of
the gastrointestinal tract and to determine whether the disease has spread
beyond the sigmoid portion of the large intestine. The tube used with a
sigmoidoscope is shorter than that used with colonoscopy; alternatively, the
scope used with colonoscopy is longer and more flexible. Flexible
sigmoidoscopy is also particularly effective when a patient is suffering from
inflammation that is located primarily in the rectum but not in other parts of
the large intestine. It may also be used for patients with Crohn’s disease,
59
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
but because Crohn’s tends to impact more areas of the gastrointestinal tract
distal to the sigmoid colon, sigmoidoscopy is less often used as a first-line
method of diagnosis.
A diagnosis of IBD is initially made based on the appearance of the intestinal
tract. The tissue may have a grainy texture and it bleeds easily when
touched. In severe cases, the lining of the gastrointestinal tract may ooze or
bleed freely with no stimulation. The greater the severity of the disease and
the longer time period a patient has been struggling with symptoms, the
clinician can expect to see more tissue damage upon colonoscopy. Over
time, the appearance of the intestinal lining becomes pocked and has deep
grooves; the ulcerations may extend to form one or two very large areas of
macerated tissue, rather than single areas of ulcers. Abscesses and infection
may lead to the release of pus or purulent exudate.
Crohn’s disease demonstrates a cobblestone appearance, deep ulcers with
skip lesions, and potential involvement of the ileocecum. Fistulas are often
more common with Crohn’s disease when compared to ulcerative colitis and
there may be rectal sparing, in which the rest of the colon is affected but the
rectum is not. Alternatively, characteristics that differentiate ulcerative colitis
from Crohn’s disease include continuous areas of inflammation that may
extend into the rectum and the anus, abnormal blood vessel patterns, and
superficial ulcerations. Ulcerative colitis also sometimes demonstrates a
cecal patch of inflammation, in which disease features center around the
appendix and the cecum. Strictures and narrowing associated with colonic
obstruction tend to be less common in ulcerative colitis and are more
frequently seen with Crohn’s disease.
60
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
A patient should undergo colonoscopy if there is evidence of complications of
IBD, such as toxic megacolon. The procedure of performing a colonoscopy is
relatively straightforward and typically painless for the patient. Most people
have more trouble with the preparation requirements of the procedure,
rather than the actual process, as preparation often requires clearing the
colon with a laxative and following a clear liquid diet beforehand. Patients
should avoid any elements that may give evidence of intestinal
inflammation, such as by using NSAIDs, prior to colonoscopy. If
inflammatory markers are not present in the stool, a patient with suspected
IBD may still need colonoscopy to officially evaluate the intestinal tract.
Colonoscopy should be done for any patient who is suffering from severe
symptoms suggestive of IBD, such as iron deficiency anemia, rectal
bleeding, and weight loss, to examine the intestinal tract and to determine
whether the symptoms have an inflammatory cause or if they are related to
another type of gastrointestinal illness.
Biopsy
Biopsy of the mucosal tissue is an essential part of the diagnostic process.
Mucosal biopsy is needed to determine whether a patient is suffering from a
type of inflammatory bowel disease or another form of illness that causes
intermittent inflammation and/or tissue damage. Following biopsy, the tissue
is examined for histologic manifestations specifically associated with certain
types of IBD. Because distinctive forms of inflammatory bowel disease may
manifest differently when examined microscopically, histological evidence is
needed through biopsy to confirm. For example, microscopic colitis, which
consists of lymphocytic and collagenous forms, appears differently when
examined under a microscope when compared to some other segments of
inflammatory bowel.
61
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
There is not one specific type of histological criteria available that
differentiates IBD from other types of colitis. In other words, examination of
a tissue biopsy can only pinpoint what is most likely to be IBD based on
inflammation and the presence of certain biomarkers, but the presence of
inflammation upon biopsy examination does not definitively diagnose IBD.
More than one tissue sample is often needed to get an accurate picture of
the condition. During the initial evaluation, the American Society for
Gastrointestinal Endoscopy (ASGE) suggests taking at least 2 biopsy
specimens from 5 sites throughout the portion of the bowel examined,
including the ileum and the rectum.
A patient undergoing testing for IBD diagnosis may have a colonoscopy with
one or more tissue samples taken to distinguish the type of inflammatory
condition present. A tissue biopsy allows the pathologist to determine
whether IBD is present and to differentiate what type of inflammatory
disease has developed; and, a tissue biopsy provides information to assess a
patient’s clinical state and the progression of the disease. Depending on how
long a patient had the disease, the tissue samples for biopsy may show
variations in cellular appearance suggestive of different stages of disease
and healing. James Kyle, author of the book Crohn’s Disease, suggests that
histopathological examination of tissues during biopsy should be considered
on a spectrum, rather than having a single, exact manifestation. Cellular
manifestations that lie within this spectrum could be better indications of an
IBD diagnosis.
Upon biopsy examination, Crohn’s disease exhibits a granulomatous
appearance and the tissue may be thickened, solidified, and inflamed.
Because Crohn’s disease is most common in the ileocecal region of the
intestinal tract, there is often a greater amount of affected tissue located in
62
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
the terminal ileum when compared to other areas of the colon. The surface
of the mucosa appears wrinkled with the cobblestone appearance; upon
microscopic examination, there may be pockets or clusters of cells and small
nodules. There are often collections of white blood cells present due to
inflammation and some blood vessels may be more prominent in the
submucosal layer of tissue. Alternatively, ulcerative colitis may appear
differently upon histological examination. The tissue is damaged from the
inflammation and there are often greater numbers of neutrophils present.
These white blood cells may have invaded the crypts of the intestinal wall
layers and the depths of the crypts may be shortened somewhat. The Paneth
cells may have an abnormal appearance and there are greater numbers of
certain cells present, including lymphocytes and plasma cells.
Diagnosis of other types of IBD often requires biopsy of tissue, as diagnosis
following symptoms or visual inspection of the intestinal tract does not
always provide confirmation. For example, Behcet’s disease, because it
causes skin lesions in addition to gastrointestinal inflammation, often
requires a skin biopsy to confirm this specific type of IBD. Diagnosis of
Behcet’s may be made following a biopsy of lesions from the mouth,
genitals, or skin that develop with this disease.
In some cases, strictures are present in the gastrointestinal tract; these
occur when the intestinal lumen is narrowed, often from damage due to
inflammation. There is a small risk that strictures develop because of tissue
hyperplasia, in which the tissue grows abnormally out of control because it
contains cancerous cells. When strictures are present, a patient may need to
have a biopsy of some of the tissue to determine its substance and to ensure
that the tissue is not malignant. Cancerous cells are much less commonly
the cause of strictures; instead, they are more likely to develop due to
63
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
inflammation and tissue damage, but it is still important to rule out
malignancy when strictures develop.
