MODULE 1 : PATHOPHYSIOLOGIC

CONCEPTS IN CELLULAR
 Benign Neoplasm
ABERRATIONS
A harmless growth that does not invade or spread
 The experience of cancer precipitates many to other tissues.
stressful feelings and reactions, such as anxiety,  Neoplasia
anger, denial, shame, guilt and uncertainty. Abnormal cellular changes and growth of new
 The diagnostic tests, the medical treatment, the tissues.
prognosis, the body changes, the reactions of the  Hyperplasia
family and friends, the process and experience of Increase in cell number.
hospitalization, the financial difficulty and the  Hypertrophy
perceived changes in life style and quality of life – Increase in cell size.
all take part in the outcome of the disease process  Metaplasia
– CANCER. Replacement of one adult cell type by a different
 Cancer is as old as the ages. It was recognized by adult cell type.
skilled observers who gave the name CANCER  Dysplasia
(Latin, cancri, which means crab) because it Changes in adult cell size, shape and organization
stretches out in many directions like the legs of the that arises from glandular tissue.
crab.  Anaplasia
 Cancer should be regarded as a disease process Reverse cellular development in a more primitive
which begins when abnormal cells are derived from or embryonic cell type.
normal cell by some poorly understood mechanism  Metastases
of change. Spread of cancer cells to distant parts of the body
 It should be noted that cancer is not a single to set up new tumors.
disease with one cause, rather it is a group of  Oncology
distinct diseases with different etiologies, The medical specialty that deals with the
manifestations, treatments and nursing care. diagnosis, treatment and study of cancers.
 Despite the significant advances in cancer detection  Adenocarcinoma
and treatment, it continues to be the second Cancer that arises from glandular tissues.
leading cause of death globally in 2018. Example: Cancer of the breast, lung, thyroid,
 Health education on cancer prevention and early colon and pancreas.
detection is one great role the nurse must venture  Carcinoma
into. A form of cancer that is composed of epithelial
 The nurse is also expected to give individualized cells, develops in tissues covering or lining organs
care to clients under her/his care. of the body such as skin, uterus or breast.
 Similarly, she/he should be knowledgeable on the  Sarcoma
disease process, side effects of drugs and A cancer of supporting or connective tissues such
treatments and most of all give emphasis on the as cartilage, bones, muscles or fats.
essentials of CARING.  Carcinogens
Factors associated with cancer causation.
A. Definition of Concepts Example: Radiation, chemicals, viruses, physical
 Cancer agents.
A disease of the cell in which the normal  Fibroma
mechanisms of the control of growth and Common benign neoplasm that arises in the
proliferation have been altered. adipose tissue.
It is invasive spreading directly to the surrounding  Leiomyoma
tissues as well as to new sites in the body. Neoplasm of smooth muscle in origin, most
Also called as malignant neoplasm. common benign neoplasm in women.
  Normal cells respect the boundaries and territory
of the cells surrounding them. They will not invade
 Lipoma
a territory that is no their own.
A common neoplasm that arises in adipose tissue,
 The neighboring cell are thought to inhibit cellular
usually benign in nature.
growth through physical contact of the
 Carcinoma in Situ
surrounding cell membranes.
Neoplasm of epithelial tissue that remains
 Cancer cells grown in tissue culture are
confined to the site of origin.
characterized by loss of contact inhibition.
 Apoptosis
 These cells have no regard for cellular boundaries
Process of carcinogenesis when cell death does
and will grow on top of another and also on top of
not occur.
or between normal cells.
 Fibroma
 The rate of normal cellular proliferation (from
May grow anywhere in the body but are
time of cellular birth to the time off cellular death)
frequently found in the uterus.
differs in each body tissue.
 In some tissues such as bone marrow, hair
B. Major Dysfunctions in the Process of Cancer
follicles, and epithelial lining of the
1. Defect in Cellular Proliferation
gastrointestinal tract, the rate of cellular
 Normally, most tissues of the human body in
proliferation is rapid.
adults, contain a population of predetermined,
 On other tissues, such as myocardium and
undifferentiated cells known as STEM CELLS.
cartilage, cellular proliferation does not occur or is
 Predetermined means that the stem cells of a
slow.
particular tissue will ultimately differentiate and
 Cancer cells usually proliferate at the same rate as
become mature, functioning cells of that tissue
the normal cells of the tissue from which they
and only for that tissue.
arise.
