ONCOLOGIC NURSING

(Written Report)

Prepared by:

Briones, Liset Grace M.

Gutierrez, Emmanuel A.

Palatino, Carol Joy Z.

Submitted to:

Ms. Joanne Otilano, RN

 ONCOLOGIC NURSING

A. Overview of The Normal Cell

1. Structure and Function of the Cell

Cell is the basic structure and function unit of a modern organism. In DNA, it stores information, its
structure, and processes. It has all the machinery to build structures and performs function to keep itself
alive.

All the cells of the body are constantly bathed in a dilute saltwater solution which is derived from the
blood. It varies in length from 2mm to 3ft. It also varies in shape like disk shaped (RBC), threadlike
extensions (nerve cells), toothpick or pointed end (smooth muscle cells), cubelike (epithelial cells).

According to the presence or absence of nucleus:

Prokaryotes- “pre nucleus or before nucleus”, found in bacteria/archaebacteria, all the

components including DNA, mingle freely in the cell’s interior, a single compartment.

Eukaryotes- “true nucleus”, found in plants, animals, fungi... a cell that contains a nucleus and a
membrane bound organelles.

The Major Parts of the Cell

1. Nucleus
 Headquarter or control center of the cell
 Contains the genetic materials (DNA)- a type of nucleic acid- blueprint that contains all the
instructions needed for building the body
 It controls both biochemical reactions that occur in the cell and the production of the cell
 The nucleus decide what the cell needs and uses DNA to print out instructions for the rest of the
cell to produce that need

 Nuclear membrane
 It seperates the chromosomes from the rest of the cells
 Encloses a jelly-like fluid called NUCLEOPLASM in which the nucleoli and
chromatin are suspended
 The nucleus communicates through holes in the envelope called nuclear
pores.
 Nucleolus
 “pacemaker of the cell”
 It is responsible in the synthesis of ribosomal RNA
  It is the site where the ribosomal RNA is synthesized and ribosomes sub-
units are assemble.
 The nucleolus is like a “tiny nucleus” inside the actual nucleus. It
contains RNA, a type of nucleic acid.
 Chromatin granules
 Composed primarily of CHON and RNA
 Smaller than nucleoli and are irregular in size and shape.
2. Cytoplasm
 Factory area of the cell
 Is the general storage and working area of the cell with the organelles and inclusions
 Kinds of cytoplasm:
a. Ectoplasm- provides semisolid gel-liked support for the cell membrane. It is
beneath the cell membrane frequently contains an interwoven mat of
microfilaments composed mainly of actin fibrilae
b. Endoplasm- the cytoplasm between the cortex and the nuclear membrane.
 Inclusions- are lifeless accumulation of metabolites or cell products such as
stored CHON, crystals pigment. They are dispensable and often temporary
constituents of the cell.
 Cytoplasmic organelles (little organ)- are compartmentalized structures that are
perform a specialized function within a cell.
 Endoplasmic reticulum
 Ribosomes
 Mitochondria
 Lysosomes
 Perixisomes
 Golgi apparatus
 Secretory vesicles
 Centrioles
 Filaments
 Microtubules
 Cytoskeleton
 3. Cell membrane
 Plasma membrane of plasmalemma, is the limiting membrane of the cell
 It is made of phospholipids, which have CHO heads and lipid tails
 An important characteristic is selective permeability which determines the kinds and amount of
substance passing into and out the cell.
 It serves as recognition sites acting as antigenic determinants which render the cell surface its
immune-chemical properties. Proteins embedded into the membrane send and receive signals
to communicate with other cells.

2. Cell Cycle

The cell cycle is composed of four distinct phases during which the cell prepares for and undergoes
mitosis.

The G1 phase consists of cells that have recently completed division and are committed to continued
proliferation. After a variable period, these cells begin synthesis DNA, marking the beginning of the S
phase. After DNA synthesis is complete, the end of the S phase is followed by the premitotic rest interval
called the G2 phase. Finally, chromosome condensation occurs and the cells divide during the mitotic M
phase. Resting diploid cells that are not actively dividing are described as being in the G 0 phase. The
transition between cell-cycle phases is strictly regulated by specific signalling proteins; however, these
cell-cycle checkpoints may become aberrant in some tumor types.

State Phase Abbreviation Description

Quiescent Gap 0 G0 A resting phase where the cell has left the cycle and has
/ stopped dividing
senescent
Interphase Gap 1 G1 Cells increase in size in Gap 1. The G 1 checkpoint control
mechanism ensures that everything is ready for DNA
synthesis
Interphase synthesis S DNA replication occurs during this phase
Interphase Gap 2 G2 During the gap between DNA synthesis and mitosis, the cell
will continue to grow. The G2 checkpoint control mechanism
ensures that everything is ready to enter the M phase and
divide.
Cell Mitosis M Cell growths stops at this stage and cellular energy are
division focused on the orderly division into two daughter cells. A
checkpoint in the middle of mitosis ensures that the cell is
ready to complete cell division.

B. Alteration in Cell Function

AGING CELL

A number of cellular structures or events appear to be involved in the process of aging. The major
theories of aging concentrate on molecules within the cell, such as lipids, proteins, and nucleis acids. It is
estimated that at least 35% of the factors affecting aging are genetic.

1. Cellular clock. One theory on aging suggests that there is a cellular clock, which, after a certain
passage of time or a certain number of cell divisions, results in death of a given cell line.
2. Death genes. Another theory suggests that there are “death genes”, which turn on late in life, or
sometimes prematurely, causing cells to deteriorate and die.
3. DNA damage. Other theories suggest that through time, DNA is damaged, resulting in cell
degeneration and death.
4. Free radicals. DNA is also susceptible to direct damage, resulting in mutations, which may result
in cellular dysfunction and ultimately, cell death. One of the major sources of DNA damage is
apparently from free radicals, which are atoms or molecules with an unpaired electron.
5. Mitochondrial damage. It may be that mitochondrial DNA is more sensitive to free-radical
damage than is nuclear DNA. Mitochondrial DNA damage may result in loss of proteins critical to
mitochondrial function. Because the mitochondria is a source of ATP, loss of mitochondrial
function may result in the loss of energy critical to cell function and ultimately, to cell death.
One proposal suggest that reduced caloric intake may reduce free radical damage to
mitochondria.

INJURED CELL

Causes

o Hypoxia
o Physical Agents: (mechanical trauma, burns, frostbite, sudden changes in pressure
(barotrauma), radiation, electric shock).
o Chemical Agents: glucose, salt, water, poisons (toxins), drugs, pollutants, insecticides,
herbicides, carbon monoxide, asbestos, alcohol, narcotics, tobacco.
o Infectious Agents: prions, viruses, rickettsiae, bacteria, fungi, parasites.
 o Immunologic Reactions: anaphylaxis, autoimmune disease.
o Genetic Derangements: Congenital malformations, normal proteins (hemoglobinopathies),
enzymes (storage diseases).
o Nutritional Imbalances: protein-calorie deficiencies, vitamin deficiencies; excess food intake
(obesity, atherosclerosis).