A colonoscopy with biopsy is often performed when considering a patient
with IBD as a possible surgical candidate. Patients with abnormal cell
proliferation in the intestinal tract, as seen with colonoscopy, become
surgical candidates for colectomy because of the increased risk of cancer due
to cell abnormalities. This abnormal cell proliferation, known as dysplasia, is
graded according to its appearance and size. Many surgeons, upon
discovering dysplasia in the large intestine, will consider a patient as a
colectomy candidate to reduce cancer risk. In fact, the presence of
dysplasia, regardless of its size and grade, is an indication for colectomy.
Ulcerative colitis and Crohn’s disease increase the risk of colorectal cancer
when compared to those in the general population. People who have more
severe conditions of colitis and larger portions of the colon affected seem to
be at greater risk of colorectal cancer when compared to those who have
milder cases of the disease. Additionally, those who have one-third or more
of the colon affected seem to have a higher risk of cancer development,
according to the Crohn’s and Colitis Foundation of America (CCFA).
Patients with extensive disease and symptoms should have routine
colonoscopies as directed by their physicians; these tests should also include
tissue biopsies from different sections of the intestinal tract to assess for
cancerous lesions. Colonoscopy and biopsy are used as part of diagnosis of
inflammatory bowel disease in its initial presentation and to differentiate the
specific form of the disease; additionally, biopsy may be needed when there
are signs of malignancy, and also after a patient has been diagnosed with
64
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
IBD due to the increased risk of cancer associated with this type of bowel
disease.
Summary
Despite some of the differences in clinical manifestations and histology
between the different forms of inflammatory bowel disease (IBD), there has
yet to be confirmation of the exact reason why some people develop the
intestinal inflammation and tissue damage associated with this illness. There
are various theories on the potential causes of IBD. Research investigations
have focused on several contributing factors of gut inflammation with
promising outcomes identifying the reason why some people develop IBD.
However, despite thorough research and extensive results in this area,
questions still remain.
There are only possible causes for IBD such as changes in the levels of
microorganisms (both aggressive and beneficial) in the gut, genetic factors,
predisposition to the disease, and the significance of family history;
additionally, important considerations include the role of diet, and the
pathophysiological effects of a break in the protective mucosal barrier of the
intestinal tract. Understanding the potential causes of inflammatory bowel
disease has improved. This has and will continue to improve the chances
that this illness can be successfully treated or may someday be prevented
from developing at all.
Please take time to help NurseCe4Less.com course planners evaluate the
nursing knowledge needs met by completing the self-assessment of
Knowledge Questions after reading the article, and providing feedback in
the online course evaluation.
Completing the study questions is optional and is NOT a course
requirement.
65
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
1.
The exact reason why some people develop intestinal
inflammation and tissue damage associated with inflammatory
bowel disease (IBD) is
a.
b.
c.
d.
2.
increased levels of microorganisms in the gut.
genetic; i.e., a patient will get IBD if an ancestor had it.
not exactly known.
always due to poor diet.
True or False: Dysbiosis is an imbalance in the number of
beneficial and aggressive bacteria normally found in the
intestinal tract.
a. True
b. False
3.
The gastrointestinal tract contains trillions of bacteria that are
said to
a.
b.
c.
d.
4.
Two of the most common forms include those from the
_________________________ phyla.
a.
b.
c.
d.
5.
interfere with metabolites.
be beneficial to sustaining normal intestinal functioning.
generally encourage harmful bacteria.
interfere with equilibrium in the gut.
Firmicutes and the Bacteroidetes
Eubacterium and Lactobacillus
Escherichia coli and Mycobacterium avium
Enterobacteriaceae and Listeria monocytogenes
Normally, the amounts of gut microbiota vary until age ___, and
microorganism levels remain stable until approximately age 70.
a.
b.
c.
d.
3
12
21
30
66
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
6.
People who have lower numbers of microbial genes are more
likely to have higher counts of
a.
b.
c.
d.
7.
Factors that may impact levels of gut microbiota include all of
the following EXCEPT
a.
b.
c.
d.
8.
pro-inflammatory bacteria in the intestinal tract.
antimicrobial molecules known as defensins.
microbiota that transform polyphenols.
Firmicutes and the Bacteroidetes.
diet.
socioeconomic status.
intestinal homeostasis.
use of antibiotics.
True or False: Irritable bowel syndrome is the most common
form of inflammatory bowel disease.
a. True
b. False
9.
When Clostridium difficile is present in the gastrointestinal tract,
it secretes small amounts of
a.
b.
c.
d.
microorganisms known as fungi.
Eubacterium and Lactobacillus.
toxins A and B.
tumor necrosis factor.
10. People with inflammatory bowel disease may have reduced
levels of beneficial bacteria such as
a.
b.
c.
d.
Lactobacillus.
Mycobacterium avium.
Enterobacteriaceae.
Listeria monocytogenes.
67
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
11. One of the most common, extra-intestinal manifestations of
inflammatory bowel disease that is not specifically associated
with bowel function is
a.
b.
c.
d.
Clostridium difficile.
dysbiosis.
intestinal homeostasis.
anemia.
12. Escherichia coli contribute to inflammation by adhering to
epithelial cells in the mucosa and secreting
a.
b.
c.
d.
toxins A and B.
hepcidin.
harmful bacteria.
tumor necrosis factor.
13. True or False: It is well-known that many patients with
inflammatory bowel disease have a family history of some type
of IBD.
a. True
b. False
14. Red blood cells carry oxygen to the body’s tissues but this
process may be affected because decreased iron in the body can
impact which of the following processes?
a.
b.
c.
d.
Production of biomarkers
An increase in hepcidin synthesis
Erythropoiesis
Autophagy
15. Variations in genes, such as a variant in the ATG16L1 gene, may
alter the immune system’s functioning and actually stimulate
cell destruction of normal tissue by the body, which is known as
a.
b.
c.
d.
autophagy.
intestinal homeostasis.
dysbiosis.
necrosis.
68
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
16. When iron is absorbed by the small intestine, it is bound to the
protein _______________ and then transported by this protein
to erythrocytes where it is used for erythropoiesis.
a.
b.
c.
d.
transferrin
defensin
hepcidin
ferroportin
17. True or False: When iron deficiency develops, hepcidin
production is suppressed; alternatively, when plasma iron stores
are elevated, hepcidin synthesis is increased.
a. True
b. False
18. Malabsorption of iron due to damaged intestinal tissue is seen
more commonly in patients with ________________ who have
involvement of the small intestine.
a.
b.
c.
d.
irritable bowel syndrome
ulcerative colitis
Crohn’s disease
Behcet’s disease
19. Generally, the better option for pain relief for a patient who has
severe abdominal pain associated with an acute flare of
ulcerative colitis is the use of
a.
b.
c.
d.
pain relievers.
antispasmodic medications.
non-steroidal anti-inflammatory agents (NSAIDs).
opioid analgesics.
20. A C-reactive protein (CRP) blood test may be ordered for a
patient with IBD symptoms to determine the presence of what
condition?
a.
b.
c.
d.
