Chapter I

INTRODUCTION

At the time of the creation of the World Health Organization (WHO), in 1948,
Health was defined as being "a state of complete physical, mental, and social wellbeing and not merely the absence of disease or infirmity. This definition invited nations
to expand the conceptual framework of their health systems beyond issues related to
the physical condition of individuals and their diseases, and it motivated us to focus our
attention on what we now call social determinants of health. Consequently, WHO
challenged political, academic, community, and professional organizations devoted to
improving or preserving health to make the scope of their work explicit, including their
rationale for allocating resources.

Colon adenocarcinoma is the most common type of gastrointestinal cancer, with

about 140,000 cases each year in the United States, according of the National Cancer
Institute. This type of cancer begins in the cells of glandular structures in the inner layer
of the colon and spreads first into the wall of the colon and potentially into the lymphatic
system and other organs. Colon denocarcinoma can be treated, with 50 percent of
patients surviving for at least five years. Early-stage colon cancers have survival rates
of 70 to 80 percent. Colon adenocarcinoma progresses slowly and may not present
symptoms for up to five years. As the cancer grows, symptoms become more likely
and can include rectal bleeding, fatigue, shortness of breath, angina, changes in bowel
habits, abdominal discomfort, anemia, or bowel obstruction.

Colon cancer stems from colon polyps that turn cancerous, and individuals who
develop polyps are at the highest risk of colon cancer. For this reason, individuals with a
family history of adenomatous polyposis or Gardners syndromeboth marked by the
growth of multiple colon and rectal polypsare at highrisk. Individuals age 50 or older
who are not screened regularly for polyps are at higher risk, as well, since polyps grow
in 30 percent of individuals past the age of 50. Colon cancer also is associated with a
diet high in fat and beef and low in fiber. Other risk factors include a personal history of
previous cancer or inflammatory bowel disease.
Although the incidence and mortality from colon cancer have been on a slow
decline over the past 20 years in the United States, colorectal cancers remain the third
most common cancer and the third most common cause of cancer-related mortality in
the US. The American Cancer Society estimates that 96,830 individuals will be
diagnosed with colon cancer in the United States in 2014. Combined estimates for colon
and rectal cancer are for 50,310 deaths in 2014. Recent trends in the United States
suggest a disproportionally higher incidence and death from colon cancer in African
Americans than in whites. Hispanics have the lowest incidence and mortality from
colorectal cancer.

The incidence of colorectal cancer is about equal for males and females. The
American Cancer Society estimates that colon cancer will be diagnosed in 48,450 men
and 48,380 women in the United States in 2014. Age is a well-known risk factor for
colorectal cancer, as it is for many other solid tumors. The timeline for progression from
early premalignant lesion to malignant cancer ranges from 10-20 years. The incidence
of colorectal cancer peaks at about age 65 years.

Many Asian countries, including China, Japan, South Korea, and Singapore,
have experienced an increase of two to four times in the incidence of colorectal cancer
during the past few decades. The rising trend in incidence and mortality from colorectal
cancer is more striking in affluent than in poorer societies and differs substantially
among ethnic groups. Although changes in dietary habits and lifestyle are believed to be
the reasons underlying the increase, the interaction between these factors and genetic
characteristics of the Asian populations might also have a pivotal role.

This case was chosen because of increasing rate of Colorectal cancer in the
Philippines. 90% of colorectal cancer patients are 50 years or older and the average
age of diagnosis is 64. In the Philippines, 5,787 new cases of colorectal cancer are
diagnosed yearly.

1 out of 100 persons would have had a likelihood of getting

colorectal cancer before age 75. While the five-year survival rate of colorectal cancer
patients from advanced countries like the United states, Singapore and South Korea is
60% or higher, the five-year survival rate of Filipinos living in the Philippines is
significantly lower at only 40%.

