CELLULAR ABBERATION

 Epidemiology of cancer
 Pathophysiology of the malignant process 967
 Detection and prevention of cancers
TYPES OF CANCERS
1. Laryngeal 1495
2. Esophageal 3422 [3423-3426]
3. Breast 4572
4. Lung 1654 [1679]
5. Pancreatic 3864 [3868]
6. Gastric 3461 [3468]
7. Bladder 4338 [4341] skip
8. Colorectal 3568 [3584]
9. Prostate 4648 [4673]
10. Uterine 4521 [4524]
11. Cervical 4517 [4522]
CELL CYCLE: 996
REPORT: CHEMOTHERAPEUTIC DRUGS = 997

EPIDEMIOLOGY

Cancer nursing practice

 overlaps with numerous nursing specialties

 covers all age groups
 carried out in various settings (acute care inst., OP centers, rehab faci, home, etc)
 ONCOLOGY: scope, responsibilities, and goals of cancer nursing
 Care for pt throughout cancer trajectory from prevention – end-of-life care
Precision medicine

 “personalized medicine”
 An innovative approach to tailoring disease prevention and treatment that takes into account
differences in people's genes, environments, and lifestyles.
Cancer health disparities

 differences or inequalities in how cancer affects different groups of people.

 A result from multiple, complex interrelated factors (ex. Socioeconomic stat, cultyre, diet, stress,
environment, biology)
 High in non-Hispanic race; Low in Hispanic/Latino (but infection-related CA are 2x higher)

PATHOPHYSIOLOGY OF THE MALIGNANT PROCESS

 Cancer: a disease that begins in mutations of or cellular DNA (deoxyribonucleic acid)

DNA mutations → Abnormal cell behavior → altered cells form a clone → proliferates abnormally
evading normal in & extracellular growth regulating processes / signals the immune system defense
mech
Genetic mutations → abnormal cell signal transduction process

Carcinogenesis: How normal cells transform into cancer cells

3 STEP PROCESS
Initiation:

 Carcinogens cause mutations in the cellular DNA (normally reversed thru apoptosis or cell
senescence: DNA repair mech)
Promotion:

 Repeated exposure to promoting agents → proliferation and expansion of initiated cells

(w/increased expression or manifestation of AN gene info.
 It is reversible when promoting substance is REMOVED.
Progression

 Altered cells exhibit increasingly malignant behavior

  These cells acquire the ability to stimulate angiogenesis (growth of new BV allowing CA cells to
grow) → invade adjacent tissues, metastasize
 Cellular oncogenes (has the ability to cause cancer under mutations): responsible for vital
functions; proliferation, differentiation.
o Cellular proto-oncogenes:
 Normal, non-mutated genes found in healthy cells; regulates cell growth,
differentiation, and various cellular processes. (ex. EGFR, c-Myc, kirsten ras)
o KRAS: Pancreatic, Lung, Colorectal CA association
 Acts as “on switches” for cellular growth
 ↑ oncogenes or overexpression → uncontrolled proliferation
o Cancer suppressor genes:
o Turns off or regulate unneeded cell proliferation
o When MUTATED → loss of function or expression → cells produce mutant cell
populations (diff from the orig cell ancestors)

PROLIFERATIVE PATTERNS
 Cancerous cells demonstrate neoplasia, or uncontrolled cell growth that follows no physiologic
demand.
ETIOLOGY
Viruses & bacteria

 10- 20% cancers linked to viral infections

 Pathophysio: Infection → virus insert DNA to infected cell genes → cell division (w/DNA of the
virus): lacks normal controls on growth.
Examples:
o (HPV) Human Papilloma Virus: cervix, head, neck
o (HBV) Hep B virus: liver
o (EBV) Epstein-Barr virus: Burkitt lymphoma, nasopharyngeal
 Little evidence of bacterial link to CA: secondary responses (carcinogenic metabolites and infalmm
reactions) suspects CA development

Examples:
o Helicobacter pylori: stomach CA
o Salmonella enteritidis: colon CA
o Chlamydia trachomatis: ovarian, cervical CA

Physical Agents

 Exposure to sunlight, radiation, chronic irritation or inflammation, tobacco carcinogens, industrial

chemicals, and asbestos.
 Excessive UV ray’s exposure
o Skin CA
o ↑ risk for fair skinned
 Ionizing radiation exposure (rad therapy, repetitive x-ray)
o ↑ incidence of leukemia, multiple myeloma, breast-thyroid-other tissues CA
o Background rad from natural decay process → lung CA
o INTERVENTION: proper ventilation to allow gas to disperse into the atmosphere

Chemical Agents

 Tobacco use
o Single most lethal chem carcinogen (accounting 30% of lung CA)
 Environmental tobacco smoke
o Second hand smoke
o Linked to lung CA
 Electronic nicotine delivery system (ENDS)
o E-cigars, pens, pipes, hookah
o NO nicotine, but w/ harmful substances: volatile org compounds, formaldehyde, flavoring
chem
 Smokeless tobacco
o Chewing, snuffing, snusing
o ↑ risk for oral, pancreatic, esophageal CA
 Chemical substances
o aromatic amines and aniline dyes
o pesticides and formaldehydes
o arsenic, soot, and tars
o asbestos
o benzene
o cadmium
 o chromium compounds
o nickel and zinc ores
o wood dust; beryllium compounds
o polyvinyl chloride
o betel quid (chewed in some cultures)

Genetics and Familial Factors

 CA has been associated w/ extra chromosomes, too few chromosomes, or translocated

chromosomes
 5% - 10% shows familial predisposition
 Hallmarks of hereditary cancer syndrome
o CA in 2 or more 1st degree relatives
o Onset of CA in fam member <50 y.o.
o Same type of CA in several fam members
o Indiv fam members with >1 type of CA
o Rare CA in ≥ 1 fam members
 Advances in recognition, isolation & identification of genetic mutation responsible of inherited CA
susceptibility syndromes
o Hereditary breast & ovarian CA: BRCA1, BRCA 2
o Multiple endocrine neoplasia syndrome: MEN1, MEN2
o Others: nephroblastoma, pheochromocytomas, colorectal, stomach, thyroid, renal, prostate,
lung CAs
Lifestyle Factors

 Alcohol intake, poor diet, physical inactivity, smoking.