Anemia
Infection
Electrolyte imbalances
Inflammation
69
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
21. Radiographic images, including abdominal x-rays, are performed
as part of diagnostic testing for IBD
a.
b.
c.
d.
because it is less invasive than endoscopy.
only if endoscopy would damage the gastrointestinal tract.
on a routine basis.
if the type of IBD is indeterminate.
22. True or False: Iron deficiency and anemia develop when too
much iron is excreted, not because of a lack of iron absorption.
a. True
b. False
23. Vomiting that occurs as a result of pain from inflammation or
slowed motility (unrelated to gastric outlet obstruction) could
be managed with
a.
b.
c.
d.
antiemetic medications.
opioid analgesics.
pain relievers.
iron supplements.
24. The main test used for diagnosis of IBD is the
a.
b.
c.
d.
x-ray.
colonoscopy.
digital examination.
C-reactive protein (CRP) blood test.
25. A patient with regular vomiting may also try the following:
a.
b.
c.
d.
eat larger meals but less often.
try to eat smaller meals but more often.
consume more dairy products.
drink less to avoid vomiting.
70
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
26. The flexible sigmoidoscopy is particularly effective when a
patient is suffering from inflammation that is located primarily
in what part of the gastrointestinal tract?
a.
b.
c.
d.
The transverse colon
The large intestine
The rectum
All of the above
27. True or False: Based on the appearance of the affected tissue,
colonoscopy cannot only identify inflammatory bowel disease,
but it can often differentiate between ulcerative colitis and
Crohn’s disease.
a. True
b. False
28. Flexible sigmoidoscopy may also be used for patients with
Crohn’s disease
a.
b.
c.
d.
as a first-line method of diagnosis.
because this disease impacts the entire gastrointestinal tract.
impacts the ileum.
but not as a first-line method of diagnosis.
29. _______________________, a severe form of ulcerative colitis,
may occur in certain patients and can be the cause of significant
complications, including toxic megacolon and bowel perforation.
a.
b.
c.
d.
Irritable bowel syndrome
Diverticulitis
Fulminant colitis
Behcet’s disease
30. In some cases, strictures are present in the gastrointestinal
tract; these occur when the intestinal lumen is ____________,
often from damage due to inflammation.
a.
b.
c.
d.
perforated
narrowed
cancerous
widened
71
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
31. When strictures are present, a patient may need to have a
biopsy of some of the tissue to determine its substance and
a.
b.
c.
d.
to
to
to
to
ensure that the tissue is not malignant.
ensure that the tissue is not perforated.
identify the type of IBD.
identify gastric outlet obstruction.
32. True or False: Lactoferrin is a type of inflammatory biomarker
that may be detected in the stool of patients with inflammatory
bowel disease.
a. True
b. False
33. The term fulminant, which refers to a form of ulcerative colitis,
describes a condition that develops
a.
b.
c.
d.
very suddenly and severely.
slowing.
anywhere along the gastrointestinal tract.
inflammatory tissue over time.
34. Diarrhea associated with fulminant ulcerative colitis
a.
b.
c.
d.
is not usually accompanied by rectal bleeding.
typically occurs once a week.
is often sudden and explosive.
is rarely present.
35. True or False: Colonoscopy is effective in distinguishing between
ulcerative colitis and Crohn’s disease in 90 percent of cases.
a. True
b. False
36. Patients with dysplasia in the intestinal tract have what
condition?
a.
b.
c.
d.
Tumor necrosis factor
Imbalance in beneficial and aggressive bacteria
Severe anemia
Abnormal cell proliferation
72
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
37. Fulminant colitis is sometimes called
a.
b.
c.
d.
abdominal colitis.
irritable bowel syndrome.
toxic colitis.
diverticulitis.
38. True or False: Cancerous cells are commonly caused by
strictures.
a. True
b. False
39. In the case of Behcet’s disease, an affected patient may have
_________________ abdominal pain, rectal bleeding, and
diarrhea that occur over the course of several months.
a.
b.
c.
d.
intermittent
mild
daily
severe, hourly
40. A visual inspection of the anus and ________________ may be
necessary if the patient complains of rectal bleeding or has
lesions and ulcerations on the anus.
a.
b.
c.
d.
the transverse colon
the ileum
the perineum
All of the above
73
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
CORRECT ANSWERS:
1.
The exact reason why some people develop intestinal
inflammation and tissue damage associated with inflammatory
bowel disease (IBD) is
c. not exactly known.
p. 5: “Despite some of the differences in clinical manifestations and
histology between the different forms of inflammatory bowel
disease (IBD), there has yet to be confirmation of the exact reason
why some people develop the intestinal inflammation and tissue
damage associated with this illness.”
2.
True or False: Dysbiosis is an imbalance in the number of
beneficial and aggressive bacteria normally found in the
intestinal tract.
a. True
p. 7: “A condition known as intestinal dysbiosis occurs when there
is an imbalance of beneficial and harmful bacteria or organisms.”
3.
The gastrointestinal tract contains trillions of bacteria that are
said to
b. be beneficial to sustaining normal intestinal functioning.
p. 6: “Normally, the gastrointestinal tract contains trillions of
bacteria that are said to be beneficial to sustaining normal intestinal
functioning.”
4.
Two of the most common forms include those from the
_________________________ phyla.
a. Firmicutes and the Bacteroidetes.
p. 6: “There are various species of bacteria existing in the intestinal
tract; however, two of the most common forms include those from
the Firmicutes and the Bacteroidetes phyla.”
74
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
5.
Normally, the amounts of gut microbiota vary until age ______,
and microorganism levels remain stable until approximately age
70.
d. 30
p. 7: “Age is related to the number of microbes found in the gut;
the intestinal tracts of newborn infants are colonized at birth, while
children and adolescents may have varying proportions of
microorganisms, followed by stability of microorganism levels by
the age of 30 and remaining so until approximately age 70.”
6.
People who have lower numbers of microbial genes are more
likely to have higher counts of
a. pro-inflammatory bacteria in the intestinal tract.
p. 23: “People who are considered to have lower numbers of
microbial genes are more likely to have higher counts of proinflammatory bacteria in the intestinal tract, which may contribute
to inflammatory bowel disease.”
7.
Factors that may impact levels of gut microbiota include all of
the following EXCEPT
c. intestinal homeostasis.
p. 7: “A condition known as intestinal dysbiosis occurs when there
is an imbalance of beneficial and harmful bacteria or organisms.
Other elements that can impact levels of gut microbiota include
diet, use of antibiotics, ethnicity, and even socioeconomic status.”
8.
True or False: Irritable bowel syndrome is the most common
form of inflammatory bowel disease.
b. False
p. 37: “While IBD may be confused with irritable bowel syndrome,
the two conditions are not the same. However, there is mounting
evidence of a connection between inflammatory bowel disease and
irritable bowel syndrome (IBS).”
75
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
9.
When Clostridium difficile is present in the gastrointestinal tract,
it secretes small amounts of
c. toxins A and B.
p. 9: “For example, C. difficile, when present in the gastrointestinal
tract, secretes small amounts of toxins A and B, which can destroy
intestinal cells.”