Principles of Cell Injury

Dependent upon the etiology, duration, severity of the inciting injury, cell type, stage of the cell cycle or
cell adaptability

o Cellular membranes, mitochondria, endoplasmic reticulum and the genetic apparatus are
particularly vulnerable.
o Injury at one focus often has a cascade effect.
o Morphologic reactions occur only after critical biochemical damage.

CELLULAR ALTERATION – response of cell to any etiological factor; vulnerable to any pathophysiological
changes

a) Physiologic reaction
b) Pathologic reaction
c)
4 Cardinal Factors of Cellular Change:

1) Maintenance of cell membrane

 cellular change = ↑ membrane permeability
2) Adenosine triphosphate (ATP) – energy currency of the cell
 Lesser ATP = lesser membrane permeability
3) Dioxyribonucleic acid (DNA) – one of the last processes protected by the cell
4) Cellular protein (enzymes)

CELLULAR DEATH – does not occur instantaneously because of adaptation

2 Types of Cellular Death:

1) Necrosis – death of living cells or tissues

2) Apoptosis – programmed cell death; important in development

4 Mechanisms of Necrosis:

1) Coagulative - Caused by ischemia; ischemia results in decreased ATP, increased cytosolic Ca ++,
and free radical formation, which each eventually cause membrane damage ( e.g  Infarct:
localized area of ischemic necrosis as in myocardial infarct )
a. Decreased ATP results in increased anaerobic glycolysis, accumulation of lactic acid, and
therefore decreased intracellular pH.
 b. Decreased ATP causes decreased action of Na + / K+ pumps in the cell membranes,
leading to increased Na+ and water within the cell (cell swelling).
c. Other changes: Ribosomal detachment from endoplasmic reticulum; blebs on cell
membranes, swelling of endoplasmic reticulum and mitochondria.
d. Up to here, the changes are reversible if oxygenation is restored by reversing the
ischemia. If the ischemia continues, necrosis results, causing the cytoplasm to become
eosinophilic, the nuclei to lyse or fragment or become pyknotic (hyperchromatic and
shrunken). In the early stages of necrosis, the cells remain for several days as ghosts of
their former selves, allowing one to still identify them and the tissue (in contrast to the
other types of necrosis). The cellular reaction is polys, followed by a granulation tissue
response.
2) Liquefactive – Usually caused by focal bacterial infections, because they can attract
polymorphonuclear leukocytes. The enzymes in the polys are released to fight the bacteria, but
also dissolve the tissues nearby, causing an accumulation of pus, effectively liquefying the tissue.
( e.g. Abscess )
3) Caseous – A distinct form of coagulative necrosis seen in mycobacterial infections (e.g.,
tuberculosis), or in tumor necrosis, in which the coagulated tissue no longer resembles the cells,
but is in chunks of unrecognizable debris. Usually there is a giant cell and granulomatous
reaction, sometimes with polys, making the appearance distinctive.
4) Fat Necrosis - A term for necrosis in fat, caused either by release of pancreatic enzymes from
pancreas or gut (enzymic fat necrosis) or by trauma to fat, either by a physical blow or by
surgery (traumatic fat necrosis). The effect of the enzymes (lipases) is to release free fatty acids,
which then can combine with calcium to produce detergents (soapy deposits in the tissues).
Histologically, one sees shadowy outlines of fat cells (like coagulative necrosis), but with Ca ++
deposits, foam cells, and a surrounding inflammatory reaction.
5) Gangrene – special type; combination of coagulative and liquefactive; occurs in limbs ( e.g.
Diabetes Mellitus )

TYPES OF ADAPTATION:

1) Hypertrophy
 Increase in cell size
 Produces proteins ( growth factors )
 Physiologic
2) Hyperplasia
 Increase in the number of cells
 Stem cell
 E.g. benign prostatic hyperplasia
 Physiologic
3) Atrophy
 Decrease in the size of cells
 Neither / either physiologic or pathologic
 Depends on etiology or condition of the patient
4) Metaplasia
 Replacement of one adult cell type by a different adult cell type
 Physiologic
 DNA adapts
 5) Dysplasia
 Changes in cell size, shape and organization
 DNA is totally destroyed
6) Neoplasia
 Abnormal cellular changes and growth of new tissues
 Happens in cancer

C. Etiologic Factors

Viruses
Chemical Carcinogens
Physical Agents
Hormones
Genetics

VIR
USES

 “Oncogenic viruses” may be one of the multiple agents acting to initiate carcinogenesis.
 Prolonged or frequent viral infections may cause breakdown of the immune system or
overwhelm of the immune system.
 Viral infections that increase risk of certain forms of cancer are as follows:
1. Human papilloma virus – Cervical cancer
2. Epstein-Barr virus – Lymphoma
3. Hepatitis B and C – Hepatocellular cancer
4. Helicobacter pylori – Gastric cancer

CHEMICAL CARCINOGENS

 These factors act by causing cell mutation or alteration in cell enzymes and proteins causing
altered cell replication.
 Chemical carcinogens are as follows:
1. Industrial Compounds
- Vinyl chloride ( used for plastic manufacture, asbestos factories, construction works )
- Polycyclic aromatic hydrocarbons ( such as from refuse burning, auto and truck
emissions, oil refineries, air pollution )
- Fertilizers, weed killers
- Dyes ( analine dyes used in beauty shops, hair bleach )
2. Drugs

- Tobacco, 90% of all cases of lung cancer are due to smoking

- Alcohol
- Cytotoxic drugs
3. Hormones

- Estrogen
- Diethylstilbestrol (DES)
 4. Foods, preservatives

- Nitrites ( bacon, smoked meat )

- Talc ( polished rice, salami, chewing gum )
- Food sweeteners
- Nitrosamines ( rubber baby nipples )
- Aflatoxins ( mold in nuts and grains, milk, cheese, peanut butter )
5. Polycyclic hydrocarbons
- Charcoal broiling
PHYSICAL AGENTS

1. Radiation from x-rays or radioactive isotopes; from sunlight / ultraviolet rays

2. Physical irritation / trauma from pipe smoking, multiple deliveries, jagged tooth, irritation of
the tongue, overuse of any organ / body part
HORMONES

 Estrogen as replacement therapy has been found to increase incidence of vaginal,

cervical and uterine cancers.
GENETICS

 When oncogene ( hidden or repressed genetic code for cancer that exists in all
individuals ) is exposed to carcinogens, changes in cell structure occurs, malignant tumor
develops.
 Regardless of the cause, several cancers are associated with familial patterns ( e.g.
retinoblastoma, pheochromocytoma, Wilm’s tumor, lung cancer, breast cancer )

D. Predisposing Factors

Age
Sex
Urban residence
Geographic distribution
Occupation
Heredity
Stress
Precancerous lesions
Obesity

AGE

 Older individuals are more prone to cancer because they have been exposed to
carcinogens longer. In addition, they have developed alterations in the immune system.

SEX
 The most common type of cancer in females is breast cancer. Whereas, the most
common type of cancer in males is prostate cancer.
URBAN vs. RURAL RESIDENCE
 Cancer is more common among urban dwellers than among rural residents. This is
probably due to greater exposure to carcinogens, more stressful lifestyle, and greater
consumption of preservative-cured foods among urban dwellers.

