ch 16 cancer a

8/8/2019 Ch 16 Cancer A

http://slidepdf.com/reader/full/ch-16-cancer-a 1/20

CANCER –CH 16

Cancer

− Group of more than 200 diseases

− Characterized by uncontrolled and unregulated growth of cells

− Declining due to preventive efforts: colorectal, lung, oral, pharyngeal cancers

− Rising: non-Hodgkin’s lymphoma, skin cancer, especially MELANOMA (due to genetic

predisposition and sun exposure)− Mostly >55 years, but ALL age groups can be affected

− Men > women

− African American > whites and other minority group

− Yet, differences in survival from cancer are attributed primarily to a combination of severalfactors:

o Poverty

o Difficult access to health care

o More comorbid conditions

o Differences in tumor biology

− Nurses position – lead efforts at changing attitudes and behaviors about cancero Goal : implement educational interventions that will assist individuals to

Understand, reduce, or eliminate their risk of cancer development

Comply with cancer management regimens

Cope with effects of cancer and related treatment

Biology of Cancer

Cancer encompasses a broad range of diseases of multiple causes that can arise in ANY CELL of thebody capable of evading regulatory controls over proliferation and differentiation.o Two major dysfunction:

1) Defect in cellular Proliferation2) Defective cellular differentiation

Defect in Cellular ProliferationNORMALLY:

o Stem cell (predetermined**, undifferentiated) begins by entering cell cycle

generation time of the cell mature cell functions until degenerates and dies.o Predetermined** : stem cells of a particular tissue will ultimately differentiate and become

mature, functioning cells of that tissue and ONLY that tissue.

o Generation time of the cell : time from when a cell enters the cell cycle cell divides into

two identical cells

ProliferationControll

NORMAL CELLS CANCER CELLS

Intracellular

mechanism

State of equilibrium is constantly

maintained(cellular proliferation = cell death)o Cellular proliferation occurs only

in the presence of cellulardegeneration and death.

o Cellular proliferation also occur

when body has physiologic needsfor more cells (ex; ↑WBC wheninfection)

− Don’t have state of dynamic

equilibrium.− Proliferation of cancer cells

divide indiscriminatlyhaphazardly, andcontinuously. (ex; producemore than two cells at thetime of mitosis)

− They have a pyramid effect.

124816…Timerequired for a tumor mass todouble in size is known as its

8/8/2019 Ch 16 Cancer A


doubling time.

Contactinhibition

− Normal cells have contact inhibition:they inhibit cellular growth throughphysical contact of their neighboringcells.

− Normal cells DO NOT invade aterritory that is not their own byrespecting boundaries and territory of

the cells surrounding them.

− Cancer cells lack contactinhibition: they have NOREGARD for cellularboundaries, (ex; they growon top of one another, also ontop of or between normalcells)

Rate of normalcellularproliferation (timeof cell birth to timeof cell death)

Rate of proliferation differs in each bodytissueRapid cellular proliferation rate: bonemarrow, hair follicles, epithelial lining of GI tract etcNO or slow proliferation rate:myocardium and cartilage

− Cancer cells usually proliferateat the same rate as normalcells

Defect in Cellular DifferentiationNORMALLY

− Cellular differentiation is an orderly processo Progresses from a state of immaturity to maturityo All cells have the potential to perform all body functions b/c body cells are derived from the

fertilized ova.o differentiated cell is stable and WILL NOT dedifferentiate(will not revert to a previous

undifferentiated state)o exact mechanism is not completely understood.

− two types of normal genes: protooncogenes and tumor suppressor genes

can be affected by mutation: function as oncogenes (tumor-inducing genes) protooncogenes

Normal cellular genes:

− “genetic lock” - Importantregulators of normal cellular

processes− Promote growth

− Genetic lock that keeps the cell inits mature functioning state

Oncogenes:

− “unlocked” through exposure to carcinogens

(agents that cause cancer), or oncogenic viruses

genetic alteration mutation occurs function asoncogenes

− Cancer cells regains fetal appearance and functionby producing proteins or hormones that characterizeembryonic and fetal periods of lifeo some cancer cells produce new proteins located on

the cell membrane includes:

Carcinoembryonic antigen (CEA) -monitor lab for treatmenteffectiveness,,should ↓

STEM CELL THEORY Cancer cells originate from the mutation of stem cell. They loss intracellular control of proliferation resulting from a mutation of the stem cells.

DNA of stem cell is substituted or rearranged stem cell mutation one of three thingscan occurcell can die either fromDamage resulting from mutation, ORBy apoptosis: initiating a programmed cellular suicideself repair: cell can recognize the damage and repair itself Survive : mutated cell survives and passes along the damage to its daughter cellsPotential to become malignant (cells with invasive and metastatic potential)

8/8/2019 Ch 16 Cancer A


α-fetoprotein(FP)o small cell carcinoma of lung produce hormones

(ordinarily produced by embryonic cells as tumorcells)

tumor suppressor genes

− Regulate cell growth bysuppressing growth

−

Examples of tumor suppressorgene:

BRCA- 1 and BRCA -2

APC gene

P53

Mutation:

− Inactivate genes, resulting in a loss of their tumor-suppressing action

− Alteration in BRCA-1 or BRCA-2 : ↑ risk for breast andovarian cancer

− Alteration in APC gene : ↑risk for familial adenomatouspolyposis (precursor for colorectal cancer)

− Alteration in P53 : found in bladder, breast, colorectal,esophageal, liver, lung and ovarian cancer

benign VS. malignant neoplasms

** the degree of anaplasia (lack of differentiation) determines the malignant potential.

Development of Cancer

− Likely to be multifactorial

−

Common belief: development of cancer is rapid, haphazard event− Natural history of cancer: Occurs over a period of time by an orderly process comprising

several stages.