10. People with inflammatory bowel disease may have reduced
levels of beneficial bacteria such as
a. Lactobacillus.
p. 11: “In addition to the presence of increased levels of certain
bacteria that contribute to inflammation with IBD, people with
inflammatory bowel disease have also been shown to have reduced
levels of certain types of microbiota in the intestinal tract, especially
those that are considered beneficial bacteria, including Eubacterium
and Lactobacillus.”
11. One of the most common, extra-intestinal manifestations of
inflammatory bowel disease that is not specifically associated
with bowel function is
d. anemia.
p. 26: “One of the most common manifestations of inflammatory
bowel disease that is not specifically associated with bowel function
is anemia, which is known as an extra-intestinal manifestation of
IBD.”
12. Escherichia coli contribute to inflammation by adhering to
epithelial cells in the mucosa and secreting
d. tumor necrosis factor.
p. 9: “E. coli contribute to inflammation by adhering to epithelial
cells in the mucosa and secreting tumor necrosis factor.”
76
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
13. True or False: It is well-known that many patients with
inflammatory bowel disease have a family history of some type
of IBD.
a. True
p. 21: “It is well known that many patients with inflammatory bowel
disease have a family history of some type of IBD.”
14. Red blood cells carry oxygen to the body’s tissues but this
process may be affected because decreased iron in the body can
impact which of the following processes?
c. Erythropoiesis.
p. 27: “Decreased iron in the body, whether through inadequate
iron stores, poor dietary intake, malabsorption, or through blood
loss can impact erythropoiesis and results in poor oxygen delivery
through diminished production of hemoglobin.”
15. Variations in genes, such as a variant in the ATG16L1 gene, may
alter the immune system’s functioning and actually stimulate
cell destruction of normal tissue by the body, which is known as
a. autophagy.
pp. 23-24: “There are some genetic polymorphisms of ATG16L1
that alter the immune system’s functioning and actually stimulate
cell destruction of normal tissue. When the immune system is
stimulated to this destruction, known as autophagy, the process
affects how antigens are exhibited and the immune response may
not be activated at the appropriate times. In other words, when
autophagy occurs, the body may be destroying healthy cells but
failing to recognize the presentation of antigens that it should be
fighting off instead.”
77
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
16. When iron is absorbed by the small intestine, it is bound to the
protein _______________ and then transported by this protein
to erythrocytes where it is used for erythropoiesis.
a. transferrin
p. 27: “When iron is absorbed by the small intestine, it is shifted to
transferrin, which is created in the liver. This transferrin can then
move iron to erythrocytes where it is needed for erythropoiesis.”
17. True or False: When iron deficiency develops, hepcidin
production is suppressed; alternatively, when plasma iron stores
are elevated, hepcidin synthesis is increased.
a. True
p. 27: “When iron deficiency develops, hepcidin production is
suppressed. Alternatively, when plasma iron stores are elevated,
hepcidin synthesis is increased.”
18. Malabsorption of iron due to damaged intestinal tissue is seen
more commonly in patients with ________________ who have
involvement of the small intestine.
c. Crohn’s disease
p. 28: “Malabsorption of iron due to damaged intestinal tissue is
another cause of iron deficiency anemia. This condition is seen
more commonly in patients with Crohn’s disease who have
involvement of the small intestine.”
19. Generally, the better option for pain relief for a patient who has
severe abdominal pain associated with an acute flare of
ulcerative colitis is the use of
d. opioid analgesics.
p. 35: “A patient who is having an acute flare of ulcerative colitis
may complain of severe abdominal pain that is unrelieved by pain
relievers or antispasmodic medications designed to treat cramps
and spasms in the gut.… Use of non-steroidal anti-inflammatory
agents (NSAIDs), while effective in managing a patient’s pain and
inflammation from extra-intestinal symptoms, are not usually
warranted for abdominal pain associated with IBD.… Other options
78
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
that have been used as alternatives for pain relief include opioid
analgesics, antidepressants, and anticonvulsants.”
20. A C-reactive protein (CRP) blood test may be ordered for a
patient with IBD symptoms to determine the presence of what
condition?
d. Inflammation
pp. 53-54: “Some diagnostic tests are routine for anyone seeking
help for IBD symptoms. A patient may need initial laboratory
testing, such as a complete blood count and metabolic panel, to
determine if underlying factors are present, including anemia,
infection, or electrolyte imbalances. C-reactive protein (CRP) is
often ordered initially to determine the presence of inflammation;
an erythrocyte sedimentation rate (ESR) may or may not be
included as part of an initial examination as well.”
21. Radiographic images, including abdominal x-rays, are performed
as part of diagnostic testing for IBD
b. only if endoscopy would damage the gastrointestinal tract.
p. 54: “Radiographic images, including abdominal x-rays, are
normally not performed as part of diagnostic testing, unless a
patient is suffering from such severe symptoms that performing
endoscopic procedures would be damaging and too invasive.”
22. True or False: Iron deficiency and anemia develop when too
much iron is excreted, not because of a lack of iron absorption.
b. False
p. 29: “As a result, iron deficiency and anemia develop not when
too much iron is excreted, but rather as a lack of appropriate iron
absorption.”
79
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
23. Vomiting that occurs as a result of pain from inflammation or
slowed motility (unrelated to gastric outlet obstruction) could
be managed with
a. antiemetic medications.
p. 42: “Treatment of vomiting often depends on its cause. Vomiting
that occurs as a result of pain from inflammation or slowed motility
(unrelated to gastric outlet obstruction) could be managed with
antiemetic medications.”
24. The main test used for diagnosis of IBD is the
b. colonoscopy.
p. 58: “The main test used for diagnosis of IBD is colonoscopy, a
visual inspection of the components of the large intestine.”
25. A patient with regular vomiting may also try the following:
b. try to eat smaller meals but more often.
p. 42: “A patient with regular vomiting may also try to eat smaller,
more frequent meals and should continue to try to drink fluids to
avoid dehydration.”
26. The flexible sigmoidoscopy is particularly effective when a
patient is suffering from inflammation that is located primarily
in what part of the gastrointestinal tract?
c. The rectum
p. 59: “Flexible sigmoidoscopy is also particularly effective when a
patient is suffering from inflammation that is located primarily in
the rectum but not in other parts of the large intestine.”
80
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
27. True or False: Based on the appearance of the affected tissue,
colonoscopy cannot only identify inflammatory bowel disease,
but it can often differentiate between ulcerative colitis and
Crohn’s disease.
a. True
p. 59: “Based on the appearance of the affected tissue, colonoscopy
cannot only identify inflammatory bowel disease, but it can often
differentiate between ulcerative colitis and Crohn’s disease.”
28. Flexible sigmoidoscopy may also be used for patients with
Crohn’s disease
d. but not as a first-line method of diagnosis.
p. 59: “Flexible sigmoidoscopy is also particularly effective when a
patient is suffering from inflammation that is located primarily in
the rectum but not in other parts of the large intestine. It may also
be used for patients with Crohn’s disease, but because Crohn’s
tends to impact more areas of the gastrointestinal tract distal to the
sigmoid colon, sigmoidoscopy is less often used as a first-line
method of diagnosis.”
