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CANCER TERMINOLOGY
Anaplastic :- tumor cells are completely
undifferentiated and bear no resemblance
to cells of tissues of their origin.

Hyperplasia :- an increase in the number of

normal cells in a normal arrangement in a
tissue or organ; usually leads to increase
in the size or part and an increase in
functional activity.
 CANCER TERMINOLOGY
Metaplasia :- the replacement of one type of fully
differentiated cell by another fully differentiated cell in
another parts of the body where the second cell type does
not normally occur.

Dysplasia :- an alteration in the size ,shape, and organization

of differentiated cells; cells lose their regularity and show
variability in size and shape, usually in response to an
irritant; cells may revert to normal when the irritant is
removed but may transform to a neoplasia.
CANCER TERMINOLOGY
Metastasis :- the ability of neoplastic cells to spread from the
original site of the tumor to distant organs ,spreading as the
same cell type as the original neoplastic tissue.

Carcinoma :- A form of cancer that is composed of epithelial

cells that tend to infiltrate surrounding tissues and may
eventually spread to distant sites .
 CANCER TERMINOLOGY
Oncogenes :- cancer genes that are altered versions of
normal genes.
Proto- oncogenes :- repressed oncogenes existing in
normal cells which can be activated by many different
factors and cause the host cells to become malignant.

Tumor : usually synonymous with neoplasm.

Neoplasm :- the word neoplasm is derive from Greek word
neos , new ,and plasis ,molding. Thus, neoplasm is defined
as an abnormal new growth or formation ,of tissue that
serves no useful purpose and may harm the host organism.
ETIOLOGY-MULTISTEP PROCESS OF
CARCINOGENESIS
ETIOLOGY
 Viruses
 Chemical agents
tar,soot,asphalt ,aniline dyes ,hydrocarbons, crude
paraffin oil, fuel oil, nickel.
 Physical agents

adiation (uv radiations and ionizing radiations) and asbestos
 Drugs and hormones
RISK FACTORS OF CANCER
ENDOGENOUS
1. Age
cancer incidence increase with age.
2.Genetic heritage
some cancers exhibit a clear inheritance pattern.
3.Hormonal factors
Donot act as primary carcinogens, but appear to
influence the process of carcinogenesis.
4.Immunologic factors
malignant cells are antigenically different & should be
recognized & destroyed by an intact immune system.
 EXTERNAL RISK FACTORS
 DRUGS &CHEMICAL
 RADIATIONS
 TOBACCO
 NUTRITION :-
DIET HIGH IN FAT AND CALORIES
 SEXUAL PRACTICES
EARLY ONSET SEX & MULTIPLE PARTNERS .
 VIRUSES
 PSYCHOSOCIAL FACTORS
CLASSIFICATION OF CANCER
Tumor can be classified according to :-
 Anatomic site
 istology (grading )
 xtend of disease (staging)
Purposes of classification :-
1. To communicate the status of the cancer to all members
of health team.
2. Assist in determining the most effective treatment plan.
3. valuation of treatment .
4. Compare like groups for statistical purposes.
 ANATOMIC SITE CLASSIFICATION
 CARCINOMA originating from embryonal ectoderm (skin &
glands ) and endoderm (mucus membranes linings of the
respiratory tract ,gastrointestinal tract ,and genitourinary
tracts)

 SARCOMAS originating from embryonal mesoderm

(connective tissue,muscle,bone,and fat)

 LYMPHOMAS & LEUKEMIAS originating from the

hematopoietic system.
 HISTOLOGIC CLASSIFICATION
 G
AD  : cells differ slightly from the normal cells (mild
dysplasia ) & are well differentiated.

 G
AD  : cells are more abnormal (moderate dysplasia )&

moderately differentiated.

 G
AD  :cells are very abnormal (severe dysplasia ) &

poorly differentiated.