GEOGRAPHIC DISTRIBUTION
 The most common type of cancer in Japan is gastric cancer while the most common type
of cancer in US is breast cancer. This may be due to influence of environmental factors such as
national diet ( raw foods greatly consist Japanese diet ), ethnic customs, and types of pollutions.

OCCUPATION
 There is a greater risk of exposure to carcinogens among chemical factory workers,
farmers, and radiology department personnel.

HEREDITY
 Positive family history of cancer increases the risk to develop the disease. In adults,
approximately 34% of cancers have familial basis. Cancers that may have familial link include
breast, ovarian, colorectal, prostate, melanoma, uterine, leukemia, sarcomas, and primary brain
tumors.

STRESS
 Depression, grief, anger, aggression, despair or life stresses decrease
immunocompetence because of affectation of hypothalamus and pituitary gland.
Immunodeficiency may spur the growth and proliferation of cancer cells.

PRECANCEROUS LESIONS
 Pigmented moles, burn scars, senile keratosis, leukoplakia, benign polyps or adenoma of
the colon or stomach, fibrocystic disease of the breast, may undergo transformation into
cancerous lesions and tumors.

OBESITY
 Studies have linked obesity to breast and colorectal cancer.

E. Pathophysiology of Cancer

Over the past two decades, hundreds of cancer-associated genes have been discovered. Some, such
as p53, are mutated in many different cancers; others, such as ABL1, are affected only in one or few.
Each of the cancer-associated genes has a specific function, the dysregulation of which contributes to
the origin or progression of malignancy. It is traditional to describe cancer-associated genes on the basis
of their presumed function. It is beneficial, however, to consider cancer-related genes in the context
ofseven fundamental changes in cell physiology that together determine malignant phenotype.(Another
important change for tumor development is escape from immune attack. The seven key changes are the
following:

 Self-sufficiency in growth signals: Tumors have the capacity to proliferate without external
stimuli, usually as a consequence of oncogene activation.
 Insensitivity to growth-inhibitory signals: Tumors may not respond to molecules that are
inhibitory to the proliferation of normal cells such as transforming growth factor β (TGF-β) and
direct inhibitors of cyclin-dependent kinases (CDKIs).
 Evasion of apoptosis: Tumors may be resistant to programmed cell death, as a consequence of
inactivation of p53 or activation of anti-apoptotic genes.
 Limitless replicative potential: Tumor cells have unrestricted proliferative capacity, avoiding
cellular senescence and mitotic catastrophe.
 Sustained angiogenesis: Tumor cells, like normal cells, are not able to grow without formation of
a vascular supply to bring nutrients and oxygen and remove waste products. Hence, tumors
must induce angiogenesis.
 Ability to invade and metastasize: Tumor metastases are the cause of the vast majority of cancer
deaths and depend on processes that are intrinsic to the cell or are initiated by signals from the
tissue environment.
 Defects in DNA repair: Tumors may fail to repair DNA damage caused by carcinogens or incurred
during unregulated cellular proliferation, leading to genomic instability and mutations in proto-
oncogenes and tumor suppressor genes.

Mutations in one or more genes that regulate these cellular traits are seen in every cancer.
However, the precise genetic pathways that give rise to these attributes differ between
individual cancers, even within the same organ. It is widely believed that the occurrence of
mutations in cancer-related genes is conditioned by the robustness of the DNA-repair
machinery, as well as protective mechanisms such as apoptosis and senescence that prevent the
proliferation of cells with damaged DNA. Indeed, recent studies in a variety of human tumors,
such as melanoma and prostate adenocarcinoma, have shown that oncogene-induced
senescence, wherein mutation of a proto-oncogene drives cells into senescence rather than
proliferation, is an important barrier to carcinogenesis. 33 Some limits to neoplastic growth are
even physical. If a tumor is to grow larger than 1 to 2 mm, mechanisms that allow the delivery of
nutrients and the elimination of waste products must be provided (angiogenesis). Furthermore,
epithelia are separated from the interstitial matrix by a basement membrane, composed of
extracellular matrix molecules, that must be broken down by invasive carcinoma cells. These
protective barriers, both intrinsic and extrinsic to the cell, must be breached, and feedback loops
that normally prevent uncontrolled cell division must be disabled by mutations before a fully
malignant tumor can emerge.
F. Classification of Neoplasm

A tumor is said to be benign when its microscopic and gross characteristics are considered relatively
innocent, implying that it will remain localized, it cannot spread to other sites, and it is generally
amenable to local surgical removal; the patient generally survives. It should be noted, however, that
benign tumors can produce more than localized lumps, and sometimes they are responsible for serious
disease.

Malignant tumors are collectively referred to as cancers, derived from the Latin word for crab, because
they adhere to any part that they seize on in an obstinate manner, similar to a crab. Malignant, as
applied to a neoplasm, implies that the lesion can invade and destroy adjacent structures and spread to
distant sites (metastasize) to cause death. Not all cancers pursue so deadly a course. Some are
discovered early and are treated successfully, but the designation malignant always raises a red flag.

All tumors, benign and malignant, have two basic components: (1) clonal neoplastic cells that constitute
their parenchyma and (2) reactive stroma made up of connective tissue, blood vessels, and variable
numbers of macrophages and lymphocytes. Although the neoplastic cells largely determine a tumor's
behavior and pathologic consequences, their growth and evolution is critically dependent on their
stroma. An adequate stromal blood supply is requisite for the tumor cells to live and divide, and the
stromal connective tissue provides the structural framework essential for the growing cells. In addition,
there is cross-talk between tumor cells and stromal cells that directly influences the growth of tumors.
In some tumors, the stromal support is scant and so the neoplasm is soft and fleshy. In other cases the
parenchymal cells stimulate the formation of an abundant collagenous stroma, referred to
as desmoplasia. Some demoplastic tumors-for example, some cancers of the female breast-are stony
hard or scirrhous. The nomenclature of tumors and their biologic behavior are based primarily on the
parenchymal component.

Benign Tumors
In general, benign tumors are designated by attaching the suffix -oma to the cell of origin. Tumors of
mesenchymal cells generally follow this rule. For example, a benign tumor arising in fibrous tisssue is
called a fibroma, whereas a benign cartilaginous tumor is a chondroma. In contrast, the nomenclature of
benign epithelial tumors is more complex. These are variously classified, some based on their cells of
origin, others on microscopic pattern, and still others on their macroscopic architecture.

Adenoma is applied to a benign epithelial neoplasm derived from glands, although they may or may not
form glandular structures. On this basis, a benign epithelial neoplasm that arises from renal tubular cells
growing in the form of numerous tightly clustered small glands would be termed an  adenoma, as would
a heterogeneous mass of adrenal cortical cells growing as a solid sheet. Benign epithelial neoplasms
producing microscopically or macroscopically visible finger-like or warty projections from epithelial
surfaces are referred to as papillomas. Those that form large cystic masses, as in the ovary, are referred
to as cystadenomas. Some tumors produce papillary patterns that protrude into cystic spaces and are
called papillary cystadenomas. When a neoplasm, benign or malignant, produces a macroscopically
visible projection above a mucosal surface and projects, for example, into the gastric or colonic lumen, it
is termed a polyp.