− Stages include: initiation promotion progression1st Stage : Initiation Stage (Irreversible)

− Mutation in the cell’s genetic structure potential for developing into a clone of neoplasticcells (NOT ALL go on to establish a tumor b/c many undergo apoptosis)

o Caused by inherited mutation (an error that occurs during DNA replication, OR

o Exposure to a chemical, radiation, or viral agent.

− Does not have the ability to self-replicate and growtherefore, NOT A TUMOR CELL YETo May remain undetected throughout lifetime unless further events stimulate the tumor to

develop

Carcinogens : cancer-causing agents capable of producing cellular alterations

− Many are detoxified by protective enzymes and harmlessly excreted

But, if protective mechanism fails carcinogens enter cell’s nucleus and alter DNA

− Some cells die or repair itself

But if not before cell division cell replicates into daughter cells, each with same geneticalteration

− Characteristics : irreversible and additive

ChemicalCarcinogens

Certain chemicals (identified as cancer causing agents in later eighteenth century by

Percival Pott) Ex; sootscrotum cancero Later on..evidence indicated that people who are exposed to certain chemicals

over time had a higher incidence of getting cancer than others.

Benign neoplasms Malignant neoplasms

− Usually encapsulated − Rarely encapsulated

− Normally well differentiated − Poorly differentiated

− No metastasis − YES metastasis (MAJOR DIFFERENCES)

− Recurrence is rare − Recurrence is possible

− Slight vascularity − Moderate to marked vascularity

− Mode of growth is expansive, but notinfiltrates

− Infiltrate and expansive growth

− Cell characteristics: Fairly normal; similar toparent cells

− Cells abnormal, become more unlike parentcells

8/8/2019 Ch 16 Cancer A


Certain drugso that interacts with the DNA are identified as carcinogens. Ex; Pts w/ HL or NHL

or Multiple myeloma treated with alkylating agents either alone orw/radiation therapy (cyclophosphamide[cytoxan] and nitrogen mustard) &

immunosuppressive agents increased incidence of acute myelogenousleukemia (Secondary leukemia)

Secondary Leukemiao Relatively refractory to induction of remission with combination chemotherapy

o Also been observed in those who had transplant surgery and takingimmunosuppressive drugs.

Radiation − Ionizing radiation can cause cancer in almost any human body tissue.

− When cells are exposed, one or both strands of DNA are damaged.

− Certain malignancies correlates w/radiation as a carcinogenic agent:

o Hiroshima and Nagasaki atomic bomb explosions ↑leukemia, lymphoma,

thyroid cancer, and other cancers.o Certain occupations such as radiologists, radiation chemists, and uranium

miners ↑incidence of bone cancero Those who received radiation to head and neck area for treatment such as

acne, tonsillitis, sore throat, or enlarged thyroid gland ↑ incidence in thyroidcancer

o Children exposed to radiation during fetal life ↑ incidence of childhoodcancers

o UV radiation melanoma and squamous and basal cell carcinoma of the skin

(skin cancer is poorly responsive to systemic treatment)

ViralCarcinogens

− Certain DNA and RNA viruses (called oncogenic)

transforms cells that they infect

induce malignant transformation.

o Epstein-Barr virus (EBV) in vitro Burkitt’s lymphoma and infectious

mononucleosis

− why an infectious dz in some persons and lymphoma in others is notknown

o AIDS ↑ incidence of Kaposi sarcoma

o Hepatitis B virus hepatocellular carcinomao human papillomavirus ↑lesions that progress to squamous cell

carcinomas, such as cervical cancersGeneticsusceptibility

− Cancer-related genes ↑ individual’s susceptibility to development of certaincancers

− Ex; those who carries genes BRCA1 or BRCA 2 has a 40% to 80% risk of developing breast cancer in her lifetime. But, in reality, 95% of wome who developbreast cancer do not have these genes.

− it is believed that ONLY 10% of cancers have a strong genetic link

2nd stage: Promotion (Reversible)

• Characterized by reversible proliferation of the altered cells (an important distinction

between initiation and promotion is the activity of promoters is reversible)key concept incancer prevention

o With the presence of promoting factors, the odds of cancer development are increased. Factors

include:

Dietary fat

Obesity

Cigarette smoking

Alcohol consumptiono Several promoting agents exert activity against specific types of tissues or organs.

− ex; smoking is a promoting agent in bronchogenic carcinoma.

8/8/2019 Ch 16 Cancer A


− Ex; smoking w/ alcohol promotes esophageal and bladder cancers)o Complete carcinogens are capable of both INITIATING and PROMOTING the development of

cancer.

− ex; cigarette smoking is a complete carcinogeno latent period: a period of time ranging from 1 to 40 yrs elapses between the initial genetic

alteration and the actual clinical evidence of cancer.

− Latent period is associated w/ the mitotic rate of the tissue of origin and environmentalfactors

o cell must reach a critical mass to become clinically evident (Most cancers develops in years or

even decades in lengths)

1 cm tumor – usually detected by palpation

0.5 cm tumor – the smallest that can be detected by MRI

Final stage: Progression

o Characterized by

1) increased growth rate of the tumor,2) increased invasiveness, and3) spread of the cancer to a distant site (metastasis)

− certain cancers have an affinity for particular tissue or organ as a site of metastasis (ex;colon cancer spreads to liver)

− others are unpredictable (ex; melanoma)− most frequent sites of metastasis : lungs, brain, bone, liver, and adrenal glands

o Metastasis is a multistep process

− Begins with rapid growth of primary tumor

− Develops tumor angiogenesis: process of the formation of blood vessels within the tumoritself. Tumor angiogenesis is facilitated by tumor angiogenesis factors produced by thecancer cells.

