Republic of the Philippines

CENTRAL MINDANAO UNIVERSITY

COLLEGE OF NURSING
University Town, Musuan, Maramag, Bukidnon
E-mail: nursing@cmu.edu.ph

NCM74
Care of Clients with Problems in Nutrition and Gastrointestinal,
Metabolism, and Endocrine, Perception and
Coordination, Acute and Chronic

Inflammatory Bowel Disease – Manuscript

Submitted by:
Leonar, Maryjhan Pillar A.
Lumod, Rachel Anne O.

Submitted to:
Ms. Neda Joy L. Espina MAN, RN
Clinical Instructor

February 24, 2022

ETIOLOGY
The exact cause of IBD is unknown, but IBD is the result of a defective immune system.
Inflammatory bowel disease (IBD) occurs in genetically susceptible individuals after an
inappropriate immune response to the intestinal flora. To date, the cause of IBD remains
a mystery. Many causes have been implicated but none is universally present in all
patients.

RISK FACTORS
Predisposing Factors

 Age. People between the ages of 20 and 29 are at greatest risk for Crohn’s
disease; whereas, people between the ages of 15 and 30 are at greatest risk and
those older than 60 years of age are at slightly greater risk for ulcerative colitis.
 Family history. Family history predisposes people to IBD, particularly if you have
a close relative — such as a parent, sibling or child — with the disease.
 Race or Ethnicity. Other risk factors for IBD, include being Caucasian of
Ashkenazi Jewish background
 Genetics. Viral illnesses in people genetically predisposed to developing an IBD
can trigger the cell-mediated immune response (antimicrobial peptides,
autophagy, handling of bacteria, cytokines) that results in the inflammatory
changes that characterized IBDs.
 Location. Living in a northern climate, and living in an urban area
 Sex. Males are at a slightly higher risk for ulcerative colitis; whereas, females are
at greater risk for Crohn’s disease.

Precipitating Factors

 Diet. Crohn's disease is common in industrialized nations where the diet is low in
fiber and high in processed food.
 Smoking & Environmental Triggers. Current smokers are at risk for Crohn’s
disease, but those who are ex-smokers or nonsmokers are at risk for ulcerative
colitis.
 Infection. Systemic Infections may Cause release of inflammatory cytokines or
may indirectly affect the trafficking of inflammatory cells to the intestine.
 Drugs. Oral contraceptives increase risk of developing UC and CD. NSAIDs Cause
IBD Flare-ups. Antibiotics may Cause IBD Flare-ups.
 Stress. Stress hypothalamus-pituitary-adrenal axis and autonomic nervous
system axis affect immune and inflammatory functions neuropeptides and pro
 inflammatory mediators increased intestinal mucosal permeability and
inflammation. Although the majority of studies evaluating the association of
stressful events and flare of IBD suggest a relationship, the definitive answer is
yet unknown.

PATHOPHYSIOLOGY
 Impaired Barrier Function, Environmental Triggers
 M-cell are specialized intestinal epithelial cells that provide the main machinery
for sampling luminal microbes for mucosal immune surveillance– responsible for
active sampling of intestinal antigen initiates regulated immune responses that
ensure intestinal homeostasis
 Microbial translocation occurs when the bacteria (or bacterial products) that
should be in the lumen of the intestine translocate across the tight epithelial
barrier into systemic circulation, where they contribute to inflammation and
pathogenesis
 Activation of immune cells
 Macrophages –work as the innate immune cells through phagocytosis and
sterilization of foreign substances such as bacteria, and play a central role in
defending the host from infection.
 Antigen presenting cell activated – presentation to the t-cells – CD4 T-cell
activation
- Further stimulates macrophages
- Release heaps of cytokines
1. TNF – α
2. IL 1
3. IL 6
CONTINOUOS RELEASE
1. Angionesis - an important component of pathogenesis of inflammatory
bowel disease (IBD). It leads to formation of new blood vessels. This process
involves the migration, growth, and differentiation of endothelial cells, which
line the inside wall of blood vessels.
2. Paneth cell necrosis - contain an abundance of antimicrobial peptides and
immunomodulating proteins that function to regulate the composition of the
intestinal flora
3. Intestinal Epithelial cells (IEC) – death (Impaired Barrier Function)
4. Increased immune response (further damage)
5. Myofibrils induced tissue obstruction stimulates myofibrils to release proteases
causes myofibril induce destruction within the area
Chronic Inflammation results;

Crohn’s Disease - transmural inflammation (distal ileum and ascending colon)

Ulcerative Colitis - mucosal inflammation (rectum & colon)

SIGNS & SYPMTOMS

Crohn’s Disease
 RLQ Pain
 Abdominal Tenderness & Cramps
 Diarrhea (Steatorrhea)
 Reduced Appetite
 Anorexia & Vomiting
 Weight loss
 Nutritional Deficiencies
 Fever
 Granulomas
 Perianal fistula & abscess
 Cobblestone appearance
 String sign
Ulcerative Colitis