 Dietary substances:
o Fats
o Alcohol
o Salt cured or smoked meats
o nitrate- and nitrite-containing foods
o red and processed meats
 Heavy alcohol use:
o ↑ risks for mouth, pharynx, larynx, esophagus, liver, colon, rectum, and breast Cas
 Obesity:
o Possible mechanisms:
 Chronic inflammation (due to excess fat) → DNA damage
 ↑ levels of hormones (estrogen, insulin, adipokines)
 Disruptions in levels of cell growth regulators (AMP-activated protein kinase,
mammalian target of rapamycin)
Hormonal agents

 Hormonal imbalance: endogenous (body’s own), admin or exogenous hormones

 Prenatal exposure to diethylstilbestrol → clear cell adenocarcinoma of lower GI tract
 Reproductive cycle changes:
o BREAST CA RISKS
 Early menarche before 12
 Delayed onset of menopause after 55
 Nulliparity (haven’t given birth)
 Delayed childbirth after 30
  Taking estrogen after menopause ↓ risk for breast CA, ↑ endometrial CA
o Estrogen replacement alone is not used (w/o hysterectomy)
o Estrogen + progesterone therapy = ↑ risk for breast CA (subside after therapy)

ROLE OF IMMUNE SYSTEM

Normal immune Response
Intact immune system: Immune surveillance → recognize and combat cancer cells 9thru multiple,
interacting cells and actions of the innate, humoral, and cellular components of IS.

 Tumor-associated Antigens (TAAs)

o Found on membranes of many cancer cells
o Is processed by antigen presenting cells APCs (ex. Macrophages, dendritic cells: presents
antigens to both T & B lymphocytes) → presented to T lymphocytes → recognized as
foreign → release of cytokines that elicits various immune system actions:
 Proliferation of cytotoxic T lymphocytes (cell-killing)
 Induction of apoptosis
 Recruitment of additional immune system cells: destruction and degradation of
cancer cells
Immune System Evasion

 Body fails to recognize TAAs on cancer cells → NO immune response stimulation

 CANCER CELLS: present in altered cell membranes, interfering APC binding and presentation to
T lymphocytes
o Have been found to release cytokines that inhibit APCs & other cells of immune system
 Tumors: express molecules that induce T-lymphocyte anergy or tolerance (PD-1)
o Molecules → bind to PD-1 proteins on T-lymphocytes → block the killing of tumor/ induce
cell death in the lymphocytes
o When tumor do not possess TAAs (labels them foreign) NO alertation of immune response
→ tumor grows too large to be managed
 Immunogenicity: can be altered thru mutations → evade immune cell recognition.
o Mutations are source for some TAAs
o Tumor antigens (may) + antibodies by IS (disguise from immune defense mech)
o Tumor antigen-antibody complexes: evade recognition → false message → decrease of
antibody productions
 Overexpression of host suppressor T lymphocytes:
o → induced thru release of cytokines (by malignant cells) → downregulate immune response
→ permitting uncontrolled cell growth
o NORMALLY: T-lymphocytes assist regulating lymphocytes production & diminishing
immune responses when no longer required
 Low levels of antibodies + high levels of suppressor cells →multiple myeloma;
associated w/hypoammaglobulinemia (low serum antibodies)
 Proliferation of T-lymphoctes is impaired by cytokines [produced by cancer cells]
o Without T helper lymphocytes = limited immune response → continued proliferation

Detection and Prevention of Cancer

Primary Secondary Tertiary

- Reducing risks of disease - Involves screening and - Focus on monitoring for &
thru health education early detection = identify preventing recurrence of
and risk reduction precancerous lesions & primary cancer as well
strategies. early stage for those who as screening for 2nd
 - Use of immunization lack S/S malignancies.
- It reduces cost, use of
resources, morbidity
- Risk evaluation
programs: in-depth
assessment, screening,
education, counseling,
follow-up monitoring (high
risk)
Diagnosis of Cancer

 It is based on assessment of physiologic and functional changes and results of diagnostic

evaluation
 PT with suspected cancer undergo extensive screening to:
1. Determine presence and extent of CA
2. Identify possible disease metastasis
3. Eval func of involved & uninvolved body systems and organs
4. Obtain tissue and cells for analysis (eval of stage & grade)

o Diagnostic eval:
 ROS
 PE
 Imaging studies
 Lab tests of blood, urine, other body fluids
 Procedures and pathologic analysis
 NURSE INTERVETION
o Address the patient’s fear and anxiety by explaining the tests to be performed
o Encourages the PT and family to voice their fears
o Support the family throughout the diagnostic eval
o Reinforce and clarifies info conveyed
o Encourage to communicate, share concerns, discuss questions.

Tumor Staging and Grading

 Accomplished prior to treatment to provide baseline data for evaluating outcomes of therapy and to
maintain a systematic and consistent approach to ongoing diagnosis and treatment.
 Cancer prognosis are based on:
o Cancer type
o Stage and grade of cancer
o Indiv health status and response to treatment

Staging

 Describes the size of the tumor, existence of local invasion, lymph node involvement, distant
metastasis.
 TNM system: Tumor, Nodules, Metastasis
Grading

 Pathologic classification of tumor cells.

 Seeks to define the type of tissue from which the tumor originated and the degree to which the
tumor cells retain the functional and histologic characteristics of the tissue of origin (differentiation)
 Cells can be obtained thru:
o Tissue scrapings
o Body fluids
o Secretions
o Washings
o Biopsy surgical excision
 This predicts the behavior and prognosis of various tumors
 GRADE:
o 1: well differentiated tumors, closely resembles tissue of origin in structure and func
o 4: opposite “poorly differentiated”, more aggressive, less responsive to treatment, poorer
prognosis

LARYNGEAL CANCER

 Accounts for approx. half of all head and neck cancers.