OBJECTIVES

This study aims to show the causes, factors, anatomy and physiology,
complications and importance of studying this disease which is the Adenocarcinoma of
the Ascending Colon. In order for us to be aware of this kind of disease, I, as a student
nurse have gathered needed information for us to know the signs and symptoms and
how to avoid the said disease.

General Objectives:
This study aims to provide the researcher, student, and audiences all information
about Adenocarcinoma of the Ascending Colon regarding for us to be knowledgeable
about it.
Specifically the study aims to:

Present an Introduction regarding Adenocarcinoma of the Ascending Colon.

Present the Initial Database of the patient.

Discuss the present and past health history of the patient.

Trace the lifestyle that could be the cause.

Present physical assessment.

Discuss anatomy and physiology.

Trace the Pathophysiology of Adenocarcinoma of the Ascending Colon.

Discuss the interpretation of the laboratory results.

Discuss the medical and nursing management (ideal and actual) rendered to
the patient with Adenocarcinoma of the Ascending Colon.

Discuss the List problems and which problem should be prioritized.

Discuss the functional health pattern of the patient.

Present the Nursing Care Plan that is needed to the patient.

CHAPTER II
Review of Related Literature and Studies

Anatomy of the Colon

The colon is approximately five feet (1.5 meters) in length, begins at the ileocecal
valve, and ends at the rectosigmoid junction. Arterial blood supply to the colon from
cecum to splenic flexure is through the superior mesenteric artery which gives rise to
the ileocolic, right colic, and middle colic arteries. The left and sigmoid colon is supplied
by the inferior mesenteric artery which gives rise to the left colic and sigmoidal arteries.
There can be several anatomic variations in the colic arteries including absent middle
colic artery, absent right colic artery, common trunk for right and ileocolic artery, and the
presence of an Arc of Riolan between the middle and left colic artery. The colonic wall
histologically from lumen outward consists of: (1) a simple columnar epithelium which
forms crypts, (2) lamina propria, (3) muscularis mucosa, (4) submucosa, (5) muscularis
propria formed by an inner circular and outer longitudinal layer of smooth muscle, and
(6) serosa.

The typical colonic malignancy is an adenocarcinoma. Once the neoplastic

epithelial cells penetrate the muscularis mucosa and into the submucosa, a malignant
(the ability to metastasize) adenocarcinoma is formed. The mainstay for treatment is
operative resection of the involved colonic segment along with the draining lymph nodes
located in the mesentery. Neoplastic cells confined by the muscularis mucosa are
termed carcinoma-in-situ or severe dysplasia and are not as yet malignant thereby
typically eliminating the need for segmental colonic resection.
The outer longitudinal smooth muscle of the colon thickens in three locations
called tenia coli. The rectosigmoid junction is the
point at which the three tenia fan out and form a
complete outer longitudinal layer. This anatomic
point

has

clinical

significance.

Carcinomas

proximal to this point are colonic; whereas distal

tumors are rectal and as such may benefit from
adjuvant radiation therapy. Likewise, operative
resection for classic sigmoid diverticular disease should include the rectosigmoid
junction with the anastomosis located at the upper rectum.

The function of the colon is (1) absorption of water and electrolytes, and (2)
propulsion and storage of unabsorbed fecal waste for evacuation. Approximately one
liter of fluid chyme enters the cecum each day with an average of only 100cc excreted
in the feces. Parasympathetic innervation by preganglionic vagal fibers and pelvic fibers
result in colonic motility. Sympathetic innervation by the superior mesenteric plexus,
inferior mesenteric plexus, and the hypogastric plexus inhibits colonic motility. It

appears that the major control of motility depends on the colonic wall intrinsic plexus. An
absence of intrinsic plexuses occurs in Hirschsprungs Disease resulting in tonic wall
contraction and functional obstruction.