29. _______________________, a severe form of ulcerative colitis,
may occur in certain patients and can be the cause of significant
complications, including toxic megacolon and bowel perforation.
c. Fulminant colitis
p. 44: “Fulminant colitis, a severe form of ulcerative colitis, may
occur in certain patients and can be the cause of significant
complications, including toxic megacolon and bowel perforation.”
30. In some cases, strictures are present in the gastrointestinal
tract; these occur when the intestinal lumen is ____________,
often from damage due to inflammation.
b. narrowed
p. 63: “In some cases, strictures are present in the gastrointestinal
tract; these occur when the intestinal lumen is narrowed, often
from damage due to inflammation.
81
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
31. When strictures are present, a patient may need to have a
biopsy of some of the tissue to determine its substance
a. and to ensure that the tissue is not malignant.
p. 63: “When strictures are present, a patient may need to have a
biopsy of some of the tissue to determine its substance and to
ensure that the tissue is not malignant.”
32. True or False: Lactoferrin is type of inflammatory biomarker that
may be detected in the stool of patients with inflammatory
bowel disease.
a. True
p. 57: “A second type of inflammatory biomarker, lactoferrin, may
also be detected in stool in patients with inflammatory bowel
disease.”
33. The term fulminant, which refers to a form of ulcerative colitis,
describes a condition that develops
a. very suddenly and severely.
p. 44: “Fulminant colitis, a severe form of ulcerative colitis, may
occur in certain patients and can be the cause of significant
complications, including toxic megacolon and bowel perforation. The
term fulminant describes a condition that develops very suddenly
and severely.”
34. Diarrhea associated with fulminant ulcerative colitis
c. is often sudden and explosive.
p. 44: “The term fulminant describes a condition that develops very
suddenly and severely. People with fulminant ulcerative colitis tend
to have significant diarrhea, evidenced by over 10 loose stools each
day, as well as continuous rectal bleeding. The diarrhea associated
with fulminant ulcerative colitis is often sudden and explosive,
leading to loss of large volumes of stool and fluid.”
82
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
35. True or False: Colonoscopy is effective in distinguishing between
ulcerative colitis and Crohn’s disease in 90 percent of cases.
a. True
p. 59: “Based on the appearance of the affected tissue, colonoscopy
cannot only identify inflammatory bowel disease, but it can often
differentiate between ulcerative colitis and Crohn’s disease. This
type of examination is effective in distinguishing between the two
conditions in 90 percent of cases.”
36. Patients with dysplasia in the intestinal tract have what
condition?
d. Abnormal cell proliferation
p. 64: A colonoscopy with biopsy is often performed when
considering a patient with IBD as a possible surgical candidate.
Patients with abnormal cell proliferation in the intestinal tract,
dysplasia as seen with colonoscopy, become surgical candidates for
colectomy because of the increased risk of cancer due to cell
abnormalities. This abnormal cell proliferation, known as dysplasia,
is graded according to its appearance and size. Many surgeons,
upon discovering dysplasia in the large intestine, will consider a
patient as a colectomy candidate to reduce cancer risk. In fact, the
presence of dysplasia, regardless of its size and grade, is an
indication for colectomy.”
37. Fulminant colitis is sometimes called
c. toxic colitis.
p. 44: “In addition to severe diarrhea, other symptoms associated
with fulminant colitis include abdominal pain and bloating, anorexia,
and fever. The condition is also sometimes called toxic colitis.”
38. True or False: Cancerous cells are commonly caused by
strictures.
b. False
pp. 63-64: “Cancerous cells are much less commonly the cause of
strictures; instead, they are more likely to develop due to
inflammation and tissue damage, but it is still important to rule out
83
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
malignancy when strictures develop.”
39. In the case of Behcet’s disease, an affected patient may have
_________________ abdominal pain, rectal bleeding, and
diarrhea that occur over the course of several months.
a. intermittent
p. 53: “For example, in the case of Behcet’s disease, an affected
patient may have intermittent abdominal pain, rectal bleeding, and
diarrhea that occur over the course of several months.”
40. A visual inspection of the anus and ________________ may be
necessary if the patient complains of rectal bleeding or has
lesions and ulcerations on the anus.
c. the perineum
p. 55: “A visual inspection of the anus and the perineum may be
necessary if the patient complains of rectal bleeding or has lesions
and ulcerations on the anus.”
References Section
The References below include published works and in-text citations of
published works that are intended as helpful material for your further
reading.
1.
2.
3.
Nair, M., Peate, I. (2015). Pathophysiology for nurses at a glance.
Malden, MA: John Wiley & Sons, Ltd.
Peppercorn, M., Kane, S. (2016, Sep.). Patient education: Ulcerative
colitis (beyond the basics). Retrieved from
http://www.uptodate.com/contents/ulcerative-colitis-beyond-thebasics
Parray, F., Wani, M., Malik, A., Wani, S., Bijli, A., Irshad, I., Ul-Hassan,
N. (2012, Nov.). Ulcerative colitis: A challenge to surgeons. Int J Prev
Med. 3(11): 749-763. Retrieved from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3506086/
84
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
National Institute of Arthritis and Musculoskeletal and Skin Diseases.
(2015, Aug.). Questions and answers about Behçet’s disease. Retrieved
from
http://www.niams.nih.gov/health_info/Behcets_Disease/default.asp
National Organization for Rare Disorders (NORD). (2015). Behçet’s
syndrome. Retrieved from http://rarediseases.org/rarediseases/behcets-syndrome/
Skef, W., Hamilton, M., Arayssi, T. (2015, Apr.). Gastrointestinal
Behçet’s disease: A review. World J Gastroenterol. 21(13): 3801-3812
Alves, R., Miszputen, S., Figueiredo, S. (2014, Apr.). Anemia and
inflammatory bowel disease: prevalence, differential diagnosis and
association with clinical and laboratory variables. Sao Paulo Med J.
132(3). Retrieved from
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S151631802014000300140
Crohn’s & Colitis.com. (2016). Understanding Crohn’s disease.
Retrieved from https://www.crohnsandcolitis.com/crohns
University of Maryland Medical Center. (2012, Dec.). Crohn’s disease.
Retrieved from
http://umm.edu/health/medical/reports/articles/crohns-disease
Kim, S. and Koh, H. (2015). Nutritional aspect of pediatric
inflammatory bowel disease: its clinical importance. Korean J. Pediatr.
Available online at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4644763/.
Crohn’s and Colitis Foundation of America. (2015, Jan.). Intestinal
complications. Retrieved from
http://www.ccfa.org/assets/pdfs/intestinalcomps.pdf
Crohn’s and Colitis Foundation of America. (2012, Sep.). Understanding
your risk: C. diff. Retrieved from
http://online.ccfa.org/site/PageNavigator/2012_09_enews_landing.htm
l
Crohn’s and Colitis Foundation of America. (2015, Jan.). Arthritis and
joint pain. Retrieved from
http://www.ccfa.org/assets/pdfs/arthritiscomplications.pdf
Jandhyala, S.M., et al. (2015). Role of the normal gut microbiota.