 5-year relative survival rate: ranges from 32% - 90% location and stage dependent
 Most common: Older than 65 years old, MEN
Risk factors

 Carcinogens:
o Tobacco
o Heavy alcohol consumption
o Tobacco + alcohol effects
o Asbestos, paint fumes, wood dust
o Chemicals used in metalworking, petroleum, plastics, and textiles.
 Other factors:
o Nutritional deficiencies
o Genetic predisposition
o Age (>65 yo)
 o Gender: men
o Race: African Americans and whites
o Weakened immune system
 Arises most in surface epithelium: squamous cell carcinoma
Clinical Manifestations

 Hoarseness of > 2 weeks [glottic area CA]: impedes action of vocal cords
 Harsh, raspy, lower in pitch
 Persistent cough or sore throat and pain and burning throat (esp. hot liquids or citrus juices)
 Lump; neck
 Later symptoms:
o Dysphagia, dyspnea, unilateral nasal obstruction or discharge
o Persistent hoarseness, persistent ulceration, and foul breath.
o Cervical lymphadenopathy
o Unintentional weight loss
o General debilitated state
o Pain radiating to the ears (metastasis)

Assessment and Diagnostic Findings

 Complete history, physical exam of head and neck

 Identification of risk factors:
o Family history
o Underlying med condition
 Assess mobility of vocal cords: w/limited movement → growth may affect muscle, tissue, even
airway.
 Palpate thyroid gland and lymph nodes of the neck.
Diagnostic procedures

 Fine-needle aspiration biopsy

 Barium swallow
 Endoscopy
 CT or MRI scan
 Positron Emission tomography scan

Indirect laryngoscopy Use of flexible endoscope, is initially performed in

the otolaryngologist’s office to evaluate pharynx,
larynx, and possible tumor.
Fine Needle Aspiration Biopsy Initial screening to obtain samples of enlarged
lymph nodes in the neck
Barium swallow Done when pt initially presents CC of dysphagia
Direct laryngoscopic exam Tumor of larynx is suspected.
Performed under general or local anesthesia
CT scan and MRI Used to assess regional adenopathy and soft
tissues
Used to stage and determine extent of tumor
MRI Post treatment follow-up to detect recurrence
PET scan Detect recurrence of laryngeal tumor after
treatment.

Medical Management
  GOALS of laryngeal cancer: cure, preservation of safe, effective swallowing, preservation of
useful voice, avoidance of permanent tracheostoma
 TREATMENT OPTIONS:
o Surgery
o Rad therapy
o Adjuvant chemoradiation therapy (cisplatin)
 Treatment plan depends whether initial diagnosis or recurrence
 BEFORE treatment begins: Dental exam (dental oncologist) → detect oral disease
EARLY STAGE

 Stage I- II, lesions w/o lymph nodes involvement:

 External beam radiation therapy or conservation therapy (less invasive surgery)
 Transoral endoscopic laser excision or partial laryngectomy.
LATER STAGE

 With resectable tumors:

o Total laryngostomies w/ w/o postoperative radiation therapy
o Radiation therapy w/adjuvant chemotherapy
o Surgical resection (aimed to preserve larynx) organ preservation surgery
 Late stage tumor extending cartilage and into soft tissues → total laryngectomies with postop
rad therapy
 Involved lymph nodes: surgery, chemoradiation, or both
Surgical Management

 Aims to minimize effects of surgery to speech, swallowing, breathing while maximizing likelihood of
cure.

Vocal Cord Striping  Removal of mucosa of the edge of the vocal cord; using an operating
microscope
 Treat dysplasia [abnormal cell growth], hyperkeratosis, leukoplakia.
 Early vocal cord lesions: treated with rad therapy
Cordectomy  excision of the vocal cord, usually via transoral laser
 used for lesions limited to middle third of the vocal cord
 result of voice post op depends on the extent of tissue removed.
Laser surgery  several advantages for early glottic cancers
 less costly, fewer side effects, short treatment and recovery
 CO 2 laser treatment for many laryngeal tumors [exception to large
vascular tumors]
 Method of choice for early laryngeal cancers based on pt outcomes
Partial
Laryngectomy  Removal of a portion of the larynx, keeping other structures remain;
airway intact; w/o dysphagia
 Often used for early stages in glottic area where 1 vocal cord is affected
 Associated w/high cure rate
 Used for recurrence when high-dose rad fails
 VOICE quality may change, or pt may sound hoarse.

Total laryngectomy  Total removal of the larynx providing a cure for advance stage of
cancers
 Removes laryngeal structures, including hyoid bone, epiglottis,
cricoid cartilage, 2-3 rings of trachea
  Preserves: tongue, pharyngeal walls, most of trachea.
 Results in PERMANENT LOSS OF VOICE, change in airway →
permanent tracheostomy
 Requires prosthetic devices: BLOM-SINGER valve

COMPLICATIONS
 Salivary leak
 Wound infection from the dev of pharyngocutaneous fistula
 Stomal stenosis
 Dysphagia secondary to esophageal stricture

Radiation therapy

 GOAL: eradicate the cancer and preserve the function of the larynx.
 Decision is based on factors: stage, overall status, lifestyle (occupation), personal preference.
 Excellent results in early stages glottic tumors involving 1 vocal cords (w/phonation)
o With therapy: Pt retain near-normal voice
o A few may; develop chondritis or stenosis= later results laryngectomy

Used PRE-OP

 reduce tumor size

COMPLICATIONS

 Acute mucositis
 Ulceration of mucous membranes
 Pain
 Xerostomia [dry mouth]
 Loss of taste
 Dysphasia
 Fatigue
 Skin reactions
Later complications: laryngeal necrosis, edema, fibrosis.
Speech therapy

 Means of communication:
o Writing
o Lip speaking and reading
o Communication or word boards or smart phones, or other e-devices
 Stablish a system of communication w/PT, family, healthcare team.
 Long-term post-op communication plan for a laryngeal communication
o TECHNIQUES:
 Esophageal speech:
 ability to compress air into the esophagus and expel it setting off a vibration
of the pharyngeal esophageal segment for esophageal speech.
 Technique can be taught when Pt begins oral feeding [appx, 1 week]
 PT belch → conscious belching action is transformed into simple explosions
of air from the esophagus for speech purposes.
 Artificial larynx (electric larynx)
 Battery powered apparatus projects sounds in the oral cavity
  Tracheoesophageal puncture
 Valve is placed in the tracheal stoma divert air into the esophagus and out
the mouth

ESOPHAGEAL CANCER

 Adenocarcinoma: Common in whites

 Squamous cell carcinoma: African Americans
 Survival rates: of 20% in 5-year span
 Primarily found in distal esophagus and gastroesophageal junction
Risk factors

 Chronic esophageal irritation or GERD

 United states: associated with alcohol consumption and tobacco use
 Apparent association between GERD and adenocarcinoma
 Higher incidence in PT with BE
Squamous Cell Carcinoma