Malignant Tumors
The nomenclature of malignant tumors essentially follows the same schema used for benign neoplasms,
with certain additions. Malignant tumors arising in mesenchymal tissue are usually called
sarcomas (Greek sar = fleshy), because they have little connective tissue stroma and so are fleshy (e.g.,
fibrosarcoma, chondrosarcoma, leiomyosarcoma, and rhabdomyosarcoma). Malignant neoplasms of
epithelial cell origin, derived from any of the three germ layers, are called carcinomas. Thus, cancer
arising in the epidermis of ectodermal origin is a carcinoma, as is a cancer arising in the mesodermally
derived cells of the renal tubules and the endodermally derived cells of the lining of the gastrointestinal
tract. Carcinomas may be further qualified. Squamous cell carcinoma would denote a cancer in which
the tumor cells resemble stratified squamous epithelium, and adenocarcinoma denotes a lesion in which
the neoplastic epithelial cells grow in glandular patterns. Sometimes the tissue or organ of origin can be
identified, as in the designation of renal cell adenocarcinoma or bronchogenic squamous cell carcinoma.
Not infrequently, however, a cancer is composed of undifferentiated cells of unknown tissue origin, and
must be designated merely as an undifferentiated malignant tumor.

In many benign and malignant neoplasms, the parenchymal cells bear a close resemblance to each
other, as though all were derived from a single cell. Indeed, neoplasms are of monoclonal origin, as is
documented later. Infrequently, divergent differentiation of a single neoplastic clone along two lineages
creates what are called mixed tumors.The best example of this is the mixed tumor of salivary gland
origin. These tumors contain epithelial components scattered within a myxoid stroma that sometimes
contains islands of cartilage or bone. All these elements, it is believed, arise from a single clone capable
of giving rise to epithelial and myoepithelial cells; thus, the preferred designation of these neoplasms
is pleomorphic adenoma. The great majority of neoplasms, even mixed tumors, are composed of cells
representative of a single germ layer. The multifaceted mixed tumors should not be confused with
a teratoma, which contains recognizable mature or immature cells or tissues representative of more
than one germ cell layer and sometimes all three. Teratomas originate from totipotential cells such as
those normally present in the ovary and testis and sometimes abnormally present in sequestered
midline embryonic rests. Such cells have the capacity to differentiate into any of the cell types found in
the adult body and so, not surprisingly, may give rise to neoplasms that mimic, in a helter-skelter
fashion, bits of bone, epithelium, muscle, fat, nerve, and other tissues. When all the component parts
are well differentiated, it is a benign (mature) teratoma; when less well differentiated, it is an immature,
potentially or overtly, malignant teratoma. A particularly common pattern is seen in the ovarian cystic
teratoma (dermoid cyst), which differentiates principally along ectodermal lines to create a cystic tumor
lined by skin replete with hair, sebaceous glands, and tooth structures.

For generations, benign-sounding designations such as lymphoma, melanoma, mesothelioma, and

seminoma have been used for certain malignant neoplasms. The converse is also true; ominous terms
may be applied to trivial lesions. Hamartomas present as disorganized but benign-appearing masses
composed of cells indigenous to the particular site. They were once thought to be a developmental
malformation, unworthy of the -oma designation. For example, pulmonary chondroid harmatoma
contains islands of disorganized, but histologically normal cartilage, bronchi, and vessels. However,
many hamartomas, including pulmonary chondroid hamartoma, have clonal, recurrent translocations
involving genes encoding certain chromatin proteins. Thus, through molecular biology they have finally
earned their -oma designation. Another misnomer is the term choristoma. This congenital anomaly is
better described as a heterotopic rest of cells. For example, a small nodule of well-developed and
normally organized pancreatic substance may be found in the submucosa of the stomach, duodenum, or
small intestine. This heterotopic rest may be replete with islets of Langerhans and exocrine glands. The
term choristoma, connoting a neoplasm, imparts to the heterotopic rest a gravity far beyond its usual
trivial significance. Although regrettably the terminology of neoplasms is not simple, it is important
because it is the language by which the nature and significance of tumors are categorized.

G. Metastasis

Metastases are tumor implants discontinuous with the primary tumor. Metastasis unequivocally marks
a tumor as malignant because benign neoplasms do not metastasize. The invasiveness of cancers
permits them to penetrate into blood vessels, lymphatics, and body cavities, providing the opportunity
for spread. With few exceptions, all malignant tumors can metastasize. The major exceptions are most
malignant neoplasms of the glial cells in the central nervous system, called gliomas, and basal cell
carcinomas of the skin. Both are locally invasive forms of cancer, but they rarely metastasize. It is
evident then that the properties of invasion and metastasis are separable.

In general, the more aggressive, the more rapidly growing, and the larger the primary neoplasm, the
greater the likelihood that it will metastasize or already has metastasized. There are innumerable
exceptions, however. Small, well-differentiated, slowly growing lesions sometimes metastasize widely;
conversely, some rapidly growing, large lesions remain localized for years. Many factors relating to both
invader and host are involved.

Approximately 30% of newly diagnosed individuals with solid tumors (excluding skin cancers other than
melanomas) present with metastases. Metastatic spread strongly reduces the possibility of cure; hence,
short of prevention of cancer, no achievement would be of greater benefit to patients than methods to
block metastases.

Pathways of Spread
Dissemination of cancers may occur through one of three pathways: (1) direct seeding of body cavities
or surfaces, (2) lymphatic spread, and (3) hematogenous spread. Although direct transplantation of
tumor cells, as for example on surgical instruments, may theoretically occur, it is rare and we do not
discuss this artificial mode of dissemination further. Each of the three major pathways is described
separately.

1. Seeding of Body Cavities and Surfaces

Seeding of body cavities and surfaces may occur whenever a malignant neoplasm penetrates into a
natural "open field." Most often involved is the peritoneal cavity (Fig. 7-16), but any other cavity-pleural,
pericardial, subarachnoid, and joint space-may be affected. Such seeding is particularly characteristic of
carcinomas arising in the ovaries, when, not infrequently, all peritoneal surfaces become coated with a
heavy layer of cancerous glaze. Remarkably, the tumor cells may remain confined to the surface of the
coated abdominal viscera without penetrating into the substance. Sometimes mucus-secreting
appendiceal carcinomas fill the peritoneal cavity with a gelatinous neoplastic mass referred to
as pseudomyxoma peritonei.

2. Lymphatic Spread
Transport through lymphatics is the most common pathway for the initial dissemination of carcinomas
and sarcomas may also use this route. Tumors do not contain functional lymphatics, but lymphatic
vessels located at the tumor margins are apparently sufficient for the lymphatic spread of tumor
cells.11 The emphasis on lymphatic spread for carcinomas and hematogenous spread for sarcomas is
misleading, because ultimately there are numerous interconnections between the vascular and the
lymphatic systems. The pattern of lymph node involvement follows the natural routes of lymphatic
drainage. Because carcinomas of the breast usually arise in the upper outer quadrants, they generally
disseminate first to the axillary lymph nodes. Cancers of the inner quadrants drain to the nodes along
the internal mammary arteries. Thereafter the infraclavicular and supraclavicular nodes may become
involved. Carcinomas of the lung arising in the major respiratory passages metastasize first to the
perihilar tracheobronchial and mediastinal nodes. Local lymph nodes, however, may be bypassed-so-
called "skip metastasis"-because of venous-lymphatic anastomoses or because inflammation or
radiation has obliterated lymphatic channels.