Disorders of colonic motility including irritable bowel syndrome, slow-transit

constipation, colonic pseudo-obstruction, and post-operative ileus are poorly understood
but may represent an imbalance in this autonomic imput to the smooth muscle wall of
the colon. Normal colon transit arbitrarily results in one to three bowel movements per
day to one bowel movement every 3 days. Colonic transit is measured by obtaining
abdominal radiographs after ingesting radiopaque markers. Markedly constipated
patients with slow-transit constipation (markers remaining disbursed throughout the
colon after 5 days) but with normal defecation mechanics may benefit from abdominal
colectomy.

Rectum
The rectum is the terminal portion of the large intestine beginning at the
confluence of the three tenia coli of the sigmoid colon and ending at the anal canal.
Generally the rectum is 15 cm in length, is
intraperitoneal at its proximal and anterior
end, and is extraperitoneal at its distal and
posterior end. The epithelial lining or
mucosa of the rectum is of a simple
columnar

mucous

secreting

variety.

Therefore, the characteristic malignancy of

the rectum is an adenocarcinoma.

Anal Canal

The anal canal begins a few centimeters proximal to the classic and well
visualized dentate line and it ends at the anal verge. The anal canal is about 5 cm in
length. Histologically the proximal end of the anal canal is the point at which the
columnar epithelium of the rectum becomes a transitional epithelium. This epithelium
transitions to a stratified squamous variety at the dentate line. The distal most end of the
anal canal is the anal verge which is the point where the stratified squamous epithelium
becomes true skin marked by the presence of hair follicles and sweat glands.

The anal verge is readily identified by noting the point at which hair shafts are
seen. The anoderm is a term used to describe the zone between the dentate line and
the anal verge. Perianal skin then describes the anatomic area beyond the anal verge.
Malignancies of the perianal skin are typical skin cancers usually squamous cell
carcinomas. Anal canal carcinomas are described as epidermoid carcinoma, squamous

cell carcinoma, cloacogenic carcinoma, or baseloid carcinoma depending on their

particular histologic features. The importance of locating and anatomically defining the
particular malignancy of the anorectal region is in their treatment.

The dentate line is a clearly observed undulating line near the midpoint of the
anal canal. It is at this location where the anal crypts are found. Anal glands secrete
mucus that empty into the anal crypts by way of anal ducts. The pathologic significance
of anal glands, ducts, and crypts is infection. Cryptoglandular infection can occur
leading to anorectal abcess and its sequelae anorectal fistula.

Autonomic nerves supply the rectum and upper anal canal whereas somatic
nerves supply the lower anal canal and perianal skin. Rectal polyps, tumors, and
mucosa can be biopsied without anesthesia. Internal hemorrhoids located beneath the
autonomically innervated upper anal canal classically present as painless bleeding and
can be treated without anesthesia using simple fixation techniques. Conversely, lesions
of the distal anal canal and perianal skin such as anal fissure and external hemorrhoids
are painful.

The blood supply to the anorectal region is rich. The terminal branch of the
inferior mesenteric artery is the superior hemmorrhoidal (rectal) artery. The superior
hemorrhoidal artery branches into right and left branches; the right branch further
divides into anterior and posterior branches. The classic hemorrhoidal plexes are then
located at the left later, right anterolateral, and right posterolateral locations. The middle
hemorrhoidal (rectal) arteries are direct branches from the internal iliac arteries. The
inferior hemorrhoidal (rectal) arteries are branches off the pudendal arteries which also

arise from the internal iliac arteries. The superior, middle, and inferior hemorrhoidal
arteries then complete the rich arterial supply to the anorectal region.

The venous drainage of the anorectal region consists of superior hemorrhoidal

veins draining into the portal venous system (by way of the inferior mesenteric vein) and
the middle and inferior hemorrhoidal veins draining into the caval system (by way of the
internal iliac veins). Thus the anorectal region can provide a means of portal
decompression when portal hypertension exists.

The main pathologic significance of the anorectal vasculature is in hemorrhoidal

disease. Two hemorrhoidal plexes are formed in each of the classic locations (left
lateral, right anterolateral, and right posterolateral). The internal (superior) hemorrhoidal
plexus is proximal to the dentate line and the external (inferior) hemorrhoidal plexus is
located distal to the dentate line.