 Cell proliferation originates in the stem cell and
 However, cancer cells respond differently than
begins when the cell enters the cell cycle.
normal cells to the intracellular signals that
 The time when a cell enters the cell cycle to when
regulate the dynamic equilibrium.
the cell divides into two identical cells is called the
 Cancer cells divide indiscriminately and
generation time of the cell.
haphazardly. Sometimes they produce more than
 A mature cell continues to function until it
cells at the time of the mitosis.
degenerates and dies.
 The “stem cell theory” proposes that the loss of
 All cells of the body are controlled by an
intracellular control of proliferation result from
intracellular mechanism that determines when
mutation of the stem cells.
cellular proliferation is necessary.
 The stem cells are viewed as the target or the
 Under normal conditions, a state of dynamic
origin of cancer development.
equilibrium is constantly maintained (cellular
 The deoxyribonucleic acid (DNA) of the stem cells
proliferation = cellular degeneration or death).
is substituted or permanently rearranged. When
 Normally, the process of cellular division and
this happens, the stem cell is mutated, one of
proliferation is activated by the process of cellular
these three things can occur.
degeneration or death.
The cell can die, either from damage, resulting
 Cellular proliferation will also occur if the body
from the mutation or by initiating a programmed
has a physiologic need for more cells.
cellular suicide called apoptosis.
Example: A normal increase in the WB count
The cell can recognize the damage and repair
occurs in the presence of infection.
itself.
 Another explanation for this phenomenon of
The mutated cells can survive and pass along the
cellular proliferation control in normal cells is
damage to its daughter cells.
contact inhibition.
  Mutated cells that survive have the potential to
become malignant (cells that have the potential to
invade and metastasize).
 The stem cell of cancer development theory is not
complete because malignant stem cells can
differentiate to form normal tissue cells.
 A common misconception regarding the
characteristics of cancer cells is that the rate of
proliferation is more rapid than that of any
normal body cell.
 In most situations, cancer cells proliferate at the
same rate as the normal cells of the tissue from
which they originated.
 The difference is that the proliferation of the
cancer cell is indiscriminate and continuous. In
this way, with each cell division creating two or
more offspring cells, there is continuous growth of
tumor mass: 1 2 4 8 16 and so on. This is
termed the pyramid effect.
 The time required for a tumor mass to double in
size is known as its doubling time.
2. Defect in Cellular Differentiation
 Cellular differentiation is normally an orderly
process that progresses from a state of immaturity
to a state of maturity.
 Because all body cells are derived from the
fertilized ova, all cells have the potential to
perform all body function.
 As cells differentiate, this potential is repressed
and the mature cells is capable of performing only
specific functions.
 With cellular differentiation, there is a stable and
orderly phasing out of cellular potential.
 Under normal conditions, the differentiated cells is
stable and will not dedifferentiate (revert to a
previous undifferentiated state).
 The exact mechanism that control cellular
differentiation and proliferation is not completely
understood.
 Two types of normal genes that can be affected by
mutation are proto-oncogenes and tumor
 Tumors can be classified as benign or malignant.
suppressor genes.
Proto-oncogenes are normal cellular genes that
are important regulators of normal cellular
process.
Proto-oncogenes – Promote growth.
Tumor suppressor genes such as the gene for
the tumor protein p53, suppress growth.
Mutations that alter the expression of proto-
oncogenes can activate them to function as
oncogenes (tumor inducing agents).
The proto-oncogenes have been described as
the genes lock that keep the cell in its mature
functioning state. When this lock is “unlocked”,
as may occur through exposure to carcinogens
(agents that cause cancer) or oncogenic virus,
genetic alterations and mutation occur. The
abilities and properties that the cell had in fetal
development are again expressed.
Oncogenes interfere with normal cell expression
under some conditions causing the cells to
become malignant. This cell regains a fetal
appearance and functions.
Example: Some cancer cells produce new
proteins, such as those characteristics of the
embryonic and fetal periods of life.
