Neoplasia Flashcards

1
Q

about __ of people die from cancer

A

16%

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2
Q

about __ of all deaths from cancer occur in low- and middle-income countries

A

70%

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3
Q

top 5 cancers killing men:

A

lung
liver
stomach
colorectal
prostate

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4
Q

top 5 cancers killing women:

A

breast
lung
colorectal
cervical
stomach

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5
Q

not using tobacco can help prevent cancer:

A

between 30-50% of cancers are preventable

tobacco use is the single largest preventable cause of cancer in the world

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6
Q

Cancer =

A

uncontrolled growth and division of abnormal cells

Refers to a large group of diseases characterized by uncontrolled cell proliferation and spread of abnormal cells

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7
Q

Benign:

A

localized tumor = does not invade surrounding tissue

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8
Q

Malignant:

A

cancerous tumor that invades surrounding tissue = metastasize to distant organs

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9
Q

Characteristics of benign and malignant:

A

normal ‘parenchyma’ cell mutates

expands beyond typical boundaries via uncontrolled growth

ability to produce a blood supply = angiogenesis

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10
Q

Characteristics of malignant ONLY:

A

ability to invade the basement membrane and surrounding tissue

enter the blood stream

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11
Q

ACS =

A

5-10% Genetic

90-95% Related to modifiable risk factors

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12
Q

Tumor:

A

abnormal new growth of tissue that serves no function and may harm the host competing for nutrients and blood supply

Benign or malignant

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13
Q

Cancer: Incidence

A

Estimated 1 in 2 and 1 in 3, women and men respectively, in the US will be diagnosed with some form of invasive cancer

3 of 5 will be cured and/or survive 5 years after cancer diagnosis

2nd leading cause of death in US

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14
Q

Survivorship in developing countries < 50% as compared to developed countries

A

Late diagnosis
Lack of availability of care

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15
Q

Cancer Survivorship

A

Good News = Cancer Survivorship Increase from 50% to 64% over last 30 years

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16
Q

Institute of Medicine (IOM) defines needs of survivorship:

A

Prevention and detection of new cancers and recurrent cancer

Surveillance for cancer spread, recurrence, or second cancer

Intervention for consequences of cancer and its treatment

Coordination between specialists and primary care providers to ensure that all of the survivor’s health needs are met

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17
Q

Health needs/consequences of cancer treatment:

A

Physiologic decline, quality of life decline, physical decline, lymphedema, sexual dysfunction, pain, cancer-related fatigue, psychological distress, work related stress

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18
Q

cancer deaths in the US dropped ___ from 1999 to 2019

A

27%

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19
Q

types of neoplasms:

A

adenoma = benign, glandular tissue

carcinoma = malignant, epithelial tissue

sarcoma = malignant, mesenchymal tissue

lymphoma = malignant, lymphocyte tissue

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20
Q

Benign Neoplasm Nomenclature:

A

typically ends with –oma

Adenoma = forms from glandular structures in epithelium

Fibroadenoma = commonly benign fibrous breast tumor

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21
Q

Malignant Neoplasm Nomenclature:

A

typically ends with - carcinoma or -sarcoma

Adenocarcinoma = glandular tissue

rhabdomyosarcoma = skeletal muscle, more common in children

Osteosarcoma = bone

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22
Q

Neoplasm Classification

A

Tissue of Origin
Degree of Differentiation
Benign vs Malignant

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23
Q

Cell Type: neoplasms are classified by cell tissue of origin
Main Classifications of Body Tissue

A

epithelial
bone, CT, cartilage
nerve
lymphoid
hematopoietic

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24
Q

Epithelial:

A

all external surfaces and internal space, organs, and cavities

ex) carcinomas

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25
Q

Bone, Connective Tissue, Cartilage:

A

all elastic, fibrous, and collagenous tissue

ex) sarcomas

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26
Q

Nerve:

A

brain, spinal cord, and nerves – named for the type of nerve cell

Astrocytomas (astrocytes – cells in brain and spinal cord)

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27
Q

Lymphoid:

A

lymphoid tissue – lymph nodes, spleen

ex) lymphomas

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28
Q

Hematopoietic:

A

bone marrow

ex) Leukemias, multiple myeloma

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29
Q

Degree of Differentiation:

A

Histological similarity of neoplasm tissue vs normal tissue

Describes how much or how little tumor tissue looks like the normal tissue it came from

Well-differentiated cancer cells look more like normal/original cells and tend to grow and spread more slowly than poorly differentiated or undifferentiated cancer cells

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30
Q

Grading of Neoplasms

A

Well differentiated = I
Moderately differentiated = II
Poorly differentiated = III
Nearly anaplastic = IV