− As tumor grows, it grows into areas of least resistance by mechanically invading surroundingtissues.

o Subpopulations (segments) of tumor cells are able to detach from primary tumorinvade

the tissue surrounding the tumor penetrate the walls of lymph or vascular vesselsmetastasisto a distant site

− Facilitating factors:1. Rapid proliferation causing mechanical pressure leading to penetration of surrounding

tissues

2. Certain malignant cells have decreased cell-to-cell adhesion in comparison with normalcells

o Some produce metalloproteinase enzymes: an enzyme that are capable of destroying the

basement membrane of tumor itself, lymph and blood vessels, muscles, nerves, and mostepithelial boundaries.

• Metastatic tumor cells travels to distant organs via lymphatic and hematogenous routes!o Hematogenous metastasis involves several steps

− Begins w/ penetration of blood vessels by primary tumor cells via release of metalloproteinase

enzymes cells enter the circulation travel through the body adhere to small blood

vessels of distant organs cells penetrate the blood vessels of distant organs by releasingagain metalloproteinase enzymes.

− Most tumor cells are destroyed by mechanical mechanisms (ex; turbulence of blood flow) andcells of the immune system. However, formation of a combination of tumor cells, platelets,and fibrin deposits may protect some tumor cells.

o Tumor cells may be “trapped” in the first lymph node OR

o Skip metastasis: may bypass regional lymph node and travel more distantly.

− Ex; esophageal cancers

− Tumor cells that do survive must create vascularization and evade cells of the immunesystem for their growth and development (like primary tumor site)

8/8/2019 Ch 16 Cancer A


• Vascularization is critical to the supply of nutrients to the metastatic tumor and to theremoval of waste products

Role of the Immune Systemo Recognition and destruction of tumor cells

− Immune system has the potential to distinguish cells that are normal(self) fromabnormal(nonself) cells (ex; transplanted organs are recognized by immune system as

‘nonself’ and elicit an immune responsemay result in organ rejection

− Cancer cells can be perceived as ‘nonself’ and elicit an immune response resultingrejection and destruction.

o However, immune response that is mounted against cancer cells may be inadequate

to effectively eradicate them.o May be inadequate b/c cancer cells arise from normal human cells

o immunologic surveillance: response of the immune system to antigens of malignant cells such

as TAAs.

− Cancer cells may display tumor-associated antigens (TAAs) on cell surface as a result of malignant transformation.

− Malignant transformation occurs continuously. Immune response destroys the malignant cells

Ex; lymphocytes detect and destroy abnormal cells or altered antigenic determinants.

− Immune surveillance will prevent transformed cells from developing into tumors.

Escaping from immunologic surveillanceo Immunologic escape: process by which cancer cells evade the immune system

o THEORY: cancer cells escape mechanisms from Immunologic Surveilance.

1) Suppression of factors that stimulate T cells to react to cancer cells (ex; stress2ndarycancer)

2) Weak surface antigens allowing cancer cells to “sneak through” immunologicsurveillance

3) The development of tolerance of the immune system to some tumor antigens

Immune response against TAAsCytotoxic Tcells

1. Dominant role in resisting tumor growth

2. Capable of killing tumor cells

3. Important in the production of cytokines (ex; IL-2 and y-interferon) whichstimulate t cells, natural killer cells, B cells, and macrophages

Natural killer(NK) cells

1. Directly lyse tumor cells spontaneously w/out any prior sensitization

2. Increased cytotoxic activity by the stimulation of Y-interferon and IL-2

Macrophagesand monocytes

o Important roles in tumor immunity

• Macrophages become nonspecifically lytic for tumor cells (activated by y-interferon)

1. Phagocytosis

2. Processing of target cells3. Macrophages also secrete cytokines

− Interleukin-I (IL-1) : coupled w/ processed antigen stimulates Tlymphocyte activation and production

− a-interferon : augments killing ability of NK cells

− tumor necrosis factor (TNF) : causes hemorrhagic necrosis of tumors and exerts cytocidal or cytostatic actions against tumor cells

− colony-stimulating factors: regulate production of various bloodcells in the bone marrow and stimulate function of various WBCs

Blymphocytes

1. produce specific antibodies that bind and kill tumor cells by complementfixation and lysis

− antibodies often detectable in serum and saliva of patient

− antibodies that are specific for a person’s own tumor and a similar tumor inother person have been found in some patients.

8/8/2019 Ch 16 Cancer A


4) Suppression of the immune response by products secreted by cancer cells

5) The induction of suppressor T cells by the tumor

6) Blocking antibodies that bind TAAs , thus preventing their recognition by T cells.

Oncofetal Antigenso Oncofetal Antigens: type of tumor antigen

− Found on both the surfaces and inside of cancer cells, found on fetal cells as well.

− Expression of the shift of cancerous cells to a more IMMATURE METABOLIC PATHWAY(expression usually associated with embryonic or fetal periods of life)

− Reappearance of fetal cells is not well understood. However, it is believed to occur for the cellregaining its embryonic capability to differentiate into many different types of cells.