These proteins, located on the cell membrane,
include carcinoembryonic antigen (CEA) and
alpha-fetoprotein (AFP). They can be detected
in the human blood by laboratory studies.
Tumor suppressor genes function to regulate
cell growth. Mutations that alter tumor
suppressor genes render them inactive, resulting
in a loss of their tumor – suppressing action.
Example of tumor suppressor genes: BRCA-1
and BRCA-2. Alterations in these genes
increase a person’s risk for breast and ovarian
cancer.
Another tumor suppressor gene is the APC
gene. Alterations is this gene increase a
person’s risk for familial adenomatous
polyposis, which is a precursor for colorectal
cancer.
Mutations in the p53 tumor suppressor gene
have been found in many cancers, including
bladder, breast, colorectal, esophageal, liver,
lung and ovarian.
Benign neoplasms are well differentiated.
Malignant neoplasms range from poorly
differentiated to undifferentiated.
The ability of tumor cells to invalid and
metastasize is the major difference between
benign and malignant neoplasms.

C. Pathogenesis and Development of Cancer
I. Pathogenesis of Cancer
1. Cellular Transformation and Derangement Theory
 This theory conceptualizes that normal cells may
be transformed into cancer cells due to exposure
to some etiologic agents.
2. Failure of the Immune Respond Theory
 This theory advocates that all individuals process
cancer cells. However, the cancer cells are
recognized by the immune response system. So,
the cancer cells undergo destruction. Failure of
the immune response system leads to inability to
destroy the cancer cells.
II. Cell Life Cycle and Metabolic Activity
III.
2. Promotion Phase
Development of Cancer
 The natural history of cancer is an orderly process
comprising several stage and occurring over a
period of time.
 The cause and development of each type of cancer
are likely to be multifactorial.
IV. Stages of Cancer Development
1. Initiation Phase
 Is a mutation in the cell’s genetic structure
resulting from an inherited mutation (an error
that occurs during DNA replication), or following
exposure to a chemical, radiation, or viral agent.
 This altered cell has the potential for developing
into to a clone (group of identical cells) of
neoplastic cells.
 Initiation is irreversible, but not all altered cells go
on to establish a tumor because many undergo
apoptosis.
 An initiated cell is not yet a tumor cell because it
has not established the ability to self-replicate and
grow.
 The DNA alteration may remain undetected
throughout the lifetime of an individual unless
further events stimulate development of a tumor.
 Many carcinogens (cancer-causing agents capable
of producing cellular alteration) are detoxified by
protective enzymes and are harmlessly excreted.
 If this protective mechanism fails, carcinogens can
enter the cell and may die or repair itself.
 If cell death or repair does not occur before cell
division, the cell will replicate into daughter cells,
each with the same genetic alteration.
 Carcinogens may be chemical, radiation or viral in
nature.
 In addition, some genetic anomalies increase the
susceptibility of individuals of certain cancer.
 Common characteristics of carcinogens are that
their effects in the stage of initiation are usually
irreversible and additive.
 Is characterized by the reversible proliferation of
the altered cells.
 Consequently, with an increase in the altered cells
population, the likelihood of additional mutation is
increased.
 An important distinction between initiation and
promotion is that the activity of promoters is
reversible.
 This is a key concept in cancer prevention.
 Promoting factors include such dietary fat,
obesity, cigarette smoking and alcohol
consumption.
 Changing a person’s lifestyle to modify these risk
factors can reduce the chance of cancer
development.
 A period of time ranging from 1 to 40 years,
elapses between the initial genetic alteration and
the actual clinical evidence of cancer.
 This period called the latent period, is now
believed to comprise both the initiation and the
promotion stages in the natural history of cancer.