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31
Q

Anaplasia vs benign

A

Anaplasia: lacks differentiation
Benign: Well differentiated

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32
Q

anaplasia =

A

reversion of differentiation in cells

characteristic of malignant neoplasms/tumors

implies loss of structural and functional differentiation of normal cells

most extreme disturbance in cell growth encountered in the spectrum of cellular proliferations

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33
Q

Cancer: Differentiation

A

process in which generic cell develops into a specific cell

differentiated cells have specific physiologic functions

altered cell differentiation = malignant cells

greater alterations = greater metastasis

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34
Q

Hyperplasia:

A

an increase in the number of cells in tissue, resulting in increased tissue mass = often initial stage in the development of cancer

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35
Q

Metaplasia:

A

initial change of normal cell to a different cell type = It is a reversible and benign but abnormal

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36
Q

Dysplasia:

A

progression of cellular disorder with tissue = not always malignant = dysplasia can be reversed

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37
Q

Low grade dysplasia ->

A

High grade dysplasia -> carcinoma

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38
Q

Stage 0 - 4: describes the spread, size of the tumor, and differentiation of cancer cells

A

Stage 0: Carcinoma in situ: Full-thickness dysplasia
Stage 1: small and localized
Stage 2: spread to nearby lymph nodes
Stage 3: greater spread to surrounding nodes and tissue/organs
Stage 4: Metastatic: tumor spreads to surrounding tissue and distant organs

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39
Q

There is disagreement over whether CIS should be classified as cancer

A

The term “pre-cancer” has also been used

These abnormal cells grow in their normal place, thus “in situ”

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40
Q

Physiologic hyperplasia:

A

change in breast size with lactation, formation of a bone callus during bone healing

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41
Q

Neoplastic hyperplasia:

A

increase in cell mass due to tumor formation, uncontrolled proliferation in which the dividing cell invades normal tissue

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42
Q

Metaplasia: early phase of dysplasia –

A

reversible and benign, change in one differentiated cell to another as a result of abnormal stimulus – cell can differentiate back to original cell when stimulus is removed

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43
Q

Dysplasia:

A

disorganization of cells from the norm – size, shape, or configuration

Late stage dysplasia to CIS = irreversible

Example: cigarette smoke causes Goblet cells (mucus secreting epithelial cells) found in airways to change to stratified squamous epithelium = loss in function (mucus secretion)increases likelihood of developing cancer

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44
Q

Hyperplasia & Metaplasia ->

A

Dysplasia -> Carcinoma in Situ -> Stage 1-3 -> Metastatic

once it gets to CIS it becomes irreversible

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45
Q

primary differentiation =

A

tumor that develops from a local structure  named for the original tissue type

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46
Q

secondary differentiation =

A

tumor that develops from cells that have metastasized

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47
Q

Rate of Growth:

A

Benign Neoplasms = tend to grow slower
Malignant Neoplasms = tent to grow more quickly

Well differentiated cells tend to grow slower = grade I
Anaplastic cells tend to divide rapidly = grade IV

In general, the less differentiated a tumor becomes, the faster the metastasis (spread) and the worse the prognosis

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48
Q

Malignant VS Benign

A

Sarcomas (bone and soft tissue) and carcinomas (skin and tissue lining organs) commonly metastasize

Exception -> Basal cell carcinoma does not typically metastasize - Slow growing cancer cells

30% of all malignant tumors have already metastasized by the time they are clinically detected

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49
Q

Lung cancer highest mortality in:

A

males and females

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50
Q

Males most frequent diagnosis

A

Carcinomas: prostate, lung, colon

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51
Q

Females most frequent diagnosis

A

Carcinomas: breast, lung, colon

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52
Q

Endogenous Origin:

A

Genetic Factors

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53
Q

Exogenous Origin:

A

Environmental Factors

54
Q

Cumulative Effect:

A

Suspected that most cancers develop from multiple factors in combination with an aging immune system

55
Q

Hereditary Predisposition (Endogenous):
Secondary Prevention: Screening & Early Detection

A

Prostate, breast, ovarian, and colon cancers

Early identification of high risk individuals

Breast Cancer = mammogram, BRCA 1 and BRCA 2 genes

Prostate = Digital Rectal Exam (DRE) or Prostate Specific Antigen Test (PSA)

Colon = Colonoscopy

Ovarian = Pelvic exam, blood tests, US

56
Q

Carcinogens (Exogenous):
Primary Prevention: Behavior Change

A

Tobacco, viruses, chemical agents, physical agents, drugs, alcohol, hormones

57
Q

Non-Modifiable Risk Factors

A

Genetics: 5-10% linked to a single gene

Age: Over 40
Median age for cancer diagnosis for all races and genders = 66 years

It is believed that longer exposure to carcinogens

Current research: Accumulated non-lethal DNA damage, increase proinflammatory factors, decline in DNA repair, telomere mutations, dysregulation of hormone modulators