World J. Gastroenterol. Available online at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528021/.
Mace, O.J. and Marshall, F. (2015). Pharmacology and physiology of
gastrointestinal enteroendocrine cells. Pharmacol Res Perspect.
Available online at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4506687/.
Kansal, S., Wagner, J., Kirkwood, C., Catto-Smith., A. (2013).
Enteral nutrition in Crohn’s disease: An underused therapy.
Gastroenterology Research and Practice, Volume 2013, Article ID
85
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
482108, 11 pages. Retrieved from
https://www.hindawi.com/journals/grp/2013/482108/
Ruemmele, F. (2016). Role of diet in inflammatory bowel disease. Ann
Nutr Metab. 68(suppl 1): 33-41. Retrieved from
https://www.karger.com/Article/Pdf/445392
Crohn’s and Colitis Foundation of America (CCFA). (2013, Nov.). Diet,
nutrition, and inflammatory bowel disease. New York, NY: CCFA
Cheifetz, A., Cullen, G. (2016, Sep.). Patient education: Sulfasalazine
and the 5-aminosalicylates (beyond the basics). Retrieved from
http://www.uptodate.com/contents/sulfasalazine-and-the-5aminosalicylates-beyond-the-basics
Kabir, S., Kabir, S., Richards, R., Ahmed, J., MacFie, J. (2014, Aug.).
Pathophysiology, clinical presentation and management of diversion
colitis: A review of current literature. International Journal of Surgery.
Retrieved from http://dx.doi.org/10.1016/j.ijsu.2014.08.350
Harig, J., Soergel, K., Komorowski, R., Wood, C. (1989, Jan.).
Treatment of diversion colitis with short-chain-fatty acid irrigation. N
Engl J Med 1989; 320: 23-28.
Walfish, A., Companioni, R. (2016, Jan.). Drugs for inflammatory bowel
disease. Retrieved from
https://www.merckmanuals.com/professional/gastrointestinaldisorders/inflammatory-bowel-disease-ibd/drugs-for-inflammatorybowel-disease#v26161059
Rezaie, A., Kuenzig, M., Benchimol, E., Griffiths, A., Otley, A.,
Steinhart, A., Kaplan, G, Seow, C. (2015, Jun.). Budesonide for
treatment of people with active Crohn’s disease. Retrieved from
http://www.cochrane.org/CD000296/IBD_budesonide-for-treatmentof-people-with-active-crohns-disease.
Nitzan, O., Elias, M., Peretz, A., Saliba, W. (2016, Jan.). Role of
antibiotics for treatment of inflammatory bowel disease. World J
Gastroenterol. 22 (3): 1078-1087. Retrieved from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4716021/
Kennedy, A. (2015). The inflammatory response. Retrieved from
http://primer.crohn.ie/the-inflammatory-response
Strober, W., Fuss, I. (2011, May). Pro-inflammatory cytokines in the
pathogenesis of IBD. Gastroenterology 140(6): 1756-1767. Retrieved
from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773507/
Bowen, R. (2000, May). Gross and microscopic anatomy of the large
intestine. Retrieved from
http://arbl.cvmbs.colostate.edu/hbooks/pathphys/digestion/largegut/a
natomy.html
Peppercorn, M., Farrell, R. (2016, Sep.). Management of severe
ulcerative colitis in adults. Retrieved from
86
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
http://www.uptodate.com/contents/management-of-severe-ulcerativecolitis-in-adults
University of Alberta IBD Clinic. (2016). What are extra-intestinal
manifestations of IBD? Retrieved from http://www.ibdclinic.ca/what-isibd/complications/
Bayless, T., Hanauer, S. (2011). Advanced therapy of inflammatory
bowel disease (3rd ed.), Volume 1. Shelton, CT: People’s Medical
Publishing House USA
The University of Chicago Medicine. (2016). Frequently asked questions
about colectomy (colon resection). Retrieved from
http://www.uchospitals.edu/specialties/colorectal/services/colectomy.h
tml
Sandborn, W., et al. (2015, Apr.). Budesonide foam induces remission
in patients with mild to moderate ulcerative proctitis and ulcerative
proctosigmoiditis. Gastroenterology 148(4): 740-750. Retrieved from
http://www.gastrojournal.org/article/S0016-5085(15)00154-7/fulltext
American Cancer Society. (2014, Dec.). Types of ileostomies. Retrieved
from
http://www.cancer.org/treatment/treatmentsandsideeffects/physicalsid
eeffects/ostomies/ileostomyguide/ileostomy-types
Canadian Society of Intestinal Research. (2016). Ileo-anal reservoir (Jpouch) procedure. Retrieved from http://www.badgut.org/informationcentre/ostomies/ileo-anal-reservoir-j-pouch-procedure/
Rungoe, C., Langholz, E., Andersson, M., Basit, S., Nielsen, N.,
Wohlfahrt, J., Jess, T. (2013, Sep.). Changes in medical treatment and
surgery rates in inflammatory bowel disease: a nationwide cohort study
1979-2011. Gut 2014(63). 1607-1616.
Sartor, R., Mazmanian, S. (2012). Intestinal microbes in inflammatory
bowel diseases. Am J Gastroenterol Suppl 2012(1): 15-21. Retrieved
from
http://www.nature.com/ajgsup/journal/v1/n1/full/ajgsup20124a.html
Chamberlain, N., (2016, Feb.). Infections of the large intestine.
Retrieved from
https://www.atsu.edu/faculty/chamberlain/website/lectures/infectionso
fthelargeintestine.htm
Murthy, A., et al. (2014, Feb.). A Crohn’s disease variant in Atg16l1
enhances its degradation by caspase 3. Nature, 506; 456-462.