In breast cancer, determining the involvement of axillary lymph nodes is very important for assessing
the future course of the disease and for selecting suitable therapeutic strategies. To avoid the
considerable surgical morbidity associated with a full axillary lymph node dissection, biopsy of sentinel
nodes is often used to assess the presence or absence of metastatic lesions in the lymph nodes. A
sentinel lymph node is defined as "the first node in a regional lymphatic basin that receives lymph flow
from the primary tumor." Sentinel node mapping can be done by injection of radiolabeled tracers and
blue dyes, and the use of frozen section upon the sentinel lymph node at the time of surgery can guide
the surgeon to the appropriate therapy. Sentinel node biopsy has also been used for detecting the
spread of melanomas, colon cancers, and other tumors.

In many cases the regional nodes serve as effective barriers to further dissemination of the tumor, at
least for a while. Conceivably the cells, after arrest within the node, may be destroyed by a tumor-
specific immune response. Drainage of tumor cell debris or tumor antigens, or both, also induces
reactive changes within nodes. Thus, enlargement of nodes may be caused by (1) the spread and growth
of cancer cells or (2) reactive hyperplasia. Therefore, nodal enlargement in proximity to a cancer, while
it must arouse suspicion, does not necessarily mean dissemination of the primary lesion.

3. Hematogenous Spread
Hematogenous spread is typical of sarcomas but is also seen with carcinomas. Arteries, with their
thicker walls, are less readily penetrated than are veins. Arterial spread may occur, however, when
tumor cells pass through the pulmonary capillary beds or pulmonary arteriovenous shunts or when
pulmonary metastases themselves give rise to additional tumor emboli. In such vascular spread, several
factors influence the patterns of distribution of the metastases. With venous invasion the blood-borne
cells follow the venous flow draining the site of the neoplasm, and the tumor cells often come to rest in
the first capillary bed they encounter. Understandably the liver and lungs are most frequently involved
in such hematogenous dissemination because all portal area drainage flows to the liver and all caval
blood flows to the lungs. Cancers arising in close proximity to the vertebral column often embolize
through the paravertebral plexus, and this pathway is involved in the frequent vertebral metastases of
carcinomas of the thyroid and prostate.

Certain cancers have a propensity for invasion of veins. Renal cell carcinoma often invades the branches
of the renal vein and then the renal vein itself to grow in a snakelike fashion up the inferior vena cava,
sometimes reaching the right side of the heart. Hepatocellular carcinomas often penetrate portal and
hepatic radicles to grow within them into the main venous channels. Remarkably, such intravenous
growth may not be accompanied by widespread dissemination. Histologic evidence of penetration of
small vessels at the site of the primary neoplasm is obviously an ominous feature.

H. Effects of Neoplasm

Ultimately the importance of neoplasms lies in their effects on patients. Although malignant tumors are
of course more threatening than benign tumors, any tumor, even a benign one, may cause morbidity
and mortality. Indeed, both malignant and benign tumors may cause problems because of (1) location
and impingement on adjacent structures, (2) functional activity such as hormone synthesis or the
development of paraneoplastic syndromes, (3) bleeding and infections when the tumor ulcerates
through adjacent surfaces, (4) symptoms that result from rupture or infarction, and (5) cachexia or
wasting.

Local and Hormonal Effects

Location is crucial in both benign and malignant tumors. A small (1-cm) pituitary adenoma, though
benign and possibly nonfunctional, can compress and destroy the surrounding normal gland and thus
lead to serious hypopituatarism. Cancers arising within or metastatic to an endocrine gland may cause
an endocrine insufficiency by destroying the gland. Neoplasms in the gut, both benign and malignant,
may cause obstruction as they enlarge. Infrequently, peristaltic movement telescopes the neoplasm and
its affected segment into the downstream segment, producing an obstructing intussusception.
Hormone production is seen with benign and malignant neoplasms arising in endocrine glands. Such
functional activity is more typical of benign than of malignant tumors, which may be sufficiently
undifferentiated to have lost such capability. A benign beta-cell adenoma of the pancreatic islets less
than 1 cm in diameter may produce sufficient insulin to cause fatal hypoglycemia. In addition,
nonendocrine tumors may elaborate hormones or hormone-like products and give rise to paraneoplastic
syndromes (discussed later). The erosive and destructive growth of cancers or the expansile pressure of
a benign tumor on any natural surface, such as the skin or mucosa of the gut, may cause ulcerations,
secondary infections, and bleeding. Melena (blood in the stool) and hematuria, for example, are
characteristic of neoplasms of the gut and urinary tract. Neoplasms, benign as well as malignant, may
cause problems in varied ways, but all are far less common than the cachexia of malignancy.

Cancer Cachexia
Individuals with cancer commonly suffer progressive loss of body fat and lean body mass accompanied
by profound weakness, anorexia, and anemia, referred to ascachexia. Unlike starvation, the weight loss
seen in cachexia results equally from loss of fat and lean muscle. There is some correlation between the
tumor burden and the severity of the cachexia. However, cachexia is not caused by the nutritional
demands of the tumor. In persons with cancer, the basal metabolic rate is increased, despite reduced
food intake. This is in contrast to the lower metabolic rate that occurs as an adaptational response in
starvation. Although patients with cancer are often anorexic, cachexia probably results from the action
of soluble factors such as cytokines produced by the tumor and the host rather than reduced food
intake. The basis of these metabolic abnormalities is not fully understood. It is suspected that TNF
produced by macrophages in response to tumor cells or by the tumor cells themselves mediates
cachexia. TNF at high concentrations may mobilize fats from tissue stores and suppress appetite; both
activities would contribute to cachexia. Other cytokines, such as IL-1, interferon-γ, and leukemia
inhibitory factor, synergize with TNF. Additionally, other soluble factors produced by tumors, such as
proteolysis-inducing factor and a lipid-mobilizing factor, increase the catabolism of muscle and adipose
tissue.185 These factors reduce protein synthesis by decreasing m-RNA translation and by stimulating
protein catabolism through the activation of the ATP-dependent ubiquitin-proteasome pathway. It is
now thought that there is a balance between factors that regulate muscle hypertrophy, such as IGF, and
factors that regulate muscle catabolism. In cachexia these homeostatic mechanisms are disrupted,
tilting the scales toward cachectic factors. There is currently no satisfactory treatment for cancer
cachexia other than removal of the underlying cause, the tumor. However, cachexia clearly hampers
effective chemotherapy, by reducing the dosages that can be given. Furthermore, it has been estimated
that a third of deaths of cancer are attributable to cachexia, rather than directly due to the tumor
burden itself. Identification of the molecular mechanisms involved in cancer cachexia may allow
treatment of cachexia itself.