 Chronic ingestion of hot liquids or foods

 Nutritional deficiencies
 Poor oral hygiene
 Exposure to nitrosamines in envi or food (ubiquitous carcinogens)
 Cigarette smoking
 Chronic alcohol exposure
 Esophageal medications (caustic injury)
EARLY STAGES

 Limited to mucosa or submucosa

 5-year survival rate abt 90%
LATE STAGES

 Tumor cells of both may spread beneath the esophageal mucosa or directly into, thru, and
beyond the muscle’s layers into the lymphatics
 Obstruction off the esophagus is noted [w/possible perforation in the mediastinum +
erosion into great vessels]

PATHOPHYSIOLOGY
Chronic ingestion of hot liquids, foods, and caustic injury in GERD → metaplasia in the esophagus →
stratified squamous epithelium at distal esophagus replaced by columnar epithelium → esophagus
becomes dysplastic → BARRET’S ESOPHAGUS → metaplastic cells exhibit dysplasia characterized by
cell abnormalities and disorganized growth → accumulation of genetic mutations during chronic
inflammation and cellular replication of tumor suppressor genes and oncogenes → dysplasia progresses
to intraepithelial neoplasia [involving deeper epithelium]
→ inhibit DNA repair, mutation, genetic alteration, activates proto-oncogenes, disables tumor suppressor
genes →
CLINICAL MANIFESTATIONS

 Before symptoms manifest: Ulcerated lesions of the esophagus

  Dysphagia; initially w/solid foods → liquids
 Sensation of mass in the throat
 Painful swallowing
 Substernal pain or fullness; later, regurgitation of undigested food with halitosis and hiccups
Aware w/increasing difficulty of swallowing → tumor grows → obstruction [even liquids can’t pass thru
stomach] →

 Regurgitation of food & saliva

 Hemorrhage
 Progressive weight loss & strength; inadequate nutrition
Later symptoms

 Substernal pain
 Persistent hiccup
 Respi difficulty
 Halitosis [bad breath]
ASSESSMENT AND FDIAGNOSTIC FINDINGS

 CT scan of chest & abdomen: detecting anatomic evidence of metastatic disease [esp. in lungs,
liver, and kidney]
 PET Scan: detect metastasis
 Endoscopic ultrasound: determine size and invasiveness of tumor (T4N3M2)
 Exploratory laparoscopy: best method in finding + lymph nodes in distal lesions
MEDICAL MGT
Early stage: goals direct to CURE, however usually detected in later stages

 Surgery, Radiation, Chemotherapy, Combination of these modalities [type, extent and PT status
dependent]
 Standard treatment varies:
o Endoscopic resection
o Chemoradiation followed by surgery
o Surgery alone
o Definitive chemoradiation
o Palliative measures
 Standard surgical: Esophagectomy with removal of tumor + wide-tumor free margin [eso, nodes]
o preserves nerves, employ less invasive techniques, target specific area
o MAY BE THRU: neck, thorax, abdomen [depends on loc]
o For esophageal continuity: Colon graft transfer
  Lower thoracic tumors are more amendable: GI tract maintained by ANASTOMOSING lower eso to
stomach
 Surgical resection of eso: high mortality rate die to infection, pulmonary complications, leakage
thru anastomosis
 POST-OP: Unmanipulated NGT placed, NPO until x-ray studies shows no complications
 PALLITIVE TREATMENT: Keep eso open → assist nutrition + control saliva, dilation of eso,
laser therapy, placement of endoprosthesis [stent] via EGD, radiation, chemo.
NURSING MGT

 Directed towards: improvement on

o Nutritional & physical status in prep for surgery, rad therapy, chemo.
 Program for weight gain: based on high-calorie, high-protein diet [liquid or soft
form]
 If not possible: parenteral or enteral nutrition
 Nutrition monitored throughout
 Inform postop equipment
 Closed chest drainage
 NG suction
 Parenteral fluid therapy
 Gastric intubation
 POST-OP CARE
o Place in Low-Fowler’s position after recovering from effects of anesthesia (prevent reflux
& gastric secretion)
o Observe for regurgitation and dyspnea → COMPLICATION: aspiration pneumonia
o Vigorous pulmonary plan:
 Incentive spirometry
 Sitting up in a chair
 Nebulizer treatment [if necessary]
o Temperature monitored → aspiration/seepage of fluid = esophageal leak
o Monitor for post-op chylothorax = [requires] pleural drainage
o Cardiac complication: atrial fibrillation =
 Digitalization
 Beta-blockers, calcium channel blockers, amiodarone
 o Esophageal anastomic leak = adequate drainage, broad spectrum antibiotics, nutrition via
enteral or parenteral feeding.
o NGT removed 5 days post op
o Barium swallow: before allowed to eat [anastomic leak check]
 CONTINUED CARE
o Encourage to swallow small sips of water → advances → discontinuation of parenteral
fluids
o Have PT remain upright after 2hours: allow foods to move to GI tract
o Antacids for gastric distress: metoclopramide, domperidone
o Vagotomy syndrome: “dumping syndrome”
 20 mins to 2 hours after eating [due to interruption of vagal nerve fibers → alteration
of storage func of stomach + pyloric emptying mech]
 S/S: Abdominal cramps, liquid bowel movement, rapid RR, PR, tiredness.
o DROOLING:
 Oral suction
 Wick-type of gauze [both corners of mouth]
 CONCERN: Pneumonia

BREAST CANCER

 Woman’s risk for breast cancer over lifetime is 1 out of 8 or 12%

 Risk increases with Age
 Non-Hispanic African American women: more common

TYPES
DUCTAL CARCINOMA IN SITU (DCIS) [noninvasive]

 Proliferation of malignant cells inside the milk ducts w/o invasion into the surrounding tissue: but CAN
DEVELOP to invasive cancer if not treated
 Progression: 10 years or more
 MAMMOGRAM: Breast cancer stage 0
MEDICAL MGT

 Accurate diagnosis and assessment of DCIS size and grade and margin evaluation
 Grade I—II: low grade, moderate-grade
 Grade III: high grade, grows more quickly
 Accurate grading + presence of necrosis (high nuclear grade)
 Pros and cons, weighed thru case to case basis
 Radiation therapy: choice
 Breast conservation: With very small area of concern
INFILTRATING DUCTAL CARCINOMA

 Most common histologic type of breast cancer [70-80%]

 Tumor arise from the duct system and invade surrounding tissues
o Solid, Irregular mass in the breast
o Micropapillary invasive ductal carcinoma; RARE; high rate of axillary nodes metastasis
and skin involvement
 TUBULAR CARCINOMA
o Carcinomas that’s usually small and consist of tube-shaped structures
o Uncommon axillary metastasis, thus, favorable.