  For the disease process to become clinically  These factors act by causing cell mutation or
evident, the cells must reach a critical mass. alteration in cell enzymes and proteins causing
 A 1 cm tumor (the size, usually detectable by altered cell replication.
palpation) contains 1 billion cancer cells.  Chemical carcinogens are as follows:
 A 0.5 cm tumor is the smallest that can be Industrial Compounds
detected by current diagnostics measures, such as Drugs
magnetic resonance imaging (MRI). Hormones
3. Progression Phase Food preservatives
 Is characterized by increased growth rate of the Polycyclic hydrocarbons
tumor, increased invasiveness, and spread of the 3. Physical Agents
cancer to a distant site (metastasis). Radiation
Example: Colon cancer spreads to the liver. Physical irritation/ trauma
 The most common sites of metastasis are lungs, 4. Hormones
liver, bone, brain and adrenal glands. Estrogen as replacement therapy
Stage I Metastasis Diethylstilbestrol (DES)
Invasion of cancer cells to the adjacent tissues. 5. Heredity
Stage II Metastasis  Positive family history of cancer increases the risk
Spread of cancer cells through the blood to develop the disease.
vessels and lymphatic system.  Cancers that may have familial link include:
Stage III Metastasis Breast
Establishment of secondary sites of cancer Ovarian
(LLBBA). Colorectal
Prostate
Melanoma
Uterine
Leukemia
Sarcomas
Primary brain tumor
6. Stress
Depression
Grief
Aggression
Despair
V. Cause of Cancer Life stresses
 UNKNOWN Decrease immunocompetence.
7. Precancerous Lesions
VI. Etiologic Factors of Cancer (Carcinogens)
Pigmented moles
1. Viruses
Burn scar
 Oncogenic viruses may be one of the multiple
Senile keratosis
agents acting to initiate carcinogenesis.
Leukoplakia
 Viral infections that increase risk of certain forms of
Benign polyps or adenoma of the colon or stomach
cancer are as follow:
Fibrocystic disease of the breast
Human papilloma virus – Cervical cancer
May undergo transformation into cancerous
Epstein-Barr virus – Lymphoma
lesions and tumor.
Hepatitis B and C – Hepatocellular cancer
8. Obesity
Helicobacter pylori – Gastric cancer
Breast cancer
AIDS Virus – Kaposi sarcoma
Colorectal cancer
2. Chemical Carcinogens
VII. Predisposing Factors to Cancer differentiated differentiated,
1. Age Anaplastic /
Characteristic
 Older individuals are more prone to cancer embryotic type
because they have been exposed to carcinogens of cells
longer. Mature cells Common
2. Sex Recurrence but poorly following
 Females – Breast cancer function surgery
 Males – Prostate cancer Extreme Very common
3. Urban Residence vs Rural Residence unusual when
Metastasis
 Cancer is more common among urban dwellers surgically
than among rural residence. removed
Not harmful to Always harmful
4. Geographic Distribution host unless it to host. May
 Japan – Gastric cancer compresses result in
Effects of
 US – Breast cancer tissues of necrosis,
Neoplasm
5. Occupation obstruct vital ulcerations,
 There is greater risk of exposure to carcinogens organs hemorrhage
among chemical factory workers, farmers, and infection
Very good Poor prognosis
radiology department personnel.
if cells are
6. Heredity
poorly
 Positive family history of cancer increases the risk
Prognosis differentiated
of develop the disease.
and evidence
7. Stress
of metastasis
 Depression, grief, aggression, despair, or life
exists.
stresses decrease immune-competence because
of affectation of hypothalamus and pituitary
gland, immunodeficiency may spur the growth D. Prevention, Screening and Early Detection of
and proliferation of cancer cells. Cancer
8. Precancerous Lesions 1. Primary Prevention
 Pigmented moles, burn scar, senile keratosis,  Primary prevention activities are aimed at
leukoplakia, benign polyps or adenoma of the intervention before pathologic change has begun.
colon or stomach, fibrocystic disease of the  These can help reduce cancer risk through
breast, may undergo transformation into alteration of lifestyle behaviors to eliminate or
cancerous lesions and tumor. reduce exposure to carcinogens.
9. Obesity Patient Education on Prevention and Detection of
 Studies have linked obesity to breast and Cancer
colorectal cancer.  Avoid exposure to known or suspected carcinogens
Benign VS Malignant Neoplasm and cancer – promoting agents (cigarette smoke
and sun exposure).