Paraneoplastic Syndromes
Symptom complexes in cancer-bearing individuals that cannot readily be explained, either by the local
or distant spread of the tumor or by the elaboration of hormones indigenous to the tissue from which
the tumor arose, are known as paraneoplastic syndromes.186 These occur in about 10% of persons with
malignant disease. Despite their relative infrequency, paraneoplastic syndromes are important to
recognize, for several reasons:

 They may represent the earliest manifestation of an occult neoplasm.

 In affected patients they may represent significant clinical problems and may even be lethal.
  They may mimic metastatic disease and therefore confound treatment.

I. Nine (9) Danger Signals of Cancer

“ C-A-U-U-U-T-I-O-N !!!”

C – hange in Bowel or Bladder Habits

 Alternating constipation and diarrhea is the most characteristic manifestation of colon
cancer. Change in bladder habits may signify bladder or prostate cancer.

A – Sore that does Not Heal

 A sore that does not heal characterize cancer because the tumor causes impaired
circulation and oxygenation in the area. This leads to tissue necrosis, ulceration,
bleeding and infection.

U – nusual Bleeding or Discharge

 Unusual bleeding or discharge from the body part affected by cancer is also due to
impaired circulation and oxygenation in the area. This leads to necrosis, ulceration,
bleeding and infection. Infection causes unusual discharge.

U – nexplained Sudden Weight Loss

 This is due to excessively rapid metabolism caused by the rapid multiplication of cancer
cells. The normal cells are deprived of nutrients because of the cancer cells.

U – nexplained Anemia
 Unexplained anemia is due to the following factors:
a) the cancer cells take up iron faster than the normal cells
b) bleeding contributes to anemia
c) cancer cells tend to destroy normal RBCs

T – hickening or Lump in the Breast or elsewhere

 This may signify abnormal cell growth.

I – ndigestion or Difficulty in Swallowing

 Indigestion is the usual initial manifestation of gastric cancer. Difficulty in swallowing is a
characteristic of cancer of the larynx and cancer of the esophagus.

O- bvious Change in Wart or Mole

 Sudden growth in size of wart or mole, uneven coloring, or change in the texture may
signify transformation into a cancerous lesion.

N – agging Cough or Hoarseness of Voice

 This signifies cancer of the larynx or cancer of the lungs.
J. Assessing patient with Cancer

1. History and Physical Assessment

HISTORY

1. Breast Cancer
 Early menarche
 Late menopause
 Nulliparous or older than 30 years at birth of a first child
2. Lung Cancer
 Tobacco abuse
 Asbestos
 Radiation exposure
 Air pollution
3. Colorectal Cancer
 Greater incidence in men
 Familial polyposis
 Ulcerative colitis
 High fat and Low fiber diet
4. Prostate Cancer
 Common among males who are 50 years old and older
 African Americans have the highest incidence of prostate cancer in the world.
 Positive family history
 Exposure to cadmium
5. Cervical Cancer
 Sexual behavior
- first sexual intercourse at an early age
- multiple sexual partners
- sexual partner who has had multiple sexual partner
 Human papilloma virus and AIDS
 Low socioeconomic status
 Cigarette smoking
6. Head and Neck Cancer
 More common among males
 Alcohol and tobacco use
 Poor oral hygiene
 Long term sun exposure
 Occupational exposures – asbestos, tar, nickel, textile, wood or leather work, and
machine tool experience
7. Skin Cancer
 Individuals with fair complexion
 Positive family history
 Moles ( nevi )
 Exposure to coal tar, creosote, arsenic, radium
 Sun exposure between 11 AM to 3 PM
 PHYSICAL ASSESSMENT

Symptoms of cancer metastasis depend on the location of the tumor. Roughly, cancer symptoms
can be divided into three groups:
 Local symptoms: unusual lumps or swelling (tumor), hemorrhage (bleeding), pain and/or
ulceration. Compression of surrounding tissues may cause symptoms such as jaundice
(yellowing the eyes and skin).
 Symptoms of metastasis (spreading): enlarged lymph nodes, cough and hemoptysis,
hepatomegaly (enlarged liver), bone pain, fracture of affected bones and neurological
symptoms. Although advanced cancer may cause pain, it is often not the first symptom.
 Systemic symptoms: weight loss, poor appetite, fatigue and cachexia (wasting),
excessivesweating (night sweats), anemia and specific paraneoplastic phenomena, (i.e. specific
conditions that are due to an active cancer, such as thrombosis or hormonal changes).

Every symptom in the above list can be caused by a variety of conditions. Cancer may be a common
or uncommon cause of each item.

Cancer symptoms are quite varied and depend on where the cancer is located, where it has spread,
and how big the tumor is. Some cancers can be felt or seen through the skin - a lump on the breast or
testicle can be an indicator of cancer in those locations. Skin cancer (melanoma) is often noted by a
change in a wart or mole on the skin. Some oral cancers present white patches inside the mouth or
white spots on the tongue.

Other cancers have symptoms that are less physically apparent. Some brain tumors tend to present
symptoms early in the disease as they affect important cognitive functions. Pancreas cancers are usually
too small to cause symptoms until they cause pain by pushing against nearby nerves or interfere with
liver function to cause jaundice. Symptoms also can be created as a tumor grows and pushes against
organs and blood vessels. For example, colon cancers lead to symptoms such as constipation, diarrhea,
and changes in stool size. Bladder or prostate cancers cause changes in bladder function such as more
frequent or infrequent urination.

As cancer cells use the body's energy and interfere with normal hormone function, it is possible to
present symptoms such as fever, fatigue, excessive sweating, anemia, and unexplained weight loss.
However, these symptoms are common in several other maladies as well. For example, coughing and
hoarseness can point to lung or throat cancer as well as several other conditions.

When cancer spreads, or metastasizes, additional symptoms can present themselves in the newly
affected area. Swollen or enlarged lymph nodes are common and likely to be present early. If cancer
spreads to the brain, patients may experience vertigo, headaches, or seizures. Spreading to the lungs
may cause coughing and shortness of breath. In addition, the liver may become enlarged and cause
jaundice and bones can become painful, brittle, and break easily. Symptoms of metastasis ultimately
depend on the location to which the cancer has spread.

2. Breast self Examination and Testicular Self Exam

 BREAST SELF-EXAMINATION

Inspection Before a Mirror

Look for any change in size or shape; lumps or thickenings; any rashes or other skin irritations;
dimpled or puckered skin; any discharge or change in nipples ( e.g. position or asymmetry ). Inspect the
breasts in all of the following positions:

 Stand and face the mirror with your arms relaxed at your sides or hands resting on hips;
then turn to the right and the left for a side view. Look for any flattening in the side
view.
 Bend forward from the waist with arms raised over the head.
 Stand straight with the arms raised over the head and move the arms slowly up and
down at the sides. Look for free movement of the breasts over the chest wall.
 Press your hands firmly together at chin level while elbows are raised to shoulder level.