 G
AD  : cells are immature & primitive ( anaplasia ) and

undifferentiated ;origin of cells is difficult to identify.
CLINICAL STAGING :-extend & spread of
disease .
 TAG 0 : cancer in situ

 TAG  : tumor limited to the tissues of origin; localized

tumor growth

 TAG  : limited local spread

 TAG  : extensive local & regional spread

 TAG  : metastasis
 TNM CLASSIFICATION SYSTEM
t involves three parameters :-
 Tumor size and invasiveness (T)
 Presence and absence of regional spread to the lymph
nodes(N)
 etastasis to distant organ sites .()
MANAGEMENT OF CANCER
 Complete eradication of malignant disease
(CURE )
 Prolonged survival & containment of cancer cell
growth
( CONTROL)

elief of symptoms associated with the disease

(PALLIATION )
 MULTIPLE MODALITIES IN CANCER
TREATMENT

ß urgery
ß
adiation therapy
ß Chemotherapy
ß Biologic response modifiers
(B
 ) therapy.
 SURGERY
ß Surgical removal of the entire cancer remains
the ideal and most frequently used treatment.

ß Types of surgery :-
Diagnostic surgery
Prophylactic
Palliative
Reconstructive
DIAGNOSTIC SURGERY
Such as biopsy to obtain tissue samples
for analysis of cells suspected to be
malignant.
Types of biopsy :-
ß Excisional biopsy
ß Incisional biopsy
ß Needle aspiration biopsy
PROPHYLLATIC SURGERY :-

it involves removing non vital tissues or organs that are likely

to develop cancer e.g. colectomy,mastectomy,oophorectomy.

PALLATIVE SURGERY :-

when cure is not possible ,the goals of the treatment are to

make the patients as comfortable as possible and to promote
satisfying & productive life as long as possible.

RECONSTRUCTIVE SURGERY :-

it may follow curative & radical surgery and carried out in ann
attempt to improve function or obtain a more desirable
cosmetic effect
 RADIATION THERAPY
 n this ,ionizing radiations are used to interrupt
cellular growth.
 Two types of ionizing radiations i.e.
electromagnetic rays (x ray & gamma rays ) and
particles ( electrons ,beta
particles,protons,neutrons and Alfa particles ) can
lead to tissue disruption .
 A radiosensitive tumor is one that can be
destroyed by a dose of radiation that still allows
for cell regeneration in the normal tissue
 Mechanism of action

 Radiation therapy works by damaging the DNA of

cells.
 The damage is caused by a photon, electron,
proton, neutron, or ion beam directly or indirectly
ionizing the atoms which make up the DNA chain.
 Indirect ionization happens as a result of the
ionization of water, forming free radicals, notably
hydroxyl radicals, which then damage the DNA.
 In the most common forms of radiation therapy,
most of the radiation effect is through free radicals
 Mechanism of action
 cells have mechanisms for repairing DNA damage,
breaking the DNA on both strands proves to be the most
significant technique in modifying cell characteristics.
 Because cancer cells generally are undifferentiated and
stem cell-like, they reproduce more, and have a
diminished ability to repair sub-lethal damage compared
to most healthy differentiated cells.
 The DNA damage is inherited through cell division,
accumulating damage to the cancer cells, causing them to
die or reproduce more slowly.
Dose

 The amount of radiation used in radiation therapy is

measured in gray (Gy), and varies depending on the type
and stage of cancer being treated. For curative cases, the
typical dose for a solid epithelial tumor ranges from 60 to
80 Gy, while lymphomas are treated with 20 to 40 Gy.

 Preventative (adjuvant) doses are typically around 45 - 60

Gy in 1.8 - 2 Gy fractions (for Breast, ead and Neck
cancers respectively.)
 any other factors are considered by radiation oncologists
when selecting a dose, including whether the patient is
receiving chemotherapy, patient comorbidities, whether
radiation therapy is being administered before or after
surgery, and the degree of success of surgery.
 Types of radiation therapy

istorically, the three main divisions of radiotherapy are :-

ß external beam radiotherapy (B
T or X
T) or

teletherapy

ß brachytherapy or sealed source radiotherapy, and

ß systemic radioisotope therapy or unsealed source

radiotherapy
 The placement of brachytherapy
sources
 can be temporary or permanent
 permanent brachytherapy, the sources are surgically
sealed within the body and left there, even after all of the
radiation has been given off. The remaining material (in
which the radioactive isotopes were sealed) does not cause
any discomfort or harm to the patient. Permanent
brachytherapy is a type of low-dose-rate brachytherapy.
 temporary brachytherapy, tubes (catheters) or other
carriers are used to deliver the radiation sources, and both
the carriers and the radiation sources are removed after
treatment. Temporary brachytherapy can be either low-dose-
rate or high-dose-rate treatment.
 V