Characteristics Benign Malignant  Have a balanced diet that includes vegetable and
Speed of Grows slowly Grows rapidly fresh fruits, whole grains and adequate amount of
Growth fiber, and reduce the amount of fat and
Mode of Remains Infiltrates
preservatives, including smoked and salt-cured
growth of localized surrounding
meats containing high-nitrite concentrations.
tissue tissues
 Participate in a regular exercise regimen (30
Presence of Encapsulated Not
minutes or more of moderate physical activity 5
Capsule encapsulated
times weekly).
Cell Well – Poorly
 Obtain adequate, consistent periods of rest (at
least 6 to 8 hours per night).
 Have a health examination on a regular basis that
includes a health history, a physical examination,
and specific diagnostic test for common cancers in
accordance with the guidelines published by the
American Cancer Society.
 Eliminate, reduce or change the perception of
stressors and enhance the ability to effectively cope
with stressors.
 Know the 9 warning signs of cancer (C-A-U-U-U-T-I-
O-N) – These actually detect fairly advanced
disease.
Warning Signals of Cancer
C – Change in bladder and bowel habits.
A – A sore that does not heal.
U – Unusual bleeding or discharges.
U – Unexplained sudden weight loss.
U – Unexplained anemia.
T – Thickening or lump in breast or other body
parts.
I – Indigestion or difficulty of swallowing.
O – Obvious changes in wart or mole.
N – Nagging cough or hoarseness of voice.
 Learn and practice recommended cancer  Uterus
screenings on a timely basis.
Colonoscopy in average-risk people from age 50
years and every 10 years thereafter.
Breast Self – Examination (BSE)
Testicular Self – Examination (TSE)
Seek immediate medical care if you notice a
change in what is normal for you and if cancer
is suspected.
2. Secondary Prevention
 Secondary prevention or early detection provides
the opportunity to detect precancerous lesions or
early – stage cancers, to treat them promptly.
Summary of America Cancer Society (ACS)
Recommendations for the Early Detection of Cancer
in Asymptomatic People
 Cancer – Relate Check – Up
For people aged 20-40 years:
Every 3 years
For people age 40 and older:
Every year
 Breast
Women who are 40 years and older should have:
Annual mammogram
An annual clinic breast examination (CBE)
Monthly breast self – examination (BSE)
Women aged 20 – 39 should have:
Clinical breast examination (CBE) every 3 years
Monthly breast self – examination (BSE)
 Colon and Rectum
Men and women aged 50 years or older should
follow one of the following examination schedule:
Fecal Occult Blood Test – Every year
Flexible Sigmoidoscopy – Every 5 years
Colonoscopy – Every 10 years
Double – Contrast Barium Enema – Every 5 to
10 years.
Digital Rectal Exam – Should be done at the
same time as sigmoidoscopy, colonoscopy or
double – contrast barium enema.
 Prostate
Men from age 50:
Annual prostate – specific antigen (PSA) blood
test
Annual digital rectal examination
For predisposition
Two or more affected first degree relatives.
Cervix
Begin 3 years after having vaginal intercourse
but not later than 21 years of age.
Conventional Pap Test – Annually or every two
years using liquid – based tests.
 Beginning at age 30 – 3 normal Pap Test result
in a row may get screened every 2 – 3 years
with either the conventional or liquid-based
pap test.
 70 years of age or older – 3 or more normal
Pap Test in a row and no abnormal pap test
result in the last 10 years may choose to stop
having cervical cancer screening.
 Endometrium
Menopause begins
Women at high risk for cancer of the uterus
should have a sample or endometrial tissue
exanimated.
3. Tertiary Prevention
 Orient the client in the developing risk of diseases
or C-A-U-U-U-T-I-O-N.
 Social support and psychological support.
 Alleviating and prevent impact of the disease to Long term sun exposure
the patient. Occupation exposure – Asbestos, tar, nickel,
4.Quaternary Prevention textile, wood or leather work, etc.
Comfort measures  Skin Cancer
Pain management Individuals with fair complexion
Advance directives – Do not resuscitate, do not Positive family history
treat, do not intubate. Moles (nevi)
 Allow natural death – Limit the hydration of the Exposure to coal tar, creosote, arsenic, radium
client and food. Sun exposure between 10 AM to 3PM
 Basic comfort – Pain management.
Dietary Recommendations Against Cancer
 Avoid obesity.