− Examples:Carcinoembryonic antigen (CEA)

o Found on normal fetal cells in gut, liver, and pancreas

o normally disappears during the last 3 months of fetal life.

o Malignant conditions : Also found on surface of cancer cells derived from GI tract (originally

isolated from colorectal cancer cells)o Nonmalignant conditions : ↑CEA have been found in cirrhosis of liver, ulcerative colitis, and heavy

smoking

• PRESENTLY, major value of CEA is NOW used as an INDICATOR OF THE SUCCESS OF CANCER

TREATMENT – so MONITOR

− Ex; persistence of elevated preoperated CEA titers post surgery tumor is not completelyremoved

− Ex; rise in CEA post chemo or radiation therapy recurrence or spread of the cancer.

a-fetoprotein (AFP)

o Produced by fetal liver cells

o Malignant conditions : Also produced by malignant liver cells

− Has diagnostic value in primary cancer of the liver (hepatocellular cancer)

− Also produced when metastatic liver growth occurs.o Nonmalignant conditions: testicular carcinoma, viral hepatitis, and nonmalignant liver disorders

• Detection of AFT is of value in tumor detection & determination of tumor progression

Oncofetal antigens curreintly being studied

o CA-125: found in ovarian carcinoma

o CA-19-9: found in pancreatic and gallbladder cancer

o Prostate-specific antigen(PSA): found in prostate cancer

Classification of Cancer

Classified according to

1. Anatomic site

2. Histology (grading)

3. Extent of disease (staging) Tumor classification provide a standardized way to

1. Communicate the status of the cancer to members of health care team2. Assist in determining the most effective treatment plan

3. Evaluate the treatment plan

4. Factor in determining the prognosis

5. Compare like groups for statistical purposes

Anatomic Site Classification

Identified byo tissue of origin

o anatomic site

8/8/2019 Ch 16 Cancer A


o behavior of the tumor (benign or malignant)

o Carcinomas:

− Originate from embryonal ectoderm – skin and glands

− Originate from embryonal endoderm – mucous membrane linings of the respiratorytract, gastrointestinal tract, and genitourinary [GU] tract

o Sarcomas:

− originate from embryonal mesoderm – connective tissue, muscle, bone and fato Lymphomas and leukemias originate from hematopoietic system

Histologic Classification

Pathologically evaluating the APPEARANCE of cells and the degree of DIFFERENTIATION.

4 grades used to evaluate abnormal cells based on the degree to which they resemble the tissueof origin.

• Grade I: Cells differ slightly from normal cells (mild dysplasia) and are well differentiated.

• Grade II: Cells are more abnormal (moderate dysplasia) and moderately differentiated

• Grade III: Cells are very abnormal (severe dysplasia) and poorly differentiated.

• Grade IV: Cells are immature and primitive (anaplasia) and undifferentiated; cell of

origin is difficult to determine. NOT GOOD NEWS!

• REMEMBER: tumors that poorly differentiated (undifferentiated) have a worse

prognosis than those that are closer in appearance to the normal tissue of origin.

Extent of Disease Classification

Staging: classifying the extent and spread of disease. Based on description of the extent of the disease(NOT appearance)

Ex; colon cancer; look at how much PENETRATION it went through rather than appearanceo Clinical Staging (based on American Joint Committee on Cancer (AJCC) tumor site-specific

rules)

− Determines the anatomic extent of the malignant disease process

Stage 0: cancer in situ (envelope – inside has not infiltrated)

Stage I: tumor limited to the tissue of origin; localized tumor growth

Stage II: limited local spread

Stage III: extensive local and regional spread

Stage IV: metastasis

− Used as a basis for staging a variety of tumor types (ex; cervix cancer, hodgkin’slymphoma. BUT NOT FOR Leukemia)

• Clinical staging is done after diagnostic workup,,, but before treatment begins.

o TNM Classification System (Represents the AJCC modification of clinical staging (originally

developed by the International Union Against Cancer (UICC))

− Made to achieve consistency w/American medical practice

− Used to determine anatomic extent of disease involvement according to threeparameters:

Primary Tumor (T) : Tumor size and invasiveness

T0

Tis

T1-4

Tx

No evidence of primary tumor

Carcinoma in situ (has all the histologic characteristics of cancer except invasion – primary feature of TNM)

Ascending degrees of increase in tumor size and involvement Tumor cannot be measure or found

Regional Lymph Nodes (N) : presence or absence of regional spread to the lymph nodesN0

N1-4

Nx

No evidence of disease in lymph nodesAscending degrees of nodal involvementRegional lymph nodes unable to be assessed clinically

Distant Metastases (M) : metastasis to distant organ sites

8/8/2019 Ch 16 Cancer A


M0

M1-4

Mx

No evidence of distant metastasesAscending degrees of metastatic involvement of the host, including distant nodesCannot be determined

• TNM cannot be applied to all malignancies (ex; NO for leukemia since not a solid tumor)

o Karnofsky Functional Performance Scale describes patient performance in terms of

functionality on a percentage basis.

Staging can be performed initially and at several evaluation points.o Clinical diagnostic staging done at the completion of diagnostic workup to determine most

effective treatment planDiagnostic tests:

Radiologic studies such as bone and liver scans

Ultrasonography

Computed tomography (CT)

MRIo Surgical Staging determined by surgical excision, exploration, and/or lymph node sampling

− Ex; staging hodgkin’s lymphomia: laparotony and splenectomyo During laprotomy, lymph node biopsies may be done and margins may be

marked w/ metal clips that are used when radiotherapy is used as treatment

modality.− Exploration surgical staging is less used b/c noninvasive diagnostic technology are

becoming increasingly sophisticated.

• The stage classification is NOT changed after the extent of dz is determined

• Original description remains part of the original record.

o If additional treatment is needed, or if treatment fails retreatment staging is done.

o “restaging” classification (rTNM) is differentiated from stage at diagnosis as clinical

significance may be quite different.

Prevention and Detection of Cancer

PUBLIC EDUCATIONGOAL of public education: motivate learners to change their negative health behavior patterns toachieve and maintain an optimal state of health.

− Care should be taken to minimize fear and anxiety

− Reinforce w/ large-type prints including graphics and key concepts increases success of educational efforts for elderly who may have visual and hearing deficits or difficultyprocessing info, or those who has English is a second language.