 Diarrhea w/ mucus, pus, or blood, tenesmus, passage of liquid stools 6 or more,

inability to defecate
 Bleeding & Edema followed with fatigue, anemia & pallor
 LLQ Pain - anorexia, weight loss, vomiting & cramping
 Dehydration - hypoalbuminemia, electrolyte imbalances
 Extraintestinal Manifestations
 Joint Disorders (e.g. Arthritis)
 Ocular disorders (e.g. Uveitis)
 Skin lesions (e.g. Erythema Nodosum)
 Oral ulcers (e.g. Aphthous ulcerations)

LABORATORY FINDINGS
 Leukocytosis
 Dark, tarry stools
 Elevated ESR
 Low Hemoglobin
 Elevated Serum Alkaline
DIAGNOSTIC TOOLS
 Complete Blood Count
 C-reactive Protein Test
 Abdominal x-ray
 MRI & CT-Scan
 Erythrocyte Sedimentation Rate
 Stool Examination
 Barium Studies
 Ultrasound
 Sigmoidoscopy
 Colonoscopy

NURSING DIAGNOSIS
 Diarrhea r/t inflammatory process aeb loose liquid & bloody stool
 Acute pain r/t increased peristalsis and GI inflammation
 Deficient fluid volume r/t to anorexia, nausea, and diarrhea
 Imbalanced Nutrition: Less than Body Requirement r/t dietary restrictions, nausea
and malabsorption
 Activity Intolerance r/t generalized weakness

MANAGEMENT & TREATMENT

Nutrition
■ Oral fluids & a low residue
■ High protein
■ High-calorie diet w/ supplemental vitamin therapy
■ Iron replacement
These are all prescribed to meet nutritional needs, reduce inflammation and control pain
diarrhea. Protein intake should be high to resolve problem with hypoalbuminemia.

Pharmacological

■ Antiperistaltic - sedatives, anti-diarrheal. To decrease gastric motility

■ Anti-inflammatory - aminosalicylates (azulfidine)
■ Antibiotic - metronidazole & ciprofloxacin. Used for complications such as
abscesses or fistula formation
■ Corticosteroids - prednisone, budesonide.
 ■ Immunomodulators - azathioprine, 6-mercaptopurine, and methotrexate. Used to
alter immune response. These medications are useful in maintenance regimens to
prevent relapses
Surgical Management

■ Strictureplasty – blocked or narrowed sections of the intestines are widened

leaving the intestine intact
■ Intestinal Transplant – provide improvement in quality of life but immunologic
problems remain formidable and the costs and mortality rates continue to be
high
Nursing Management

■ Feeding - Provide appropriate nursing care - oral care & (Aphthous ulcerations)
1/cup of water for every 1 teaspoon of salt.
■ Hydration – IV fluids may be needed either short term or long term to restore
hydration status. Enteral or parenteral nutrition for clients unable to maintain
adequate nutritional status
■ Pain – acknowledge and accept patient’s pain
■ Administer medications
■ Rest - decreases intestinal motility and reduces the metabolic rate when infection
or hemorrhage is a complication
■ Mobilize – turn patient every 2-3 hours, assist in getting out of the bed or
transferring from chair to bed (postural hypotension & anemic)

Non-pharmacological Management

■ Coping measures - provide opportunity to vent frustrations related to disease

process.
■ Maintaining a clean environment - Removing patient from outside stressors
promotes relaxation; helps reduce anxiety and promote a sense of well-being
■ Mind-body Therapies – stress management (i.e., guided imagery, deep breathing)
■ Provide Comfort Measures - encourage verbalization of feelings. Provide
feedback. Patient with severe diarrhea may hesitate to ask for help for fear of
becoming a burden to the staff, assuring that you are always ready to help will
provide comfort.

HEALTH EDUCATION
■ Hand Hygiene – deter the spread of organism causing infection
■ Proper food preparation – review food preparation, emphasizing adequate cooking
time and proper refrigeration or storage to prevent bacterial growth and contamination
■ Perianal skincare - preventing or minimizing additional exposure to damaging irritants
and bacteria, suggest use of incontinence pads to protect bed linens
 ■ Therapeutic regimen into ADL - exercise has theoretical benefits on the immune
response, and the limited available data suggest that exercise may improve
disease activity, quality of life, bone mineral density, and fatigue levels in patients
with IBDs.
■ Medication – do not abruptly stop taking medications. Patients who are non-
adherent may suffer a greater chance of disease relapse with severe associated
symptoms
■ Dietary Modifications – increase oral fluid intake and slowly return to normal diet
if appropriate. Even though, it cannot cure IBD it can control the progress the disease
■ Family support – family support is vital, as IBD patient become embarrassed and
have fear losing control over other aspects of their lives. They need time to
express their fears and frustrations. Discussing individual behaviors and stress
coping management can help

PROGNOSIS
■ If treated – prognosis is high at 76%, No single treatment works for IBD, and
treatment is aimed at decreasing inflammation and prevent flare ups of s/s and keep pt.
in remission (NIDDK)
■ If not treated – mortality rate is at 19-45%. Certain complications may arise that are
fatal + coexisting diseases (increased mortality over younger patients)
 Crohn’s Disease - small bowel obstruction, right-side hydronephrosis,
nephrolithiasis, colon cancer, cholelithiasis
 Ulcerative Colitis - toxic megacolon, perforation, hemorrhage, colon cancer,
pyelonephritis, cholangiocarcinoma
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