The musculature of the anorectal region forms the anal sphincter mechanism.
The internal anal sphincter is smooth, involuntary muscle and is simply the terminal
thickening of the inner visceral smooth muscle layer of the rectal wall. The role of the
internal anal sphincter in fecal continence may be for flatus control. Division of the
internal anal sphincter is the operative treatment for anal fissure and most often has no
effect on fecal continence.

The external anal sphincter is skeletal muscle and thus under voluntary control.
There is a distinct anatomic plane between the internal and external anal sphincter
occupied by longitudinal connective tissue fibers continuous with the outer longitudinal

muscle wall of the rectum. The external anal sphincter is arbitrarily separated into
subcutaneous, superficial and deep components. The puborectalis muscle is felt to
represent the deep component of the external anal sphincter and appears to be the
most significant muscle for maintainting fecal continence. The puborectalis muscle
originates and inserts on the pubis after encircling the rectum at the anorectal junction.
When contracted the puborectalis muscle creates a 90 degree angle between the anal
canal and the rectum. Puborectalis relaxation allows the anorectal angle to approach
180 degrees which in combination with relaxation of the other components of the
external allows defecation.

Lymphatic drainage of the rectum travels along the internal iliac vessels as well
as the aorta. Lymphatic drainage of the anal canal can follow the internal iliac vessels
but also may travel through channels in the inguinal region.

I D E A L

P A T H O P H Y S I O L O G Y

O F

T H E

D I S E A S E
Colon cancer arises from mucosal colonic polyps. The critical parameterof polyps in
terms of natural history, particularly malignant potential, ishistology. The two most
common histologic types are hyperplastic and adenomatous. Histologically, hyperplastic
polyps contain an increasednumber of glandular cells with decreased cytoplasmic
mucus, but lacknuclear hyperchromatism, stratification, or atypia. Adenomatous nuclei
are usually hyperchromatic, enlarged, cigar-shaped, and crowded together ina palisade
pattern. Adenomas are classified as tubular or villous.
Histologically, tubular adenomas are composed of branched tubules, whereasvillous
adenomas contain digitiform villi arranged in a frond. Tubulovillousadenomas contain
both elements.Virtually all colon cancers arise from adenomas as demonstrated
bymultiple epidemiologic, clinical, and pathologic findings. First, about onethird of
operative specimens containing colon cancer contain one or moresynchronous
adenomas, a significantly higher rate than in age-matchedcontrols without colon cancer.
Second, the risk of colon cancer markedly
increases with increasing number of adenomatous polyps. Third,adenomatous tissue is
frequently found contiguous to frank carcinoma. Fourth, patients with familial
adenomatous polyposis (FAP), who have
hundreds or thousands of adenomatous colonic polyps, inevitably develop colon cancer
if colectomy is not performed. Fifth, patients who refuse polypectomy for adenomas
develop colon cancer at a rate of about 4% after
5 years and 14% after 10 years.

Colon cancer is believed caused by a cascade of genetic mutations leading to

progressively disordered local DNA replication and accelerated colonocyte replication.
The progressive accumulation of multiple genetic mutations results in thetransition from
normal mucosa to benign adenoma to severe dysplasia tofrank carcinoma. Mutations of
the mismatch repair genes are believed to account for about 15% of sporadic colon
cancers. APCmutation is believed to account for about 80% of sporadic colon cancers.
Spontaneous somatic APC mutation in colonocytes is believed to underlie the
development of sporadic adenomatous polyps. APC gene mutationsoccur early in
adenoma development and are often found in aberrant cryptfoci, the earliest identifiable
dysplastic crypts. APC mutations are foundin about 50% of sporadic adenomas.
Adenomas usually remain benign. Malignant transformation requires further genetic
alterations. The DCC(deleted in colon cancer) gene encodes for a neural cell adhesion
molecule receptor and normally promotes apoptosis and suppresses tumors. Loss of
the normal DCCgene is believed to be important in the transition from an intermediate to
a late adenoma. Its role in this transition is supported by its frequent allelic deletion
during this transformation.
The normal p53 gene product arrests the cell cycle following DNA injury to permit
either DNA repair if the damage is correctable, or apoptosis if the damage is too severe.
The wild-type p53 protein product is up-regulated after cell stress from radiation
exposure, DNA injury, or other noxious events to prevent new DNA synthesis and halt
cell division. Loss of p53 function can promote genomic instability as genetic errors are
replicated without check, resulting in loss of heterozygosity. Mutation of the p53 geneis
believed to be important in the transition from late adenoma to frankcarcinoma.