TEACH – Nursing Implementation1. Reduce or avoid exposure to carcinogens and cancer-promoting agents (ex; cigarette smoke &

sun exposure)

2. Eat balanced diet including vegetables, freshfruits, whole grains, adequate amountsof fiber. Reduce amount of fat, preservatives, including smoked and salt-cured meats

containing high nitrite concentrations.3. Participate in regular exercise regimen (ex; ≥ 30minutes moderate physical activity 5times weekly)

4. Obtain adequate, consistent periods of rest (at least 6 to 8 hrs /night)

5. Have health examination on a regular basis including health history, physical examination,specific diagnostic tests for common cancers in accordance with the guidelines published by theAmerican Cancer Society

6. Eliminate, reduce, or change perceptions of stressors and enhance the ability to effectively copew/stressors

7. Know seven warning signs of cancer (actually detect fairly advanced disease)

7 WARNINGS SIGN OF CANCER

8/8/2019 Ch 16 Cancer A


− Change in bowel or bladder habits

− A sore that doesn’t heal

− Unusual bleeding/discharge from an orifice

− Thicking or lump in beast or elsewhere

− Indigestion or difficulty swallowing

− Obvious chage in wart or mole

− Nagging cough or hoarseness

8. Learn & practice recommended cancer screenings on a timely basis (ex; colonoscopy in average-risk people beginning at age 50 and every 10yrs thereafter)

9. Learn & practice self-examination (ex; DO testicular self-exam & SBE starting from EARLY 20’s)

10.Seek immediate medical care if notice any change in what is normal for you and if cancer issuspected.

• Remember! Early detection of cancer has positive impact on prognosis!

DIAGNOSIS OF CANCER

− When pt has a possible diagnosis of cancer,,,o Stressful time for pt and family

o Fear of the unknown.

Nursing Implementation− Be available to actively listen to concerns and skilled in techniques that will engage the in

discussion about their cancer-related fear.

− Recognize that their anxiety may arise from myths and misconceptions about cancer (ex;

cancer is a “death sentence”, cancer treatment is worse than the illness) correctingmisconceptions will ↓anxiety

− Nurses should learn to recognize their own discomfort when discussing about cancer.o AVOID closed communication patterns that may shut off further communication

o AVOID false reassurance that everything will be all right (ex; it’s probably nothing)

o AVOID redirecting the discussion (let’s discuss that later)

o AVOID generalizing (everyone feels this way)

− Pt may need repeated explanations of diagnostic workup due to HIGH ANXIETY &

FEAR. Clear and repeated/reinforced explanations may be necessary. (written info ishelpful for reinforcement)

− Diagnositic plan for those cancer is suspected : includes health hx, identifying risk factors,physical exam, specific diagnostic studies

o Health history: emphasis on risk factors such as

family or personal history of cancer

Exposure to or use of known carcinogens (exl cigarette smoking, exposure tooccupational pollutants or chemicals)

Disease characterized by chronic inflammation (exl ulcerative colitis)

Drug ingestion (ex; hormone therapy, previous anticancer therapies)

Dietary habits, ingestion of alcohol

Lifestyle

patterns and degree of coping w/ perceived stressorso Physical examination

Should be thorough

Particular attention should be given to

• respiratory system GI system (including colon, rectum and liver),

• lymphatic system (including spleen),

• breasts,

• skin,

• reproductive system (testes and prostate gland in men; cervix, uterus,and ovaries in women), and

8/8/2019 Ch 16 Cancer A


• musculoskeletal and neurologic systemo Diagnostic studies

Studies to be performed on will depend on the suspected primary or metastaticsite(s) of the cancer

Examples of studies or procedures:

• Cytology studies (ex; Papanicolaou[Pap] test, bronchial washings)

• Tissue biopsy

•Chest x-ray

• CBC, chemistry profile

• Sigmoidoscopy or colonoscopy exam (include guaiac test for occult blood)

• LFT (ex; aspartate aminotransferase[AST])

• Radiologic studies (ex; mammography, ultrasound)

• Radioisotope scans (ex; bone, lung, liver, brain)

• CT scan (ex; spiral)

• Positron emission tomography (PET) scan

• Presence of tumor markers (ex; CEA, AFP, PSA, CA-125) or geneticmarkers (ex; BRCA-1, BRCA-2)

• Bone marrow examination (if hematolymphoid malignancy is suspected orto document metastatic dz)

Biopsyo The only definitive means of diagnosing cancer

o Essential in planning a treatment plan

o Involves surgical acquisition of tissue from suspicious area for histologic examination by a

pathologist

Will determine whether tissue is benign or malignant

The anatomic tissue from which tumor arises

Degree of cellular differentiationo Needle or aspiration biopsy: used to obtain cells and tissue fragments through a large-bore

needle that is guided into tissue in question (ex; bone marrow aspiration; core biopsy of prostate gland, breast, liver, and kidney tissues)

− To determine the presence of tumor ,, cytologic analysis is performedo

Incisional biopsy: performed w/ scalpel or dermal punch− Common technique for obtaining a tissue sample for making a diagnosis of cancer

o Excisional biopsy: involves removal of entire tumor

− Used for small tumors (smaller than 2 cm), skin lesions, intestinal polyps, and breastmasses

− Considered therapeutic as well as diagnostic

− If not easily accessible major surgical procedure such as laparotomy, thoracotomy,craniotomy, is necessary to obtain a piece of tumor tissue.

o Endoscopic procedures: biopsy specimens of GI, respiratory, and GU systems

Collaborative Care

Goals and Modalities

• GOAL of cancer treatment : CURE, CONTROL, or PALLIATIONo Factors that determine therapeutic approach are:

Tumor cell type

Location

Size

And systemic extent of dz.o Other important considerations

Pt’s physiologic status (ex; presence of comorbid illness)

8/8/2019 Ch 16 Cancer A


8/8/2019 Ch 16 Cancer A


o Oldest form of local cancer treatment

o Was the only effective method of cancer diagnosis and treatment in the early days

o For many years, removing the cancer w/ surrounding tissue as much as possible was treatment of

choiceo This approach did not consider the ability of malignant cells traveling to other locations

o Made surgical cure possible only when tumor was localized and relatively small

o TODAY, surgery is employed to meet a variety of goals b/c

Surgical techniques improved

Expanded knowledge of tumor metastasis patterns

Availability of alternate therapies

Prevention

− Prophylactic removal of nonvital organs - used to eliminate or reduce risk of cancerdevelopment who have underlying conditions that ↑risk of developing cancer. (Must weigh riskvs. benefits)

o Ex; total colostomy to those who have adenomatous familial polyposis to prevent

colorectal cancero Ex; prophylactic mastectomy to those who have genetic mutations of BRCA-1 or BRCA-2

and a strong family hx of early-onset breast cancer prevent breast cancer

Cure and Control

− Objective is to remove all or as much resectable tumor as possible while sparing normaltissue.

− Good prognostic indicatiorso Small tumor size

o Clean tissue margins (free of dz surrounding the site of resection)

o Absence of node involvement

o Absence of abnormal tumor marker values

− Several principles applicable when surgery is used to cure or control cancer

1. Only as much tissue as necessary is removed

2. When appropriate, adjuvant (additional) therapy is used to treat unresectable gross

tumor or eliminate residual undetectable micrometastases. Risk for metastaic dz istumor dependent. The decision regarding adjuvant therapy is customized to pt’stumor type, stage, level of risk for residual or metastatic dz, comorbidities, and ptpreferences.

3. Preventive measures used to reduce surgical seeding of cancer cells

4. Usual sites of regional spread may be surgically removed to evaluate presence of microscopic dz or to minimize the risk of recurrence.

Supportive and Palliative Care

− When cure or control is no longer possible focus shifts to preservation of quality of life atthe highest possible level for the longest period of time.

− GOAL – supportive care and palliation of SYMPTOMS

− Surgical procedures for supportive care that maximizes bodily function or facilitates cancertreatment. Examples; (to ↑ function)

1. Gastric feeding tube insertion to maintain nutrition during head and neck cancer treatment

2. Creation of colostomy to allow healing of rectal abscess

3. Suprapubic cystostomy for pt with advanced prostatic cancer

4. Placement of venous access devices to deliver chemotherapy, pain med, parenteralnutrition, blood products, and other supplements.

− Surgical procedures for palliation of symptoms associated w/ cancer include: (to ↓pain)

1. Debulking of tumor or radiation therapy to relieve pain or pressure

8/8/2019 Ch 16 Cancer A


2. Colostomy for the relief of a bowel obstruction

3. Laminectomy for the relief of a spinal cord compression

Rehabilitative Care

− Cancer surgery can produce a change in body image and function. Conjunction with thediagnosis itself may be difficult for the pt to cope with these changes.

− Patient must be able to accept and cope with their altered body image and functionaldeficit on a daily basis in order to maintain its quality of life.

− The emphasis of rehabilitative role of surgery is greatly increasing to increase the quality of life.

1. Creation of a bladder reservoir at the time of cystectomy

2. Breast reconstruction after mastectomy

3. Spinal or joint stabilizing rods insertion to facilitate function

4. Create ostomies to facilitate function

Chemotherapy

Def: the use of chemicals as a systemic therapy for cancerMAINSTAY for treatment of most solid tumors & hematologic malignancies. (ex; leukemia,lymphoma, myeloma, and myelodysplastic syndromes).

Chemotherapy is a therapeutic option that can offero cure for certain cancers,

o control other cancers for long periods,

o and offer palliative relief of symptoms when cure or control is no longer possible

GOAL – is to eliminate or reduce number of malignant cells present in the primary tumor andmetastatic tumor sites.Several factors determine response:

1. Mitotic rate of tissue of origin

− Rapid mitotic rate, better response (ex; acute leukemia and small cell lung cancer)

2. Size of tumor

− Smaller tumor, the greater response

3. Age of tumor

− Younger the tumor, greater response. Rationale: newly developing tumors tend to have agreater percentage of proliferating cells

4. Location of tumor

− Certain anatomic sites provide protected environment from chemotherapy effects.

MOST DOES NOT CROSS BLOOD BRAIN BARRIER

− Only few drugs that cross the BBB are (ex; nitrosoureas, bleomyci,temozolomide)

New agents and techniques are being developed to cross this barrier

OR maybe given intrathecally in the spine

5. Presence of resistant tumor cells

− Resistant malignant cells pass resistance to daughter cells, which continue to proliferate andremain resistant.

Effect on Cells

Chemotherapy effects is at the cellular level : relationship to the cell cycle.

2 major categories of chemotherapeutic drugs: (often administered in combo to maximizeeffectiveness)

1) Cell cycle phase-nonspecific chemotherapeutic drugs: effect on the cells during allphases of cell cycle

− (include cellular replication & proliferation & those in resting phase(G0)

8/8/2019 Ch 16 Cancer A


2) Cell cycle phase-specific chemotherapeutic drugs: most significant effects duringspecific phases of cell cycle

− (process of cellular replication or proliferation during G1, S1, G2, or M)

When cancer first develops, most cells are actively dividing most chemoagents are mosteffective against dividing cells.