   

 n systemic radiation therapy, a patient swallows or

receives an injection of a radioactive substance, such as
radioactive iodine or a radioactive substance bound to a
monoclonal antibody.
 à   
   

ßExternal-beam radiation therapy is most often

delivered in the form of photon beams (either x-
rays or gamma rays) .
ß A photon is the basic unit of light and other
forms of electromagnetic radiation.
ß It can be thought of as a bundle of energy.
ß The amount of energy in a photon can vary.
ß For example, the photons in gamma rays have
the highest energy, followed by the photons in x-
rays.
DRUG THERAPY
 Alkylating agents
 Nitrosoureas
 Platinum drug
 Antimetabolites
 Antitumor antibiotics
 itotic inhibitors
 Topoisomerase inhibitors
 Corticosteroids
 ormone therapy
 ALKYLATING AGENTS
 Cell cycle phase ±non specific agents
 Damage DNA by causing breaks in the
double stranded helix. if repaired does not
occur cell will die immediately (cytocidal ),or
when they attempt to divide (cytostatic )
 xamples:- nitrogen mustard ;-
cyclophosphamide ,thiotepa
NT

A
Cell cycle phase- non specific agents
like alkylating agents ,break DNA helix
,interfering with DNA replication;cross
blood brain barrier.
Example :- carmustine,lomustine
PLATINUM DRUGS
 Cell cycle phase ±non specific
 Binds to DNA & RNA ,miscoding
information and /or inhibiting DNA
replication ,and cells die.
 Examples:- cisplatin,carboplatin
 ANTIMETABOLITES
 CELL CYCLE PHASE ± SPECIFIC AGENTS
 imics naturally occurring substances ,thus interfering
with enzyme function or DNA synthesis. Primarily acts
during  phase .purines & pyrimidines are building blocks
of nucleic acids needed for DNA &
NA synthesis.
 nterferes with purine metabolism-mercaptopurine
 nterferes with pyrimidine metabolism -5- flouro uracil
 nterferes with folic acid metabolism-methotrexate
 nterferes with DNA synthesis hydroxyurea.
ANT T 
ANTBTC
 Cell cycle phase ±non specific agents
 Binds directly to DNA,thus inhibiting the
synthesis of DNA and interfering with
transcription of
NA .
 xample :- doxarubicin,mitomycin
MITOTIC INHIBITORS
 Cell cycle phase ± specific agents
 Taxanes ±antimicrotubule agents that
interfers with mitosis .Acts during G 2
phase & mitosis to stabilize
microtubules ,thus inhibiting cell
division.example:- pacliaxel
 Vinca alkaloids :- acts in M phase to
inhibit mitosis. Ex.
Vincristine,vinblastine
TP
A NBT

 Cell cycle phase ± specific agents
 Inhibits the normal enzyme
topoisomerase that function to make
reversible breaks & repairs in DNA that
allows for flexibility of DNA in
replication .
 Ex. etoposide
C
TCT
D
 Cell cycle phase ±non specific agents
 Disrupts the cell memgrane and inhibits
synthesis of protien;decreased circulating
lymphocytes;inhibit mitosis;depress
immune system;increase sense of well
being.
 x. Cortisone,methylprednisolone.
 
NAL T
APY
 Cell cycle phase ±non specific agents
 Antiestrogen :- selectively attach to estrogen receptors,
causing down regulation of them and inhibiting tumor
growth ;also known as 
s ( selective estrogen receptor
modulators ) ex. Tamoxifen
 strogen :- interfers with hormone receptors and proteins
ex. stradiol.
iscellaneous
 nhibits protien synthesis ex. L-
asparaginase.
 Causes changes in DNA in leukemia cells
and degrades the fusionn protien ex.
Arsenic trioxide.
 uppresses mitosis at interphase ;appears
to alter preformed DNA,
NA ,& protien.
x. Procarbazine.
Chemotherapy can produce many side
effects, such as:
 Fatigue
 Diarrhea, constipation
Anemia, low red blood cell count  Nausea or vomiting
 Low white blood cell count (this increases  uscle and nerve
risk for infection)
problems
 air loss, or thinning hair
 Lung problems and
 Bleeding or bruising (due to low platelet difficulty breathing;
count)
coughing excessively
 Dry skin, or rashes
 Fertility and sexuality
problems
NURSING RESPONSIBILITIES
 RADIATION THERAPY
 CHEMOTHERAPY
PROBLEM ETIOLOGY NURSING MANAGEMENT