About 50% of lesions with high-grade dysplasia and about 75%of frank cancers
exhibit loss of normalp53function, usually from a missense point mutation of one allele
and deletion of the other, wild-type, The K-rasgene encodes for a protein involved in
signal transduction from the cell membrane to the nucleus. Specific mutations of this
gene result inconstitutive activation of this signal pathway and increased colonocyte
replication. These mutations are associated with exophytic growth of adenomas in the
transition to carcinoma. About 50% of colon cancers have K-ras mutations.The
accumulation of genetic mutations leads to genetic instability,manifested by loss of
heterozygosity.. Loss of heterozygosity accelerates carcinogenesis. Cells with loss of
heterozygosity have one, instead of the normal two, alleles of some genes because of
loss of individual chromosomesduring mitosis.
A tumor suppressor gene is more likely to lose normal function when only one
allele is present after loss of heterozygosity. Only one, rather than two, allelic mutations
are then required for loss of its function. DNA methylation at the promotor region can
terminate and silence gene expression without DNA mutation. In particular, DNA
methylation can inactivate suppressor genes, thereby promoting cancer. Colon cancer
is sometimes associated with methylation and inactivation of p14, normally an upstream
inducer of thep53tumor suppressor pathway. This occurs in about 25% of colon
cancers. The inactivation produces the same cancer phenotype as mutation of the
tumor

suppressor

genep53.

Methylation

of

the

tumor

designatedCDKN2, occurs in about 35% of colon cancers.

suppressor

genep16,

A C T U A L

P A T H O P H Y S I O L O G Y

O F

T H E

D I S E A S E
Obstructing Adenocarcinoma of the Ascending Colon
Mrs. GMB was diagnosed Obstructing Adenocarcinoma of the Ascending
Colon.She was predisposed to the disease by the following factors: Gender Female,
Older Age - 50years old and above, Low Fiber and Hight Fat Diet, Palpable mass in the
lower right quadrant of abdomen were also present at the month of February 2014. The
factors that aggravated the formation obstructing adenorcarcinoma of the were the
following. (Table 1)
Predisposing Factors
1. Gender (Female)

Inference
The risk overall is equal, but women have
a higher risk for colon cancer, while men
are more likely to develop rectal cancer

2. Low Fiber and Hight Fat Diet

Colon cancer may be associated with a

diet low in fiber and high in fat and
calories. Some studies have found an
increased risk of colon cancer in people
who eat diets high in red meat.

3. Palpable

mass in the lower right A palpable lump in the abdomen can be a

quadrant of abdomen

symptom of colorectal cancer. Right colon

cancers: weight loss, anaemia, occult
bleeding, mass in right iliac fossa, disease

more

likely

to

be

advanced

presentation.

CLINICAL MANIFESTATIONS

Signs and symptoms include:

A change in bowel habits, including diarrhea or constipation or a change in the

consistency of your stool.

Rectal bleeding or blood in stool.

Persistent abdominal discomfort, such as cramps, gas or pain.

A feeling that your bowel doesn't empty completely.

Weakness or fatigue

Unexplained weight loss

LABORATORY STUDIES

A laboratory test for carcinoembryonic antigen (CEA) may be ordered to help in

staging. This protein is increased in many people with colon cancer, and blood levels
generally correlate with the stage of the disease. CEA testing also can help in
determining prognosis, as increased concentrations are associated with an increased
risk of recurrence and development of metastatic disease.