Palpation: Lying Position

 Place a pillow under your right shoulder and place the right hand behind your head. This
position distributes breast tissue more evenly on the chest.
 Use the finger pads of the three middle fingers ( held together ) of your left hand to feel
for lumps.
 Press the breast tissue against the chest wall firmly enough to know how your breast
feels. A ridge of firm tissue in the lower curve of each breast is normal.
 Use small circular motions systematically all the way around the breast as many times as
necessary until the entire breast is covered.
 Bring your arm down to your side and feel under your armpit, where breast tissue is also
located.
 Repeat the exam on your left breast, using the finger pads of your right hand.

Palpation: Standing or Sitting

 Repeat the examination of both breasts while upright with one arm behind your head.
This position makes it easier to check the area where a large percentage of breast
cancers are found, the upper outer part of the breast and toward the armpit.
 Optional: Do the upright BSE in the shower. Soapy hands glide more easily over wet
skin. Report any changes to your health care provider promptly.

TESTICULAR SELF-EXAMINATION

 Choose one day of each month ( e.g. the first or the last day of each month ) to examine
yourself.
 Examine yourself when you are taking a warm shower or bath.
 Support the testicle underneath with one hand. Place the fingers of the other hand under the
testicle and the thumb on top. This may be easier to do if the leg on that side is raised.
 Roll each testicle between the thumb and fingers of your hand, feeling for lumps, thickening, or
a hardening inconsistency. The testes should feel smooth.
  Palpate the epididymis, a cordlike structure on the top and back of the testicle. The epididymis
feels soft and not as smooth as a testicle.
 Locate the spermatic cord, or vas deferens, which extends upward from the scrotum toward the
base of the penis. It should feel firm and smooth.
 Using a mirror, inspect your testicles for swelling, any enlargement, or lumps in the skin of the
testicle.
 Report any lumps or other changes to your health care provider promptly.

3. Cancer Specified Diagnostic Examination

A cancer diagnosis is based on assessment for physiologic and functional changes and results of the
diagnostic evaluation. Patients with suspected cancer undergo extensive testing to:

1. Determine the presence of tumor and its extent

2. Identify the possible spread of disease or invasion of other body tissues
3. Evaluate the function of involved and uninvolved body systems and organs
4. Obtain tissue and cells for analysis, including evaluation of tumor stage and grade.

The diagnostic evaluation is guided by information obtained through a complete history and physical
examination. Patients undergoing extensive testing are usually farfel of the procedures and anxious
about the possible test result. The nurse can help relieve the patient’s fear and anxiety by explaining the
tests to be performed, the sensations likely to be explaining the test to be performed, and the patient’s
role in the test procedures. The nurse encourages the patient and the family to voice their fears about
the results, supports the patient and family throughout the test period, and reinforces and clarifies
information and conveyed by the physician. The nurse also encourages the patient and the family to
communicate and share their concerns and to discuss their questions and concerns with each other.

Cancer Specified Diagnostic Examination

Test Description Diagnostic Exam

Tumor Marker Analysis of the substances found in blood or other body Breast , colon, lung,
Identification fluids that are made by the tumor or by the body in ovarian, testicular,
response to the tumor or by the body in response to prostate cancer
the tumor.
Magnetic Use of magnetic fields and radiofrequency signals to Neurologic, pelvic,
resonance imaging create sectional images of various body structures. abdominal, thoracic
(MRI) cancer
Computed Use of narrow-beam x-ray to scan successive layers of Neurologic, pelvic,
tomography (CT) tissue for a cross-sectional view. skeletal, abdominal,
thoracic cancers
Fluoroscopy Use of x-rays that identify contrasts in body tissue Skeletal, lungs,
densities; may involve the use of contrast agents. gastrointestinal cancers

Ultrasonography High-frequency sound waves echoing off body tissues Abdominal and pelvic
(ultrasound) are converted electronically into images; used to assess cancers
 tissues deep within the body.
Endoscopy Direct visualization of a body cavity or passageway by Bronchial,
insertion of an endoscope into a body cavity or gastrointestinal cancers
opening; allows tissue biopsy, fluid aspiration, and
excision of small tumors; both diagnostic and
therapeutic.
Nuclear medicine Uses intravenous injection or ingestion of radioisotope Bone, liver, kidney,
imaging substances followed by imaging of tissues that have spleen, brain, thyroid
concentrated the radioisotopes. glands
Positron emission Through the use of tracer; provides black and white or Lung, colon, liver,
tomography (PET) color-coded images of the biologic activity of a pancreatic, head and
particular area, rather than its structure; used in neck cancers; Hodgkin
detection of cancer or its response to treatment. and non-Hodgkin
lymphoma and
melanoma
PET fusion Use of PET scanner and CT scanner and CT scanner in Lung, colon, liver,
one machine to provide an image combining anatomic pancreatic, head and
detail, spatial resolution, and functional metabolic neck cancers; Hodgkin
abnormalities. and non-Hodgkin
lymphoma and
melanoma
Biopsy The surgical removal of a small piece of tissue to Colorectal, breast,
determine whether the area is cancerous. ovarian, head and neck
cancer; lymphoma and
Most frequently used for easily accessible tumors of the melanoma
Excisional biopsy skin, breast, upper and lower gastrointestinal tract and
upper respiratory tract. The surgeon can remove the
entire tumor and surrounding marginal tissues as well.
This removal of normal tissue beyond the tumor area
decreases the possibility that residual microscopic
disease cells may lead to a recurrence of tumor.

Is performed if the tumor mass is too large to removed.

In this case, a wedge of tissue from the tumor is
removed for analysis.
Incisional biopsy
Are performed to sample suspicious masses that are
easily accessible, such as some growths in the breasts,
thyroid, lung, liver and kidney. Needle biopsies are fast,
Needle biopsies relatively inexpensive, and easy to perform and usually
require only local anesthesia.

Mammogram It is a special x-ray examination of the breast made with Breast

specific x-ray equipment that can often find tumors too
small to be felt. A mammogram is the best radiographic
method available today to detect breast cancer early.
Colonoscopy An examination of the entire length of the colon using a Colon
 lighted, flexible tube.
Colposcopy An examination of the cervix and vagina using an Cervix, vagina
instrument called a colposcope.
PSA (Prostate A substance (tumor marker) in the blood derived from
Specific Antigen) the prostate gland. Its level may rise in prostatic cancer
and is useful as a marker to monitor the effects of
treatment. It is occasionally elevated as a result of non-
malignant conditions, such as benign prostatic
hypertrophy. Should be evaluated in conjunction with
other diagnostic tests such as digital rectal exam,
transrectal ultrasound, and/or prostatic acid
Phosphatase levels.
Papanicolaou test A screening test used in gynecology to detect Cervix
(Pap smear, Pap premalignant and malignant (cancerous) processes in
test, cervical the ectocervix.
smear, or smear
test)

Tumor Staging and Grading

Staging

It determines the size of the tumor and the existence of metastasis. Several systems exist for
classifying the anatomic extent of disease. The TNM system is frequently used. T refers to the extent of
the primary tumor, N refers to lymph node involvement and M refers to the extent of metastasis. A
variety of other staging systems are used to describe the extents of cancers that are not well described
by the TNM system. It also provide convenient shorthand notation that condenses lengthy descriptions
into manageable terms for comparisons of treatment and prognoses.