INFILTRATING LOBULAR CARCINOMA

 Tumor arise from lobular epithelium and typically occurs as area of ill-defined thickening in the
breast
 Often multicentric, can be bilateral
MEDULLARY CARCINOMA

 Diagnosed more often in women younger than 50 years.

 Tumors grow in a capsule inside a duct.
 Becomes large: mistaken as FIBROADENOMA [favorable prognosis]
MUCINOUS CARCINOMA

 Presents in women postmenopausal, 75 and older

 A mucin producer; tumor grows slow
INFLAMMATORY CARCINOMA

 Characterized by diffuse edema + erythema of the skin = “peau d’orange”

 Caused by malignant cells blocking the lymph channels in the skin
 Often a large area of indiscrete thickening
 Usually confused with INFECTION
Management

 Chemotherapy [invade disease progression], but radiation and surgery may follow.
PAGET’S DISEASE

 More common in men

 S/S: scaly, erythematous, pruritic lesions of the nipples
 Often represents DCIS in nipples (w/invasive components)

RISK FACTORS
A combination of hormonal, genetic, and environmental factors.

 Mostly sporadic, but sometime familial or genetically acquired.

 RESEARCH: obesity, alcohol consumption, smoking ↑ risks
 Some suggests: late in life weight gain, sedentary life, night shift work
PROTECTIVE FACTORS
1. Breastfeeding for at least 1 year
2. Regular moderate physical activity
3. Healthy body weight

BREAST CANCER PREVENTION IN PT AT HIGH RISK

 Consultation with abreast specialist.

LONG TERM SURVEILLANCE

 Focus on early detection; additional MRI along with yearly mammogram

 Clinical BE early as 25 years old
 Mammogram and MRI + screening tests [ultrasonography]
CHEMOPREVENTION

 the main modality aiming for prevention

 TAMOXIFEN & RALOXIFENE
o Tamoxifen:
 Reduce risk up to 50%
 Increase risk for endometrial cancer & thrombolytic events [esp. in postmenopausal]
thus, recommended in PREMENOPAUSAL.
 Advised for those w/history of LCIS [pre-menopause]
o Raloxifene:
 Recommended for post menopause
 Anastrozole + exemestane are also known.
PROPHYLACTIC MASTECTOMY

 Another primary prevention modality ↓ risks up to 90%-95%

 “risk-reducing” mastectomy
 Involves TOTAL MASECTOMY + immediate BREAST RECONSTRUCTION
 Possible candidates:
o fam history
o diagnosis of LCIS or atypical hyperplasia
 o mutation in BRCA
o previous cancer (1 breast)
 however, does not confer 100% protection.

CLINICAL MANIFESTATIONS
 Can occur anywhere in the breast: common in UPPER OUTER QUADRANT
 Generally: lesions are non-tender, fixed, rather than mobile, and hard with irregular borders
 BENIGN: Diffused breast pain & tenderness w/menstruation
 ADVANCED signs: skin dimpling, nipple retraction, skin ulceration.

ASSESSMENT AND DIAGNOSTIC FINDINGS

 Various types of biopsy
 Tumor staging and analysis of additional prognostic factors (determine prognosis and optimal
treatment)

Staging
 Classifying cancer by the extent of disease
 Based whether cancer is invasive or non, size, # of lymph nodes involved, metastasis +
hormone receptors & gene mutation.
 Identifies prognosis and treatment options
 Tool used: TNM by American Joint Committee on Cancer (AJCC)
Prognosis
 Consideration: size and metastasis (spreads to axillary lymph nodes)
 Small in size: better
 Intense of AMPLIFICATION & OVEREXPRESSION
o ERBB2: more aggressive tumors have amplification and overexpression of this oncogene
 Factors for survival rate: Proliferative rate & rapidity in growth rate (S-fraction) and DNA content
(ploidy)
SURGICAL MANAGEMENT

MODIFIED RADICAL MASTECTOMY

 For INVASIVE breast cancers

 Involves removal of breast tissues (nipple areola complex)
o Removed portion of axillary lymph nodes in axillary lymph node dissection (ALND)
 Pectoralis major & minor is intact unlike [radical mastectomy]
TOTAL MASECTOMY

 Performed w/non-invasive breast CA or in junction w/sentinel lymph node biopsy (SLNB) for pt with
invasive cancer
 Involves removal of the breast and nipple-areola complex, but DOES NOT INCLUDE ALND
 May be performed phrophylactically
BREAST CONSERVATION TREATMENT

 GOAL: excise tumor and obtain clear margins while achieving acceptable cosmetic result
 Non-invasive CA: lymph node removal not necessary
 Invasive CA: indicates lymph node removal (thru separate semicircular incision in axilla)
SENTINEL LYMPH NODE BIOPSY

 Less invasive alternative to ALND and is a standard of care for early-stage

 Sentinel lymph node: first node in the lymphatic basin receiving drainage from primary tumor in the
breast.
 Identified by injecting radioisotope or blue dye → dye travels via lymphatic pathways to the
node → doctor uses probe to locate SLN → excision → sends for pathologic analysis → (+) ALND
→ (-) not necessary

NURSING MANAGEMENT

 SNLB in conjuction w/breast conservation treatment PTs: discharged the same day
 SNLB w/total mastectomy: stays over night or longer [breast reconstruction]
 Inform frozen-section analysis is highly accurate, but may show false negative results.
 Educate that blue dye is safe, may notice blue-green discoloration in the urine or stool (first
24hrs)
 Be prepared for side effects such as:
o Lymphedema
o Decreased arm mobility
o Seroma formation (serous fluid collection) in axilla
 Listen, provide emotional support, and refer the patient to appropriate specialists when indicated.