Retrieved from
http://www.nature.com/nature/journal/v506/n7489/full/nature13044.h
tml
Bowen, R. (2009, May). Paneth cells. Retrieved from
http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/pa
neth.html
87
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
Crohn’s and Colitis Foundation of America. (n.d.). Interaction between
a virus and the Crohn’s disease gene ATG16L1. [PowerPoint
presentation]. Retrieved from http://www.ccfa.org/assets/pdfs/broadfoundation/1437-cadwell-website-version.pdf
Jandhyala, S., Talukdar, R., Subramanyam, C., Vuyyuru, H., Sasikala,
M., Reddy, D. (2015, Aug.). Role of the normal gut microbiota. World J
Gastroenterol. 21(29): 8787-8803. Retrieved from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528021/
MetaHIT. (2010). The project objectives: association of bacterial genes
with human health and disease. Retrieved from
http://www.metahit.eu/index.php?id=351
Sochan, J., (2015, Jun.). Secretory immunoglobulin A (sIgA) for
healthy gut, digestion and immunity. Retrieved from
http://naturimedica.com/secretory-immunoglobulin-a-siga-for-healthygut-digestion-and-immunity/
Crohns.net. (n.d.). Mucosal immune system. Retrieved from
https://www.crohns.net/miva/education/articles/Hanaway_Mucosal_Im
mune_System_5of7.shtml
Saraswati, S., Sitaraman, R. (2015, Jan.). Aging and the human gut
microbiota – from correlation to causality. Front Microbiol. Retrieved
from
http://journal.frontiersin.org/article/10.3389/fmicb.2014.00764/full
Chong, C., et al. (2015, Aug.). Effect of ethnicity and socioeconomic
variation to the gut microbiota composition among pre-adolescents in
Malaysia. Scientific Reports 5; Article 13338. Retrieved from
http://www.nature.com/articles/srep13338
Rogler, G., Vavricka, S. (2015, Jan.). Anemia in inflammatory bowel
disease: an under-estimated problem? Front Med. Available at
http://journal.frontiersin.org/article/10.3389/fmed.2014.00058/full
Hartree, N. (2014, Oct.). Non-anaemic iron deficiency. Retrieved from
http://patient.info/doctor/non-anaemic-iron-deficiency
Lichtin, A. (2013, May). Iron deficiency anemia. Retrieved from
http://www.merckmanuals.com/professional/hematology-andoncology/anemias-caused-by-deficient-erythropoiesis/iron-deficiencyanemia
Dudkowiak, R., Neubauer, K., Poniewierka, E. (2013). Hepcidin and its
role in inflammatory bowel disease. Adv Clin Exp Med. 22(4): 585-591.
Johns Hopkins Medicine. (n.d.). Vitamin B12 deficiency anemia.
Retrieved from
http://www.hopkinsmedicine.org/healthlibrary/conditions/hematology_
and_blood_disorders/anemia_of_b12_deficiency_pernicious_anemia_8
5,P00080/
Lichtin, A. (2013, May). Anemia of chronic disease. Retrieved from
http://www.merckmanuals.com/professional/hematology-and88
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
oncology/anemias-caused-by-deficient-erythropoiesis/anemia-ofchronic-disease
Docherty, M., Jones, R., Wallace, M. (2011, Sep.). Managing pain in
inflammatory bowel disease. Gastroenterol Hepatol (NY). 7(9): 592601. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3264972/
American College of Gastroenterology (ACG). (2012, Oct.). Possible
overlap of IBS symptoms and inflammatory bowel disease. Science
Daily. Retrieved from
https://www.sciencedaily.com/releases/2012/10/121022081236.htm
Crohn’s and Colitis Foundation of America (CCFA). (2009, Apr.).
Managing flares and other IBD symptoms. New York NY: CCFA
Dyall-Smith, D. (2016). Orofacial Crohn disease. Retrieved from
http://www.dermnetnz.org/topics/orofacial-crohn-disease/
Zbar, A., Ben-Horin, S., Beer-Gabel, M., Eliakim, R. (2012, Mar.). Oral
Crohn’s disease: Is it a separable disease from orofacial
granulomatosis? A review. Journal of Crohn’s and Colitis 6(2): 135-142.
Steckstor, M., Adam, B., Pech, O., Tannapfel, A., Riphaus, A. (2013,
Jun.). Gastroduodenal Crohn’s disease. Video Journal and Encyclopedia
of GI Endoscopy 1(1): 178-179.
Bayless, T., Hanauer, S. (2011). Advanced therapy of inflammatory
bowel disease (3rd ed.), Volume 2. Shelton, CT: People’s Medical
Publishing House USA
Stamatakos, M., Karaiskos, I., Pateras, I., Alexiou, I., Stefanaki, C.,
Kontzoglou, K. (2012). Gastrocolic fistulae; From Haller till nowadays.
International Journal of Surgery 10(3): 129-133. Retrieved from
http://www.sciencedirect.com/science/article/pii/S1743919112000295
Scheck, S., Ram, R., Loveday, B., Bhagvan, S., Beban, G. (2014,
Dec.). Crohn’s disease presenting as gastric outlet obstruction. J Surg
Case Rep. 2014(12): rju 128. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255135/
Colon & Rectal Surgery Associates. (2016). What is ulcerative proctitis?
Retrieved from
http://www.colonrectal.org/services.cfm/sid:6694/ulcerative_proctitis/i
ndex.html
Gore, R., Levine, M. (2015). Textbook of gastrointestinal radiology (4th
ed.). Philadelphia, PA: Elsevier Saunders
Ji, X., Wang, L., Lu, D. (2014, Oct.). Pulmonary manifestations of
inflammatory bowel disease. World Journal of Gastroenterology 20(37):
13501-13511. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4188901/
IBD Relief. (2016). What is perianal Crohn’s disease? Retrieved from
https://www.ibdrelief.com/learn/what-is-ibd/what-is-crohnsdisease/perianal-crohns
89
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
66.
67.
68.
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
De Zoeten, E., Pasternak, B., Mattei, P., Kramer, R., Kader, H. (2013,
Sep.). Diagnosis and treatment of perianal Crohn disease: NASPGHAN
clinical report and consensus statement. JPGN 57(3): 401-412.
National Institute of Diabetes and Digestive and Kidney Diseases.
(2014, Jun.). Microscopic colitis. Retrieved from
https://www.niddk.nih.gov/health-information/health-topics/digestivediseases/microscopic-colitis/Pages/facts.aspx
Crohn’s & Colitis Foundation of America. (2012, Oct.). Microscopic
colitis. Retrieved from http://www.ccfa.org/resources/microscopiccolitis.html?referrer=https://www.google.com/
Wickbom, A., Bohr, J., Eriksson, S., Udumyan, R., Phil, M., Nyhlin, N.,
Tysk, C. (2013, Oct.). Stable incidence of collagenous colitis and
lymphocytic colitis in Orebro, Sweden, 1999-2008: A continuous
epidemiologic study. Inflamm Bowel Dis. 19(11): 2387-2393.
Hopkins Medicine. (2013). Collagenous and lymphocytic colitis:
Introduction. Retrieved from
http://www.hopkinsmedicine.org/gastroenterology_hepatology/_pdfs/s
mall_large_intestine/collagenous_lymphocytic_colitis.pdf
IBD Relief. (2016). What is indeterminate colitis? Retrieved from
https://www.ibdrelief.com/learn/what-is-ibd/what-is-indeterminatecolitis
Mahdi, B. (2012). A review of inflammatory bowel disease unclassified
– Indeterminate colitis. Journal of Gastroenterology and Hepatology
Research 1(10). Retrieved from
http://www.ghrnet.org/index.php/joghr/article/view/214/395
Crohn’s & Colitis Foundation of America. (2009, Jan.).
Immunomodulators. Retrieved from
http://www.ccfa.org/resources/immunomodulators.html
American College of Rheumatology. (2015). Azathioprine (Imuran).
Retrieved from http://www.rheumatology.org/I-Am-A/PatientCaregiver/Treatments/Azathioprine-Imuran
Tian, H., Cronstein, B. (2007). Understanding the mechanisms of
action of methotrexate: Implications for the treatment of rheumatoid
arthritis. Bulletin of the NYU Hospital for Joint Diseases 65(3): 168173.