Grading

It refers to classification of the tumor cells. Grading systems seek to define the type of tissue
from which the tumor originated and the degree to which the tumor cells retain the functional and
histologic characteristics of the tissue origin. Samples of cells to be used to establish the grade of a
tumor may be obtained through cytology, biopsy or surgical excision.

The tumor is assigned a numeric value ranging I to IV. Grade I tumors, also known as well-differentiated
tumors, closely resemble the tissue of origin in the structure and function. Tumors that do not clearly
resemble the tissue of origin in the structure and function are described as poorly differentiated and are
assigned grade IV. These tumors tend to be more aggressive and less responsive to treatment than well
differentiated tumors.

K. Common Malignancies

 Breast cancer
  Bladder cancer
 Colon and rectal cancer
 Endometrial cancer
 Kidney cancer
 Lung cancer
 Melanoma
 Leukemia
 Non-hodgkin lymphoma
 Pancreatic cancer
 Prostate cancer
 Thyroid cancer
 Stomach cancer

K. Therapeutic and Nursing Modalities of Cancer

 Support the idea that cancer is a chronic illness that has acute exacerbations rather than one
that is synonymous with death and sufferings.
 Assess own level of knowledge relative to the pathophysiology of the disease process.
 Make use of current research findings and practices in the care o f the patient with cancer and
his or her family.
 Identify patient at high risk for cancer.
 Participate in primary and secondary prevention efforts.
 Assess the nursing care needs of the patient with cancer.
 Assess the learning needs, desires, and capabilities of the patient with cancer.
 Identify the nursing problems of the patient and the family.
 Assess the social support networks available to the patient.
 Plan appropriate interventions with the patient and the family.
 Assist the patient to identify strengths and limitations.
 Assist the patient to design short-term and long-term goals for care.
 Implement a nursing care plan that interfaces with the medical care regimen and that is
consistent with the established goals.
 Collaborative with members of a multidisciplinary team to foster continuity of care.
 Evaluate goals and resultant outcomes of care with the patient, the family, and the members of
the multidisciplinary team.
 Reassess and redesign the direction of the care as determined by the evaluation.

Surgery

Surgical removal of the entire cancer remains the ideal and most frequently used treatment method.
Surgery may be the primary method of treatment, or it may be prophylactic, palliative and
reconstructive.

Diagnostic Surgery
 Diagnostic surgery, such as biopsy, is usually performed to obtain tissue sample for analysis of
cells suspected to be malignant. Biopsy is taken from the actual tumor, but in some situations, it is
necessary to biopsy lymph nodes near the suspicious tumor.

Surgery as Primary Treatment

Two common surgical approaches used for treating primary tumors are local and wide excisions. Local
excision is warranted when the mass is small. It includes removal of the mass and a small margin of the
normal tissues that is easily accessible. Wild or radical excision include removal of the primary tumor,
lymph node, adjacent involve structures and surrounding tissue that may be at high risk for tumor
spread. This surgical method can result in disfigurement and altered functioning. However, wide
excisions are considered if the tumor can be removed completely and chances of cure and controlare
good.

Prophylactic Surgery

It involves removing nonvital tissues or organs that are likely to develop cancer. The factor s are
considered when physicians and patient discuss possible prophylactic surgery ;family history and
genetic predisposition, presence or absence of symptoms, potential risks and benefits, ability to detect
cancer at an early stage, the patient’s acceptance of the post operative outcome.

Palliative Surgery

When cure is not possible, the goals of treatment are to make the patient as comfortable as possible
and promote a satisfying and productive life for as long as possible. Palliative surgery is performed in an
attempt to relieve complications of cancer. Honest and informative communication with the patient and
family about the goal of surgery is essential to avoid false hope and disappointment.\

Reconstructive Surgery

Reconstructive surgery may follow curative and radical surgery and is carried out in an attempt to
improve function obtain a more desirable cosmetic effect. It may be performed in one operation or in
stages. Reconstructive surgery may be indicated for breast, head and neck, and skin cancers.

The nurse must recognize the patient’s needs and the impact that altered functioning and altered body
image must have on quality of life. The individual’s needs of the patient undergoing reconstructive
surgery must be accurately assessed and addressed.

Chemotherapy

In chemotherapy, antineoplastic agents are used in an attempt to destroy tumor cells by interfering with
cellular functions, including replication. Chemotherapy is used primarily to treat systemic disease rather
than localized lesions that are amenable to surgery and radiation. Chemotherapy may be combined with
surgery to reduce tumor size preoperatively, to destroy any remaining tumor cell postoperatively, or to
treat some forms of leukemia. The goals of chemotherapy (cure, control and palliation), must be realistic
because they will define medications to be used and the aggressiveness of the treatment plan.

Classification of Chemotherapeutic Agents

Chemotherapeutic agent may be classified by their relationship with to the cycle. Certain
chemotherapeutic agents are termed cell cycle-specific agents. These agent destroy cells that are
actively reproducing by means of the cell cycle, most affect cells in the S phase by interfering with the
DNA and RNA synthesis. Other agents, such as vinca or plant alkaloids, are specific to the M phase,
where they half mitotic spindle formation. Chemotherapeutic agent that act independently of the cell
cycle phases are termed cell cycle-nonspecific agents. These agents usually have a prolonged effect on
the cells, leading to cellular damage or death. Many treatment plan combined cell cycle-specific and cell
cycle-nonspecific agents to increase the number of vulnerable tumor cells killed during treatment
period.

Nursing Management in Chemotherapy

Nurses play an important role in assessing and managing of many of the problems experienced by the
patient undergoing chemotherapy. Chemotherapeutic agents have systemic effects on normal cells as
well as malignant ones, which means that these problems are often widespread, affecting body systems.

Assessing fluid and electrolyte

Anorexia, nausea, vomiting, altered taste, and diarrhea put patients at risk for nutritional and fluid and
electrolyte disturbances. It is important for the nurse to assess the patients nutritional and fluid and
electrolyte status frequently and to use creative ways to encourage an adequate fluid and dietary
intake.

Modifying risk for infection and bleeding

Nursing assessment and care focus on identifying and modifying factors that would further increased
the patient’s risk. Aseptic technique and gentle handling are indicated to prevent infections and trauma.
The patient and family members are instructed about the measures to prevent these problems at home.

Administering chemotherapy

The local effects of the chemotherapeutic agent are also of concern. The patient is closely observed
during its administration because of the risk and consequences of extravasation. Local difficulties or
problems with administration of chemotherapeutic agents are brought to the attention of the physician
promptly so that corrective measures can be taken immediately to minimize local tissue damage.

Protecting caregivers

Nurses involved in handling chemotherapeutic agents may be exposed to low doses of the agents by
direct contact, inhalation, or ingestion. Urinalyses of personnel repeatedly exposed to the cytotoxic
agents have demonstrated mutagenic activity. The Occupational Safety and Health Administration,
Oncology Nursing Society, hospitals and other health care agencies have developed specific precautions
for health care providers involved in preparation and administration of chemotherapy.