A test for epidermal growth factor receptor (EGFR) may be performed on a sample
of the tumor to help establish a prognosis and guide treatment. Tumors that express

at

EGFR tend to be more aggressive, but treatment can be targeted toward this type of
tumor; an EGFR blocking agent may be used as therapy.

A test to detect a KRAS gene mutation in tumor tissue may be used to guide cancer
treatment and to evaluate prognosis. The presence of certain mutations indicates that
anti-EGFR drug therapy will not be effective in treating the cancer and a likely poorer
prognosis.

DIAGNOSIS

Biopsy
When a suspected cancer is found during a colonoscopy, a biopsy is taken, removing
some tissue from the suspicious site for examination under a microscope by a
pathologist.

If the tissue is cancerous, the next step is to determine the stage (or extent) of
disease. Treatment will depend in part on the "stage" of the colon or rectal cancer; it is
categorized by how far it has spread from its original site. Staging systems for colon

cancer vary in different parts of the world, and some use letters instead of numbers.
One common system used to describe colon cancer stages is:

Stage 0: Very early cancer on the innermost layer of the colon or rectum
(carcinoma in situ).

Stage I: Tumor in the inner layers of the colon but has not grown through the wall
of the colon.

Stage II: Tumor in the outer layers of the colon and/or nearby tissue but has not
spread to lymph nodes.

Stage III: Tumor that has spread to the lymph nodes but not to distant organs of
the body.

Stage IV: Tumor that has spread to distant organs, such as the lungs, bone, or
liver (metastatic).

TREATMENT

Since these cancers have not grown beyond the inner lining of the colon, surgery
to take out the cancer is all that is needed. This may be done in most cases by
polypectomy (removing the polyp) or local excision through a colonoscope. Colon
resection (colectomy) may occasionally be needed if a tumor is too big to be
removed by local excision.

Chapter IV
This chapter presents the assessment of data, comprehensive database,
psychopathophysiology, medical and nursing management of the client, including the
laboratory results, diagnostic studies, prognosis of patients condition, discharge
planning and nursing care plan to the patient.

I. Biographic Data

Name:

Mrs. GMB

Age:

56 years old

Gender:

Female

Birth date:

December 23, 1957

Ordinal Position:

3rd out of 5 children

Civil Status:

married for 36 years

Number of Children:

four (4)

Residence:

Balayo Subdivion Lagao, GSC, South Cotabato 9500

Birthplace

Bohol

Nationality

Filipino

Religion

Roman Catholic

Educational Attainment

college graduate, secretarial course

Occupation

housewife

Room Number

251

Hospital

General Santos Doctors Hospital

Chief Complaint

Palpable mass in abdomen; Epigastric pain

Admitting Diagnoses

Intestinal Obstruction probably secondary to Colonic Mass

Final Diagnoses

Obstructing Adenocarcinoma of the Ascending Colon

Surgery (done by)

1. Procedure:
Performed by:

Right Hemicolectomy
Dr. Lorenzo

Date performed: November 29, 2014

Attending Physician

Dr. Balay
Dr. Lorenzo

Date of Admission

November 28,2014

Time of Admission

1:12 PM

Source of Health Care

Philhealth

II. Chief Complaint or Reason for Visit

Patient sought medical care at Geral Santos Doctors Hospital., due to
constipation, abdominal cramps, fatigue, epigastric pain and palpable mass in right
lower abdominal quadrant. Masakit masyado kasi hindi ako nakakagalaw ng maayos,
syempre may bukol , hindi din ako nakakabawas, sa isang lingo mga dalawa lang
siguro. Sumasakit tiyan ko lalo na pag kumakain ako ng matataba, kagaya ng lechon.

ACTUAL LABORATORY FINDINGS

EXAMINATION
Ionized Ca

RESULTS

NORMAL VALUE