Ananthakrishnan, A., et al. (2015, Jun.). Diabetes and risk of infections
with immunomodulator therapy in inflammatory bowel diseases.
Aliment Pharmacol Ther. 41(11): 1141-1148. Retrieved from
http://europepmc.org/articles/pmc4420684
Crohn’s & Colitis Foundation of America. (2014, Feb.). Biologic
therapies. Retrieved from http://www.ccfa.org/resources/biologictherapies.html?referrer=https://www.google.com/
Simponi® Golimumab. (2016, Mar.). Start changing your UC picture.
Retrieved from https://www.simponi.com/ulcerative-colitis/
90
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
89.
Humira® Adalimumab. (2013). Moderate to severe Crohn’s disease.
Retrieved from https://www.humira.com/crohns/consider-humira-forcrohns-treatment
Lichtenstein, G., et al. (2012, May). A pooled analysis of infections,
malignancy, and mortality in infliximab- and immunomodulator-treated
adult patients with inflammatory bowel disease. The American Journal
of Gastroenterology 2012; 107: 1051-1063. Retrieved from
http://www.nature.com/ajg/journal/v107/n7/full/ajg201289a.html
Naser, S., Sagramsingh, S., Naser, A., Thanigachalam, S. (2014, Jun.).
Mycobacterium avium subspecies paratuberculosis causes Crohn’s
disease in some inflammatory bowel disease patients. World J
Gastroenterol. 20(23): 7403-7415. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064085/
Rashid, T., Ebringer, A., Wilson, C. (2013). The role of Klebsiella in
Crohn’s disease with a potential for the use of antimicrobial measures.
International Journal of Rheumatology (2013); Article ID 610393, 8
pages. Retrieved from
https://www.hindawi.com/journals/ijr/2013/610393/
Dewint, P., et al. (2014). Adalimumab combined with ciprofloxacin is
superior to adalimumab monotherapy in perianal fistula closure in
Crohn’s disease: a randomized, double-blind, placebo controlled trial
(ADAFI). Gut 2014; 63: 292-299.
Burakoff, R., Levine, J. (2014). Medical therapy of ulcerative colitis.
New York, NY: Springer Science + Business Media New York
Lashner, B. (2013, Jan.). Crohn’s disease. Retrieved from
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanageme
nt/gastroenterology/crohns-disease/
IBD Relief. (2016). What is ileocolitis? Retrieved from
https://www.ibdrelief.com/learn/what-is-ibd/what-is-crohnsdisease/ileocolitis
Crohn’s & Colitis Foundation of America. (2016). Types of Crohn’s
disease and associated symptoms. Retrieved from
http://www.ccfa.org/what-are-crohns-and-colitis/what-is-crohnsdisease/types-of-crohnsdisease.html?referrer=https://www.google.com/
Menys, A., et al. (2013, Dec.). Small bowel strictures in Crohn’s
disease: a quantitative investigation of intestinal motility using MR
enterography. Neurogastroenterology & Motility 25(12): 967-e775.
Retrieved from
http://onlinelibrary.wiley.com/doi/10.1111/nmo.12229/full
Jonkers, D., Penders, J., Masclee, A., Pierik, M. (2012). Probiotics in
the management of inflammatory bowel disease: A systematic review
of intervention studies in adult patients. Drugs 72(6): 803-823.
91
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
90.
Antoni, L., Nuding, S., Wehkamp, J., Stange, E. (2014, Feb.). Intestinal
barrier in inflammatory bowel disease. World J Gastroenterol. 20(5):
1165-1179. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3921501/
91. Axe, J. (2016). 7 signs and symptoms you have leaky gut. Retrieved
from https://draxe.com/7-signs-symptoms-you-have-leaky-gut/
92. Emory University. (2012, Sep.). Immune system compensates for
‘leaky gut’ in inflammatory bowel disease susceptibility. Science Daily.
Retrieved from
https://www.sciencedaily.com/releases/2012/09/120913123512.htm
93. Griffiths, S. (2015, Feb.). Role of microbes in carbohydrate digestion.
Food Science and Technology. Retrieved from
http://www.fstjournal.org/features/29-1/carbohydrate-digestion
94. Conlon, M., Bird, A. (2015, Jan.). The impact of diet and lifestyle on
gut microbiota and human health. Nutrients 7(1): 17-44. Retrieved
from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303825/
95. Paik, J., Fierce, Y., Treuting, P., Brabb, T., Maggio-Price, L. (2013,
May). High-fat diet-induced obesity exacerbates inflammatory bowel
disease in genetically susceptible Mdr1a-/- male mice. The Journal of
Nutrition 143(8): 1240-1247.
96. Chalmers-Watson, T. (2008). The role of the NOD2 gene in the
pathogenesis of Crohn’s disease. [Doctoral dissertation]. Royal Free &
University College Medical School, University of London.
97. Mandal, A. (2013, Sep.). Vomiting mechanism. Retrieved from
http://www.news-medical.net/health/Vomiting-Mechanism.aspx
98. Draper, R. (2015, Jan.). Rectal bleeding in adults. Retrieved from
http://patient.info/doctor/rectal-bleeding-in-adults
99. Shea-Donohue, T., Notari, L., Sun, R., Zhao, A. (2014, Jun.).
Mechanisms of smooth muscle responses to inflammation.
Neurogastroenterol Motil. 24(9): 802-811. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4068333/
100. Lehmann, F., Burri, E., Beglinger, C. (2015, Jan.). The role and utility
of faecal markers in inflammatory bowel disease. Therap Adv
Gastroenterol. 8(1): 23-36. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4265086/
101. Smith, L., Gaya, D. (2012, Dec.). Utility of faecal calprotectin analysis
in adult inflammatory bowel disease. World J Gastroenterol. 18(46):
6782-6789. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520167/
102. Techlab. (2015). Fecal lactoferrin testing. Retrieved from
http://lactoferrintesting.com/downloads/IBD_monograph_final_ss.pdf
92
nursece4less.com nursece4less.com nursece4less.com nursece4less.com
The information presented in this course is intended solely for the use of healthcare
professionals taking this course, for credit, from NurseCe4Less.com. The information is
designed to assist healthcare professionals, including nurses, in addressing issues
associated with healthcare.
The information provided in this course is general in nature, and is not designed to address
any specific situation. This publication in no way absolves facilities of their responsibility for
the appropriate orientation of healthcare professionals. Hospitals or other organizations
using this publication as a part of their own orientation processes should review the
contents of this publication to ensure accuracy and compliance before using this publication.
Hospitals and facilities that use this publication agree to defend and indemnify, and shall
hold NurseCe4Less.com, including its parent(s), subsidiaries, affiliates, officers/directors,
and employees from liability resulting from the use of this publication.
The contents of this publication may not be reproduced without written permission from
NurseCe4Less.com.
93
nursece4less.com nursece4less.com nursece4less.com nursece4less.com