LUNG CANCER (BRONCHOGENIC CARCINOMA)

 Leading cancer killer among women and men with 1 out of 4 death
 Low long-term survival rate with 5-year survival rate of 21.7%
PATHOPHYSIOLOGY
Single transformed epithelial cell (tracheobronchial airways) → Inhaled carcinogens → carcinogens bind to
the site → damages cell’s DNA → cellular changes, abnormal cell growth, malignant cell formation → DNA
passes to daughter cells (DNA undergoes further changes) → instability
GENTIC CHANGES → EPITHELIUM UNDERGOUS MALIGNANT TRANSFORMATION → INVASIVE
CARCINOMA
CLASSIFICATION AND STAGING
2 MAJOR CATEGORIES:
1. Small Cell Lung Cancer (13%)
 Often presents already at metastatic stage
 Grows proximally near hilum
2. Non-small Cell Lung Cancer (84%)
a. Adenocarcinoma (peri)
 Most prevalent carcinoma; occurs peripherally as (mass and nodules)
 Often metastasize, involves glands of the lungs
b. Large cell (peri)
 “undifferentiated carcinoma”
 Fast-growing tumor, arising peripherally
c. Squamous (cen)
 More centrally located
 Arises in the segmental and subsegmental bronchi
 Occurs commonly at main bronchus (epithelial cell lining) = obstruction of airway
 Change from cuboidal, columnar to squamous
d. Unclassified (OTHERS) (cen)
 Bronchoalveolar cell cancer: terminal bronchi and alveoli
 Slow-growing compared to bronchogenic carcinomas

SCLC 
NSCLC

PERIPHERAL

CENTRAL

 Lung cancers are stage using TNM staging system

o Refers size
o Location
o Lymph node involvement
o Metastasis
RISK FACTORS
Most lung CA are due to cigarette smoking (voluntary/involuntary), genetic predisposition,
dietary deficits, underlying respi conditions (COPD, TB), familial predisposition (close relatives, 2-
3x higher risk)
TOBACCO SMOKE

 23x higher in men, 13x higher in women than those who don’t smoke
 Risk determined thru:
o PACK-YEAR history
o Age of initiation
o Depth of inhalation
o Tar and nicotine lvls smoked

E-NICOTINE DELIVERY SYSTEM

 Eg. E-cigars, e-pens, e-hookahs, e-pipes

 Unclear link to lung cancer (present time)
SECONDHAND SMOKE

 Cause of lung cancer of people who don’t smoke

 Increases risk as exposed in closed environment
ENVIRONMENTAL AND OCCUPATIONAL EXPOSURE

 Eg. Motor vehicle emissions, pollutant from refineries and manufacturing plants
 Research suggest: Incidence greater in URBAN areas
 Radon:
o Colorless, odorless gas in rocks and soil associated with uranium mines
o High levels of radon esp + cig smoking
o Adviced home owners to have radon levels checked and arrange special venting if high
 Industrial carcinogens:
 o Arsenic
o Asbestos
o mustard gas
o chromates
o coke oven fumes
o nickel, oil, and radiation

GENETIC MUTATIONS

 Changes lead to abnormal cell growth, sometime cancer.

 Mutations sometimes caused by environmental factors: cancer causing chemical in tobacco
smoke.
 Most common GENETIC MUTATION:
o EGFR (epidermal growth for factor receptor) 50%
o K-RAS or LAK oncogenes (dev. of NSCLC)

CLINICAL MANIFESTATIONS
Often develops insidiously and asymptomatically until late course. S/S depends on the
location, size, degree of obstruction, and metastasis to regional or distant sites.

 Starts as dry, persistent cough w/out sputum prod.

 PRODUCTIVE: Obstruction in airways
 DYSPNEA: early in disease, due to tumor occlusion, lung parenchyma, pleural effusion,
pneumonia, or complications of treatment
 HEMOPTYSIS
 CHEST or SHOULDER PAIN: chest wall or pleural involvement, pain; metastasis to bone
 RECURRING FEVER: early symptom in response to persistent infection, suspected in unresolved
URTI
 Metastasis to adjacent structures of regional lymph nodes:
o Chest pain & tightness
o Hoarseness (recurrent laryngeal compression)
o Dysphagia (esophagus compression)
o Head and neck edema (SVC compression)
o Symptoms of pleural effusion (chest pain, DOB, fever, cough, hiccups, ↑RR)
 COMMON SITES:
 Lymph nodes
 Bone
 Brain
 Contralateral lung
 Adrenal glands
 Liver
 Non-specific symptoms: anorexia, weakness, weight loss (
ASSESSMENT AND DIAGNOSTIC FINDINGS
CHEST X-RAY

 to search for pulmonary density, a solitary pulmonary nodule (coin lesion), atelectasis, and
infection.
CT SCANS

 Identify small nodules not easily visualized on the chest x-ray

  Serially examine areas for lymphadenopathy
 Low dose of CT for 55-80 years old [w/30 pack-year history, currently or have quit less than 15
years ago.
FIBEROPTIC BRONCHOSCOPY

 Provides a detailed study of the tracheobronchial tree and allows for brushings, washings, and
biopsies of suspicious areas (alternative: transthoracic biopsy)
VARIETY OF SCANS (bone, abdomen, PET, liver ultrasound)

 CT scan or brain, MRI: detect central nervous system metastases

MEDIASTINOSCOPY

 Obtain biopsy samples from lymph nodes in the mediastinum

ENDOBROCHIAL UNTRASOUND BIOPSY


MEDICAL MANAGEMENT
Goal: Cure if possible. Treatment depends on cell type, stage, and patient’s physiologic
status
NSCLC

 Surgery
 Rad therapy
 Chemotherapy
 Immunotherapy: targets patients’ immune cells → primed to more effectively kill cancer cells
 Gene therapy: Uses agents that target specific genetic mutations including EGFR mutations and
ALK and ROS1 rearrangements.
SCLC

 Surgery (only if 1 lung is affected, NO metastasis)

 Radiation therapy
 Laser therapy: open airways blocked by tumor
 Endoscopic stent placement: open airway

SURGICAL MANAGEMENT
THORACOTOMY

 Creation of a surgical opening into the thoracic cavity

 Applicable for NSCLC as SCLC metastasize fast.
 LOBECTOMY (removal of the lobe of the lung): for small, curable tumor in the lung
 PNEUMONECTOMY: removal of entire lung
RADIATION THERAPY

 Useful in controlling neoplasms that cannot be resected but responsive to radiation

