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2ND SEM · AY 17-18
Nursing Care of Clients with Cancer (Intro)
Professor Lydia Manahan
o Most cancers are curable if treated early Total number of cells in the body remains constant
II. CANCER BACKGROUND
D. Differentiation
Family of complex diseases
Is when the stem cell (from bone marrow) matures
Affect different organs and organ systems
Normal cells mutate into abnormal cells that take into a specific type of cell
Normally, after a cell has divided, it becomes either a
over tissue
Eventually harm and destroy host permanent cell or stable cell
These cells stop reproducing and become productive
Historically, cancer is a dreaded disease
Regulated by a feedback system
A. Pathophysiology Affected by various stimuli
Carcinogenesis/ Oncogenesis o Stress
Tumor development slow and insidious o Infection
Initiator-Promoter Theory o Hemorrhage
Loss of cellular control mechanisms (ie apoptosis) o Bone marrow depletion
Loss of differentiation o Drug therapy
Some books say that it takes 18 years for symptoms to IV. REACTIVE AND NEOPLASTIC GROWTH PROCESSES
appear. Differentiation
Atrophy: decrease in cell size
1. Berenblum Theory Hypertrophy: increase in cell size
INITIATION PROMOTION PROGRESSION Hyperplasia: increase in the number of normal cells
in a normal arrangement in a tissue or organ. Usually
Initiation leads to an increase in the size or part (tissue mass)
o Multiple theories as to when the genes in the
and an increase in functional activity
cells are damaged o Types:
o Possibly in utero, from physical or chemical o Physiologic: due to an external stimulus and
exposure, latent oncogenes, viruses, or a lack of subsides when the stimulus is removed
suppressor genes from our parents, and at this o Neoplastic Hyperplasia or Neoplasia: due in part
point the cell is not dividing to a heritable abnormality within the involved
Promotion cells (alter the genetic mechanisms of involved
o The stage when the abnormal cell starts to
cells)
divide, may be stimulated by environmental Metaplasia: replacement of one type of fully
changes, hormones, drugs, or irritants differentiated cell by another fully differentiated cell in
Progression another part of the body where the second cell type
o The phase when the abnormal cells have
does not normally occur
continued to grow into a Primary Tumor, may Dysplasia: alteration in the size, shape, and
produce angiogenesis factors which supply organization of differentiated cells. Pre-malignant
blood and vascular nourishment to the tumor. change. Change is usually a response to an irritant. It
The tumor may have subcolonies of cells with reverts to normal when the irritant is removed but
different genes and features. may transform to a neoplasia.
Anaplasia: tumor cells that that are completely
III. ONCOLOGY PROCESSES
A. Angiogenesis undifferentiated and bear no resemblance to cells of
tissues of their origin. Irreversible change
Angiogenetic switch: ability of the tumor to promote
formation of new capillaries from pre-existing host ** Once a cell is mutated, it can’t turn back. Dysplasia >
vessels Metaplasia, chance in developing cancer
Stimuli for angiogenesis: hypoxia, inflammation, and
genetic lesions V. BIOLOGY OF ABNORMAL CELLS
They have continuous or inappropriate, usually faster
B. Metastasis growth or larger growth patterns
The movement of cancer cells into other organs of They have no specific morphology and often do not
the body, thus creating new tumor sites. resemble their parent cells= anaplastic
They do not respond to signals for apoptosis =
C. Proliferation
programmed cell death
Normally: cells produced=cells die
Have a large nuclear - cytoplasmic ratio; the nucleus o Cancer is a genetic disease
may occupy most of the cell area o The malignant phenotype often requires
They lose some or all of their normal cell functions mutations in several different genes
They do not make fibronectin, and thus cannot o Germline cells: passed to future generations
connect easily and break off easily o Somatic cells: not passed to progeny
They are able to migrate throughout the body= Chronic Inflammation: an important factor in the
metastasis development of cancer
They invade other tissues and types of cells o Cytokine release from inflammatory cells
They are not controlled by contact o Free radicals
They have more or less chromosomes than the o Mutation promotion
parent cells= Aneuploid, or a mutation of gene. o Decreased response to DNA damage
Virus: not sufficient of cancer development but
** Cancer has exponential growth constitute one alteration in the multistep process of
cancer
VI. THEORIES OF CARCINOGENESIS
1. Cellular Mutation Implicated:
o Epstein Barr virus: Burkitt’s lymphoma
Cells begin to mutate (change the DNA to unnatural
o Hepatitis virus-hepatocellular Ca
cell reproduction)
2. Oncogenes/Tumor Suppressor Genes o HPV-cervical cancer
Abnormalities o Retrovirus-T cell leukemia
Oncogenes are genes that promote cell proliferation
C. Environmental Risk Factors
and can trigger cancer
Chemical Carcinogens
Tumor suppressor genes normally suppress
Radiation
oncogenes but are damaged
o Ionizing radiation in atomic bomb survivors
** all of us have cancer cells, it is up for us that the cancer o Sunlight and melanoma
cells do not grow faster than the anti-oncogenes. Lifestyle
Tobacco
A. Telomeres o Multipotent carcinogenic mixture
The ability to bypass telomere-based growth o Linked to cancers of the lungs, aerodigestive
limitations is a critical step in the evolution of tract, liver, pancreas, kidney, lower urinary tract,
malignancies cervix uteri, and myeloid leukemia
End of chromosomes which gradually shortens with Alcohol Consumption
every cell replication o Risk factor for oral cavity, pharynx, hypopharynx,
Replicative senescence: cell growth arrest due to larynx, esophagus, and liver cancers
loss of telomeres o Cigarette/alcohol combination multiplies the
person’s risk
B. Oncogenesis Ionizing Radiation
Cells in the replicative senescence can go through o Emission from X-rays, radioisotopes, and other
the cell cycle if the p53 and pRB are nonfunctioning radioactive sources
Telomerase: allows telomere extensions and are o Exposure causes cell death gene mutations, and
found high in cancer thus allowing cellular chromosome aberration
proliferation o Bystander effects: genetic instability
o Poor gene repair
VII. RISK FACTORS o Changes in gap junction- intercellular
A. Host Risk Factors
communication
Age
Ultraviolet Radiation
Heredity: familial predisposition and genetic make- o Physical source is sunlight
up o Ultraviolet A (UVA) and ultraviolet B (UVB)
Hormones: drives cell division of a malignant o Promotes skin inflammation and release of free
phenotype
radicals
Immunologic mechanism: o Causes basal cell carcinoma, squamous cell
o Impaired immune surveillance
carcinoma, and melanoma
o HIV-related cancers
Occupational Hazards
Exposure to Mutagens
E. Radiation Therapy
Second most common treatment radiation therapy, or
radiotherapy, uses high-energy ionizing radiation to
kill cancer.
Two types:
o External
o Internal
F. Chemotherapy
May be used to cure, prevent, or relieve cancer
symptoms
Drugs used in chemotherapy are called
antineoplastics because they inhibit the growth and
reproduction of malignant cells.
Chemotherapy is the treatment of choice for
metastatic cancers. It is also the treatment most
responsible for increasing cancer cure rates in recent
years.
G. Biotherapy
Performed with biologic response modifiers (BRMs),
agents that stimulate the body’s natural immune
system to control and destroy malignant cells.
Most BRMs are still being evaluated in trial studies.