 Cut down on total fat intake.
Common Causes of Cancer  Eat more high fiber foods.
 Breast Cancer  Include food rich in Vitamin A and C in daily diet
Early menarche (especially tomatoes) Include cruciferous
Late menopause vegetables.
Nulliparous or older than 30 years at the birth of  Be moderate in the consumption of alcoholic
a first child. beverages.
 Lung Cancer  Be moderate in the consumption of salt – cured,
Tobacco abuse smoked – cured, and nitrite – cured foods.
Asbestos
Clinical Staging
Radiation exposure
 Determines the anatomic extent of the malignant,
Air pollution
disease process by stages.
 Colorectal Cancer
Stage 0 – Cancer in situ
Greater incidence in men
Stage I – Tumor limited to the tissue of origin;
Familial polyposis
localized tumor growth
Ulcerative colitis
Stage II – Limited local spread
High – fat , Low – fiber diet
Stage III – Extensive local and regional spread
 Prostate Cancer
Stage IV – Metastasis
Common among males who are 50 years old and
older. TNM Classification System
African – Americans have the highest incidence of  Developed by the American Joint Committee of
prostate cancer the world Cancer (AJCC) that can be applied to all tumor
Positive family history types.
Exposure to cadmium T – Extent of primary tumor.
 Cervical Cancer N – Presence or absence of regional lymph node
Sexual Behavior involvement.
First intercourse at an early age M – Presence or absence of distance metastasis.
Multiple sexual partner 1. T – Extent of primary tumor.
Human papilloma virus and AIDS (acquired Tx – Primary tumor is unable to be assessed.
immunodeficiency syndrome) To – No evidence of primary tumor.
Low socioeconomic status Tis – Tumor in situ; localized; no spread
Cigarette smoking T1, T2, T3, T4 – Increasing size and/or local
 Head and Neck Cancer extent off primary tumor.
More common among males 2. N – Presence or absence or regional lymph node
Alcohol and tobacco use involvement.
Poor oral hygiene Nx – Regional lymph nodes are unable to be
assessed.
 No – No regional lymph node involvement. It is done by taking only a part of the tumor. This
N1, N2, N3, N4 – Increasing involvement of is done when the tumor is large.
regional lymph nodes. 3. Ultrasound
3. M – Absence or presence or distant metastasis. Magnetic Resonance Imaging (MRI)
Mx – Metastasis is unable to be assessed. Radiodiagnostic Test
Mo – Absence of distance metastasis. Computerized Axial Tomography (CT Scan)
M1 – Presence of distant metastasis. Endoscopic Examination
Cancer Detection Examinations 4. Laboratory Blood Tests for Cancer
1. Cytologic Examination or Papanicolaou Test  Hematologic (CBC)
 Pap’s Exam or Par Smear  Hemoglobin
 Cytologic specimen can be obtained from tumors  Hematocrit
that tend to shed cells from their surface.  Leukocytes
Gastrointestinal tract through endoscopy.  Platelets
Respiratory tract through laryngoscopy and  Tumor Markers
bronchoscopy.  AFP (Alpha – feto – protein)
Genitourinary tract through:  CEA (Carcinoembryonic Antigen
Colposcopy of the cervix and vagina
Cystoscopy of the bladder
Laparoscopy of the pelvic and abdominal
cavity.
Preparation for Pap Exam of the Cervix
 No menstruation.
 No vaginal sexual intercourse 24 hours before the
test.
 No vaginal douching 24 hours before the test.
 Avoid inserting cervical cap, cervical diaphragm,
spermicide, or condom into the vaginal 24 hours
before the test.
Interpretation of Papanicolaou Test Result
 Class I – Normal
 Class II – Inflammation
 Class III – Mild to Moderate Dysplasia
 Class IV – Probably Malignant
 Class V – Possibly Malignant
2. Biopsy
 Involves obtaining tissue samples by needle
aspiration, or incision of tumor.
 It is the only definitive means of diagnosing
cancer.
 Needle Biopsy
It is done by aspiration of tumor cells with
needle and syringe.
 Excisional Biopsy
It is done by removing the entire tumor. It is
done when the tumor is small.
 Incisional or Subtotal Biopsy