 Useful in reducing size of tumor; inoperable → operable, relieve pressure of tumor in vital
structures
 PROPHYLACTIC IRRADIATION: microscopic brain metastases
 STEREOTACTIC ABLATIVE RADIOTHERAPY:
o Delivers higher-than-typical doses of radiation directly to the tumor (for small tumor
detected early)
o Given 1-5 days in early stages of lung cancers

CHEMOTHERAPY

 To alter tumor growth patterns, to treat distant metastases or small cell cancer of the lung, and
as an adjunct to surgery or radiation therapy.
 Choice of agent depends on the growth of the tumor cell, specific cell cycle that the medication
affects.
IMMUNOTHERAPY

 Immunotherapy drugs: Checkpoint Inhibitors = unresectable stage III tumors (w/ metastasis)
 Targets cell death on PD-1 or PDL1 on T cells
 METASTATIC LUNG CA:
o Pembrolizumab (+ chemo = first line treatment for metastatic NSCLC)
o Nivolumab
o Atezolizumab
o Durvalumab: inoperable stage III NSCLC
 Delivered thru IV infusion q 2,3,or 4 weeks for several months -1 year
 With few adverse effects [tolerable compared to chemo]
 Fatigue
 Rashes
 Diarrhea
PALLIATIVE CARE
  Radiation therapy: shrink tumor → pain relief
 Bronchoscopic intervention → narrow bronchus or airway
 Pain management and other comfort measures
 Eval and referral for hospice care

COMPLICATIONS

SURGICAL RESECTION - Respiratory failure (esp. if cardio system is

compromised prior surgery)

RADIATION THERAPY - Diminished cardiopulmonary function

- Pulmonary fibrosis
- Pericarditis
- Myelitis
- Corpulmonale

CHEMOTHERAPY - Pneumonitis
- Pulmonary toxicity

NURSING MANAGEMENT
Managing symptoms - Educate PT and family abt side effects of specific
treatment and strategies to manage
- Help family to cope with therapeutic measures
Relieving Breathing - Deep-breathing exercises, chest physiotherapy,
Problems directed cough, suctioning, and in some instances,
bronchoscopy
- Bronchodilators
- Supplemental oxygen
- NURSING FOCUS: decreasing dyspnea →assume
position that promote lung expansion
- Educate abt energy conservation and airway
clearance techniques
- Pulmonary rehabilitation
Reducing fatigue -
Providing Psychological - Nurses are nurse navigators to help manage and
Support coordinate the many challenging aspects of cancer
care

PANCREATIC CANCER

 4th leading cause of cancer death in men

 5th leading cause of cancer death in women
 Increased incidence as age progress
 Develops more likely in the head of the pancreas
 Clinical manifestations depend on the site and insulin-secreting pancreatic islet cells function
 Responsible for HYPERINSULINISM.
 7% survival rate at 5 years regardless the stage.
RISK FACTORS
  High-fat diet, meat
 History of increased pack years of cig smoking
 High alcohol intake
 Diabetes, chronic pancreatitis, hereditary pancreatitis, obesity.
CLINICAL MANIFESTTAIONS

 Pain, jaundice, weight loss: CLASSIC SYMPTOMS

 OTHER: rapid profound progressive weight loss, vague upper or abdominal pain [unrelated to GI]
 Radiating boring pain midback [non-posture related]: alleviates sitting up, leaning forward
 Ascites: common
 IMPORTANT SIGNS OF INSULIN DEFICIENCY: [diabetes may be an early sign]
o Glycosuria (glucose in urine)
o Hyperglycemia (high blood glucose)
o Abnormal glucose tolerance

ASSESSMENT AND DIAGNOSTIC FINDINGS

SPIRAL HELICAL CT

 Accurate in diagnosing and staging pancreatic cancer: most useful pre-op imaging technique
 MRI/MRCP can be used
ENDOSCOPIC ULTRASOUND

 Identify small tumors and in performing fine-needle biopsy or primary tumor or lymph nodes
 Can be superior to CT at localizing small tumors (producing dramatic symptoms despite size <1cm)
GI XRAY

 Demonstrate deformities in adjacent organs due to impinging pancreatic mass

PERCUTANEOUS BIOPSY

 Used to diagnose non-resectable tumors

 Needle is inserted thru the anterior abdominal wall guided by CT, ultrasound, ERCP or imaging
techniques.
 Aspirated material: examined for malignant cells
 POTENTIAL DRAWBACKS: false-negative for small tumors are missed
PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY

 Performed to identify obstructions of biliary tract

ANGIOGRAPHY, CT SCANS, LAPAROSCOPY

 Determine whether tumor can be removed surgically.

INTRAOP UNLTRASOUND

 Determine metastasis to other organs

MEDICAL MANAGEMENT
------
NURSING MANAGEMENT

 Pain management and attention to nutritional requirements → improved pt comfort

 Skin care and nursing measure directed towards relief of pain: jaundice, anorexia, profound weight
loss
 Specialty mattresses: bony prominence pressure
 OPIODS; Patient controlled analgesia (severe escalating pain)
SYMPTOM CLUSTER

 GI
 Gustatory
 Discomfort related to symptoms

 Knowledge and awareness to symptoms clusters

 Improved nursing assessments and interventions based upon evidence
 End-of-life preferences discussion, honored.

GASTRIC CANCER

 More common diagnosis among older adults, with the mean age at diagnosis of 68 years.
 Higher incidence in MEN
 5th most common cancer diagnosis
 Majority are sporadic or occurring as a result of acquired, not inherited gene mutations; however,
with familial component (blood type A, 1st degree relative w/gastric cancer)
 PROGNOSIS: poor, at 32% in 5year survival rate
RISKS FACTORS

 Diet high in smoked, salted, or pickled foods

 Low in fruits and vegetables
 H. pylori infection
 Gastritis
 Pernicious anemia
 Smoking
 Obesity
 Achlorhydria
 Gastric ulcers
 Previous partial gastrectomy (>20y)
 Genetics
PATHOPHYSIOLOGY
Lesions involving cells on the top layer of the stomach → lesions penetrates the cells in the deeper layers
of mucosa, sub, amd stomach wall → lesions infiltrates to stomach wall → extends to other organs or
structures adjacent to stomach →

 Lymph node involvement and metastasis occurs fast: abundant lymphatic and vascular networks
of the stomach
 COMMON SITES OF METASTASIS:
 o Liver
o Peritoneum
o Lungs
o Brain

CLIINICAL MANIFESTATIONS

 Few symptoms in early stages

o Pain
 Relieved by antacids
 Resembling benign ulcers
 Seldom definitive
 Advance stages symptoms:
o Similar to peptic ulcers
o Dyspepsia
o early satiety
o Weight loss
 Result of cancer itself or blood loss from lesions infiltrating the stomach or
surrounding tissues
o Abdominal pain just above the umbilicus
o Loss or decrease in appetite
o Bloating after meals
o Nausea or vomiting

ASSESSMENT AND DIAGNOSTIC FINDINGS

 Palpable mass: advance stage

 Ascites and hepatomegaly: disease metastasized to liver
 Palpable nodules “Sister Mary Joseph’s nodules”: GI malignancy/cancer.