G YT :- pithelial cells are destroyed Assess oral mucosa daily

tomatitis,mucositis by the chemotherapy or Be aware that eating ,talking
,esophagitis radiation therapy and swallowing may be
nflammation & ulceration difficult.
occurs due to rapid cell ncourage pt to use artificial
destruction saliva to manage dryness
(radiations)
Discourage use of irritants
Apply topical anesthetics
Nausea ,vomiting 
elease of intracellular Teach pt to eat & drink
breakdown products ,when no nauseated.
stimulates vomiting centre in Administer antiemetic
the brain.  se diversional activities
G lining destroyed
Anorexia
elease of TNF & L from onitor weight
macrophages has appetite ncourage pt to eat small
suppresor effect frequent meals,high
protein,high calric
Diarrhoea Denuding of epithelial Give antidiarrheoal agents as
lining of intestines. needed.
Side effect of Encourage low fibre,low residue
chemotherapy diet.
Radiations to Encourage fluid intake ,atlrast 3
abdomen,pelvis,lumbosac litres
ral area
Constipation Decrease intestinal motility nstruct patient to
related to autonomic Take stool softeners as needed
nervous system dysfunction at high-fiber foods
Caused by neurotoxic ncrease fluid intake
effects of plant
alkaloids(vincristine,
vinblastine)

epatotoxicit Toxic effects from

y chemotherapy drugs onitor liver function tests
(usually transient and
resolves when drug is
stopped)
HEMATOLO Bone marrow
GIC SYSTEM depressed secondary to
Anemia therapy.
Malignant infiltration of
bone marrow by cancer
Leukopenia Depression of bone
marrow secondary to
chemotherapy or radiation
therapy
nfection most frequent
cause of morbidity and
death in cancer patients

espiratory and
genitourinary system
usual sites of infection
Thrombo- Bone marrow depressed
 of bleeding(petec
cyotopenia ,sec. to chemotherapy.
alignant infiltration of
bone marrow that crowds
Monitor hemoglobin and hematocrit
levels
Administer iron suppliments and
erythropoietin.
Encourage intake of foods that promote
RBC production
onitor WBC count especially neutrophils
Teach patients to report temperature
elevation & other manifestations of infection.
Teach pt to avoid large crowds& people
with infection.
Administer WBC growth factors
bserve 
hiae,ecchymosis ).
onitor platelet count.
INTEGUMENTARY Destruction of hair Suggest ways to cope with hair loss
SYSTEM:- follicles by .
ALOPECIA chemotherapy or Cut long hair before the therapy.
radiation to scalp. Avoid use of electric hair razor .
Hair loss usually Discuss impact of hair loss on self
temporary with image.
chemotherapy
,usually permanent in
response to
radiations.
kin changes from
adiation damage to
dry to moist skin
desquamation

Chemotherapy yperpigmentation Alert pt to potential skin changes .

induced skin Telangietasis ncourage pt to avoid sun exposure .
damages Photosenstivity mplement symptomatic management
Acneiform eruptions as needed .
Acral erythema Application of lotion .
Respiratory system : Radiation pneumonitis
develops 2-3 mo after
start of treatment
- After 6-12 mon ,fibrosis
occurs & is evident on x
ray
Cardiovascular system :- nflammation secondary to
myocarditis radiation injury.
Complication when chest
wall is irridiated ,may occur
to 1 yr after treatment .
s of
yperuricemia ncreased uric acid levels
due to chemotherapy
induced cell destruction
Monitor for dry ,hacking
cough,fever and exertional
dyspnea.
onitor ofr clinical
manifestations of these
disorders
onitor heart with CG
Drug therapy may be
modified ,if s
deteriorating cardiac
enzymes present .
onitor uric acid levels.
Allopurinol may be given as
prophylactic management.
ncourage fluid intake .
THANK
YOU