As tumor increases, more cells become inactive and convert to resting state (G0) duringchemo, cells can escape death by staying in the G0 phase. Therefore, a major problem is thepresence of drug-resistant resting and noncycling cells.

Classification of Chemotherapeutic Drugs

Classified in general groups according to

Molecular structure

Mechanisms of action

Particular class has many similarities. Yet, there are major differences in how drugs work, andunique side effects within each class

Preparation and Administration of Chemotherapy

• ONLY those who are SPECIFICALLY TRAINED IN CHEMOTHERAPY HANDLINGTECHNIQUES SHOULD BE INVOLVED WITH THE PREPARATION AND ADMINISTRATION OFANTINEOPLASTIC AGENTS.

− Specific guidelines for administration of chemotherapeutic drugs b/c may pose anoccupational hazard.

− Drugs may be absorbed when preparing, transporting, or administering chemotherapyo skin if there is droplet exposure,

body fluids and excretions of persons receiving chemoo Inhalation when reconstituting a powder in an open ampule

Methods of Administration

Intravenous (IV) routes - most commonIV Peripherally

o Major concerns w/ IV administration

Venous access difficulties

Device-or catheter-related infection Extravasation (infiltration of drugs into tissues

surrounding the infusion site) causing local tissuedamage & PAIN

o IRRITANTS – damage the intima of the vein, causing

phlebitis and sclerosis and limiting future peripheralvenous access- BUT WILL NOT CAUSE TISSUE DAMAGE IF

INFILTRATED

o VESICANTS – if extravasation or infiltrated into skin

(W/OUT PAIN) may cause severe local tissuebreakdown, ulceration & necrosis (or third

degree burn) potential to progress to a deep,wide crater that warrants closure with skingrafts

Nursing implementationo MONITOR for extravasation

o Promptly recognize symptoms

swelling redness

presence of vesicles on the skin,

w/out paino immediately turn OFF infusion

o protocols for drug-specific

extravasation to minimize furthertissue damange

IV pushFresh IV run w/ open saline bagAspirate q few seconds and see flashbackof blood..If seen, it is okay

But if not seen blood or if pain stopGive Antidote intradermally

Central vascular access device (CVAD)o Advantages: (can give over 4 hrs)

To minimize associated physical discomforts, emotional distress and risks of infection andinfiltration. (still IV)

Using large blood vessels and permit frequent, continuous, or intermittent administration of chemotherapy

8/8/2019 Ch 16 Cancer A


Can also be used to administer additional fluids, and electrolytes, blood products, parenteralnutrition, other meds (antiemetics) and for venous sampling

Avoiding multiple venipunctures for vascular access

↓risk for extravasation injury – but still can occur if displacement or damage to particulardevice used for central venous access

Facilitation of supportive therapies

o Disadvantages:

Risk of systemic infection (if pt becomes immunosuppressed during therapy)

− Write down what site looks like, or any signs of infection

o Used for:

Those with limited vascular access

Intensive chemotherapy

Repetitive or continous infusion of vesicant agents

Projected long-term need for vascular accessTunneled Catheter

Single-, double-, or triple lumen

Approximately 90 cm in length

Ranging from 1 to 2 mm in internal diameters

− Inserted with local or general anesthesia througha central vein

− Tip rests in distal end of superior vena cava OR rightatrium of the heart

− Other end is tunneled through subcu tissue and exitsthrough incision on chest or abdominal wall

o DACRON cuff : serves to stabilize catheter and may

↓incidence of infection by impeding bacteriamigration along the catheter beyond the cuff

o

Groshong catheter : special tube of tunneled cath− Closed ended with a slit valve(pressure activated

valve) on the side of the distal end

− Therefore, this valves opens w/infusion, flushing,or aspirating blood. When not used, valve closes,preventing backflow of blood or entry of air

− Does not need heparin flushing or clamping

o MUST VERIFY accurate placement

using CHEST-X-RAY before using

cathetero care requirements

Cap chage

Cleansing

Heparin flush

Dressing changeo complications - MONITOR

Occlusion

Sepsis

Bleeding

Venous thrombosis

Technical problems

Local infection at exit site

8/8/2019 Ch 16 Cancer A


Peripherally inserted Central Venous Catheters(PICCs)

-only MD or specially trained nurse can placethese

Single-, or double-lumen

Up to 60 cm in length

Ranging from 24 to 16 guages

Nontunneled

Polymer catheters

− Inserted at or just above the antecubital fossa

− Tip ending in the distal 1/3 of superior vena cava

− Use guide wire or forceps to advance the line.

− Primarily used in cancer care for immediate centralvenous access OR for infusion therapy that is beyondthe capacity of pt’s existing, long-term venousaccess device.

o Used for

− short term IV therapy – can be in place for up to 6mons

− frequent administration of blood products

− frequent blood drawing

− intermittent or continuous drug infusions

o Complications - MONITOR

Catheter occlusion – thrombolyticagent can be used to lyseobstructions

Phlebitis – usually appears within 7to 10 days following insertion

• Signs

−

Redness− Edema

− Tenderness along trackof catheter line

• If sign present

− Remove catheter

− Must culture tip of catheter

• Arm in which PICC is in place shouldNOT BE USED FOR BP or blooddrawings

Implanted Infusion Ports

− Consists of central venous catheter connected to animplanted, single or double subcu injection port

− Placed into desired vein and other end is connectedto a port that is sutured to the chest wall muscle

− Surgically implanted in a subcu pocket on the chestwall

− Port consists of metal sheat w/ self-sealing siliconseptum

− Accessed via septum w/special Huber Point Needlethat has a deflected tip to prevent coring of theseptum