ESOPHAGOGASTRODUODENOSCOPY  For biopsy and cytologic washings: diagnostic

study of choice
BARIUM X-RAY  examination of the upper GI tract

ENDOSCOPIC ULTRASOUND  assess tumor depth and any lymph node

involvement
CT SCAN  completes the diagnostic studies
 assess for surgical resectability of the tumor
before surgery is scheduled

CT SCANS OF CHEST, ABDOMEN, PELVIS  staging gastric Cancer

CBC  to evaluate for the presence of anemia

TUMOR MARKERS ASSESSMENT  determine the effectiveness of treatment

(carcinoembryonic antigen [CEA],
carbohydrate antigen [CA 19-9], CA 50)
MEDICAL MANAGEMENT

 Is considered MULTIMODAL. Often involving surgery, chemotherapy, targeted therapy, and radiation
therapy
 Resectable; Surgery
 Unresectable; cure is less likely, surgery for cancer growth control, chemotherapy, target therapy,
and rad therapy for palliation of symptoms
SURGICAL MANAGEMENT
TOTAL GASTRECTOMY

 For resectable cancer in the midportion or body of the stomach

 Removal of entire stomach along the duodenum
 Reconstruction of the GI tract performed thru anastomosing the end of the jejunum to the end of
esophagus: ESOHAGOJEJUNOSTOMY
RADICAL PARTIAL (SUBTOTAL) GASTRECTOMY

 For resectable tumor

 Middle and distal portion of the stomach
PROXIMAL PARTIAL (SUBTOTAL) GASTRECTOMY

 For resectable tumor

 Proximal portion of the stomach or cardia
COMPLICATIONS OF GASTRIUC SURGERY

 Hemorrhage, dumping syndrome, bile reflux, gastric outlet obstruction

DUMPING SYNDROME

 Occurs as a result of surgery due to the removal of sugnifacant portion of the stomach that includes
resection r removal or pylorus
 Rapid bolus of hypertonic food from foods to small intestines darws extracellular fluid into the
lumen of the intestines to dilute the high concentration → intestinal dilation, increased intestinal
transit, hyperglycemia, rapid onset of GU and vasomotor symptoms.
 Occurs 10-3 mins after meal
o Early satiety
o Cramping abdominal pain
o Nausea
o Vomiting
o Diarrhea
 Vasomotor symptoms: headache, flushing and feelings of warmth, diaphoresis, dizziness,
palpations, drowsiness, faintness, or syncope.
BILE REFLUX

 Occurs with any gastric surgery involving manipulation or removal of pylorus (barrier to prevent
duodenal contents back into the stomach)

Prolonged exposure of bile acid from duodenum → irritation and damage to gastric mucosa v
gastritis, esophagitis, peptic ulcer formation
  S/S:
o burning epigastric pain, increasing after meals
o vomiting
o administration of PPI and ursodiol
 Ursodiol: changes composition of bile, ↓ promote gastric healing
GASTRIC OBSTRUCTION

 May be caused by stenosis or structure formation at the surgical anastomosis site.

TREATMENTS
CHEMOTHERAPY &TARGETED THERAPY

 Non-resectable tumor: further control of tumor and palliation

 Addition to surgery as adjuvant treatment of gastric cancer.
 CHEMO AGENTS:
o Fluorouracil
o Carboplatin
o Capecitabine
o Cisplatin
o Docetaxel,
o Epirubicin
o Irinotecan
o Oxaliplatin
o Paclitaxel
 For improved tumor response rate
o Fluorouracil + other agents (cisplatin or oxaliplatin)
 TARGET THERAPY
o Trastuzumab + Fluorouracil or Capecitabine

RADIATION THERAPY

 Primarily used for ADVANCED stage to slow rate of tumor growth or for palliation of symptoms
related to: obstruction, bleeding, pain.
 Used alone or in combo with chemo before surgery (decrease size)
 COMMON APPROACH: all direct to the site of tumor
o Traditional External-Beam Rad therapy
o 3D CRT (Conformal Rad Therapy)
o Intraop rad Therapy
o IMRT Intensity-Modulated Rad Therapy

GASTRIC CANCER

 Occurs in adults older than 65 years old

 6th most common cancer: high incidence in MEN
RISK FACTORS

 Cancer arising from prostate, colon, rectum and lower gynecologic tract may METASTASIZE to
bladder
  Tobacco use: esp. cigarette

CLINICAL MANIFESTATIONS

 Usually arise at the base of the bladder and involve the ureteral orifices and bladder neck
 Common Complication: Urinary Tract Infection → frequency + urgency
 Indication of BLADDER CA: Alteration in voiding or change in urine
 Sign of metastasis: Pelvic or back pain
ASSESSMENT AND DIAGNOSTIC FINDINGS

 CYSTOGRAPHY
 EXCRETORY UROGRAPHY
 CT AND MRI SACNA
 UNLTRASONOGRAPHY
 BIMANUAL EXAMINATION
 BIOPSIES (definitive diagnostic tool)
 CYTOLOGIC EXAM: [Fresh urine & saline bladder washings] provides information abt the
prognosis and stage

MEDICAL MANAGEMENT

 Depends on the tumor grade and stage of tumor growth

 Consideration for treatment modalities: Age, physical, mental, emotional status
SURGICAL MANAGEMENT

TRANSURETHRAL RESECTION OR - For simple papilloma

FULGURATION - Eradicate the tumors through surgical
incision or electrical current [instruments
inserted through the urethra]
- Followed by intravesical administration of
Bacille Calmette–Guérin (BCG)
-