− Available w/ 90degree tips for longer invusions

o Care requirements

Regular flushingo Complications

Clotting

Catheter migration

Infection

Bleeding

Thrombosis

Air embolism

Infection at the exit site or in thepocket

Formation of “sludge” –accumulation of clotted blood anddrug precipitate may also occurwithin port septum

Infusion Pumps

− Used primarily for continous infusion of chemotherapy by IV, subcutaneous, intraarterial,and epidural rountes

− Pumps worn externally or implanted surgically

Implanted pumps are used primarily forintraarterial administrations – continous infusiondirectly to the tumor while ↓systemic effects of the drug

2nd septum can be used for bolus medicationadministration

− Most commun use:

Hepatic artery infusion for liver metastasisusually from primary colorectal cancer

o Flow rate can be affected by

Drug concentration

Length and diameter of SilasticCatheter

Pt’s body temp; dose alterationsmay be required if pt has changein temperature or travels to higheraltitutdes

o Complications

Infection

Thrombosis

Clotting of catheter

8/8/2019 Ch 16 Cancer A


− Catheter is attached to a pump apparatus consistingtwo chambers

Inner chamber: serves as the drug reservoir

Outer chamber: contains vapor pressureproviding source of power for the pump

− Pump is implanted surgically in a subcutaneouspocket

− Access to pump via a silicone septum with a Huber-point needle

Pump malfunction

Regional chemotherapy administration

Involves delivery of drug DIRECTLY TO TUMOR SITE

Advantage: Higher concentrations of drug can be delivered to the tumor with ↓systemictoxicity

Intraarterial Chemotherapy

o Delivers drug to the tumor via arterial vessel supplying the tumor

o Method: surgical placement of a catheter connected to an external infusion pump or an implanted

infusion pumpo Treatment used for

osteogenic sarcoma

Cancers of head and neck,Bladder,Brain,Cervix

Melanoma

Primary liver cancer

Metastatic liver diseaseo reduced systemic toxicity

type of toxicity experienced by pt depends on the site of tumor being treated

Intraperitoneal Chemotherapy – PERITONEAL METASTASESo Delivery of drug to peritoneal cavity.

− Generally infused into peritoneum in 1 to 2 L of fluid and allowed to “dwell” in theperitoneum for a period of 1 to 4 hrs. Following the “dwell time,” the fluid is drained fromthe peritoneum.

o Method: temporary Silastic catheters (Tenckhoff, Hickman, and Groshong) are percutaneously or

surgically placed into peritoneal cavity for short-term administration.Alternate method: implanted port can be used to administer chemotherapy intraperitoneally

o Treatment used for

Peritoneal metastases from primary colorectal and ovarian cancers

Malignant asciteso Complications

Abdominal pain

catheter occlusion, dislodgement, and migration

infectionIntrathecal or Intraventricular Chemotherapy - CNS

o Cancers that metastasize to CNS are difficult to treat b/c of BBB often prevents distribution of

chemotherapy to this area (ex; common in breast, lung, GI tumors, leukemia, and lymphoma)o Method used to treat metastasis to the CNS

Intrathecal chemotherapy:

− involves lumbar puncture and injection of chemotherapy into subarachnoid space.

− However, results in incomplete distribution of the drug in CNS, particularly to thecisternal and ventricular areas

Intraventricular Chemotherapy:

− Ommaya reservoir, Silastic, dome-shaped disk with an extension catheter that issurgically implanted through the cranium into a lateral ventricle, is inserted to ensure

8/8/2019 Ch 16 Cancer A


more uniform distribution of chemotherapy to the cisternal and ventricular areas

− Also precludes the use of repeated, painful lumbar punctureso Complications of both

HA, N/V, fever, nuchal regidityIntravesical Bladder Chemotherapy - BLADDER

o Instillation of chemotherapy into bladder via urinary catheter and retained for 1 to 3 hrs.

− Promotes destruction of cancer cells and reduces incidence of recurrent disease

−

Reduces urinary and sexual dysfunctiono Complications

Dysuria

Urinary frequency

Hematuria

Bladder spasms

Effects of Chemotherapy on Normal Tissueso Chemotherapeutic agents cannot distinguish between normal and cancer cells.

o Chemotherapy induced side effects

− result of normal cells destruction – especially those that rapidly proliferates such as bonemarrow, lining of GI system, integumentary system (skin, hair, and nails)

−Caused by general cytotoxicity and organ-specific drug toxicities

o Body’s response to products of cellular destruction:

Fatigue

Anorexia

Taste alterationso General and drug-specific adverse effects

Acutetoxicity

Occurs during and immediately after drug administration

Anaphylactic

Hypersensitivy reactions

Extravasation or a flare reaction

Anticipatory nausea and vomiting

Cardiac dysrhythmias

Delayedeffects

Delayed nausea and vomiting

Mucositis

Alopecia

Skin rashes

Bone marrow suppression

Altered bowel function (diarrhea or constipation)

A variety of cumulative neurotoxicities depending on the affected componentof the nervous system (ex; central or peripheral nervous system or cranialnerves)

Chronictoxicities

Damage to organs such as the heart, liver, kidneys, and lungs

Treatment Plano Single-drug can be and sometimes prescribed

− Combining agents– proved to be more effective in managing most cancers.o Choosing agents with different MOA and Varying toxicity profiles

− Avoids tumor cell resistance and minimizes s/eo Drug regimens are selected based on evidence used in specific cancers, and are sometimes

customized for individual ptso Chemotherapy is most effective when

Tumor burden is Low

Therapy is not interrupted

8/8/2019 Ch 16 Cancer A


Pt receives the intended dose

• REMEMBER~! Each drug is carefully calculated according to pt’s body surface area (ex; basedon body weight & height) – FOLFOX treatment

ch 16 cancer a

Documents