58
Q

Modifiable Risk Factors

A

Tobacco: 30% of cancer deaths, lung cancer leading cause in males and females

Alcohol: Linked to increased rates of mouth, pharynx, larynx, esophagus, liver, breast, colon

Obesity <-> Inactivity: Physical inactivity and obesity lead to metabolic consequences with increased hormone levels = evidence of increased rates of cancer

Unsafe Sex: Early and multiple partners linked to cervical cancer

Air Pollution

59
Q

ACS best clinical practice includes diet and exercise before, during, and after cancer dx however research is needed to support

A

> Diet/Nutrition: estimated 30% of cancer deaths in developed countries may result from dietary cause

Poor diet is thought to ‘slow’ the immune system and long-term exposure may affect cell differentiation

Epigenetics

Healthy diet is thought to detoxify carcinogens and inhibit processes associated with cell dyplasia

60
Q

Risk Factors: Ethnicity

A

African Americans: 10% higher incidence and mortality as compared white americans = Attributed to preventable risk factors such as early screening, delayed diagnosis, smoking, and diet

Hispanics/Latinos = Worldwide Hispanics have a lower incidence and death rate than non-Hispanic whites for all cancers

Asian American: leading cause of death with proportionately more cancer of infectious origin = Human papillomavirus induced cervical cancer

61
Q

Risk Factors: Stress

A

Evidence growing for link between biobehavioral and psychological factors such as stress, depression, and social isolation

Depression: Immune system dysregulation

62
Q

Hereditary Cancer:

A

mutation passed from one generation to the next

Mutations associated with development of malignancies

Mutation is not equal to development of a neoplasm

63
Q

Autosomal dominant neoplasia syndromes

A

Mutated gene inherited from one parent

64
Q

Defective DNA repair syndromes

A

repair defects can cause an accelerated aging disease &/or an increased risk of cancer

65
Q

Familial Neoplasm:

A

associated with specific inherited mutations that are seen in many generations in the same family – likely caused by genetic and environmental factors

66
Q

Familial Neoplasm Characteristics:

A

Early onset
Two or more close relatives
Multiple or bilateral tumors

Examples: breast, ovarian, and colon
BRCA-1 and BRCA-2 associated with breast cancer = 2-4% of families with breast cancer have a mutation in one or both of these genes

67
Q

carcinogens and associated neoplasms

A

aflatoxin = hepatocellular carcinoma

thorotrast = angiosarcoma of liver

vinyl chloride = angiosarcoma of liver

asbestos = mesothelioma, bronchogenic carcinoma

aniline dyes = transitional cell carcinoma of bladder

nitrosamines = gastric adenocarcinoma

polycyclic hydrocarbons = bronchogenic carcinoma

68
Q

Viruses associated with neoplasms

A

Human papillomavirus (HPV) = Squamous cell carcinoma of the cervix

Epstein-Barr virus (EBV) = Lymphoma, nasopharyngeal carcinoma

Hepatitis B virus (HBV) = Hepatocellular carcinoma

Human T-cell leukemia virus type-1 (HTLV-1) = Adult T-cell leukemia/lymphoma

69
Q

Effects of Tumors: Location

A

Location of a tumor is directly related to the effects from the tumor

A 2.0-cm tumor in the brainstem may kill a patient; a 2.0-cm tumor in the leg may not even be noticed

70
Q

Examples of tumor in different locations & Clinical Manifestations

A

Nerve cell = Neurologic deficits or pain
- Myotome and Dermatome distribution patterns

Colon = constipation & Hematochezia

Bile duct or Liver = jaundice

Bronchus = pneumonia or bronchiectasis

Bone = pathologic fracture

71
Q

Cachexia =

A

Basic description: Loss of body fat and muscle; weakness and anorexia associated with a neoplasm or other chronic conditions

symptoms:
unintentional weight loss
anorexia/loss of appetite
skeletal muscle wasting
lowered quality of life

72
Q

Paraneoplastic syndromes

A

Side effects of a neoplasm not attributable to functions normally associated with the cell type of origin or by the location of the tumor

Disorders that are triggered by an altered immune system or nervous system response to a neoplasm = nonmetastatic systemic effects that accompany malignant disease

may be the first or most prominent manifestation of a cancer

73
Q

Paraneoplastic syndromes examples =

A

Difficulty walking
Difficulty maintaining balance
Loss of muscle coordination
Loss of fine motor skills, such as picking up objects
Loss of muscle tone or weakness
Difficulty swallowing
Slurred speech or stuttering

74
Q

Carcinogenesis =

A

The initiation of the process by which normal cells are transformed into cancer cells

Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells

Simultaneous mutations = aggressive cell proliferation = tumor growth

**Mutations alone are not lethal
**Both initiators and promoters are required to cause a neoplasia

75
Q

Carcinogenesis Characteristics

A

1) Imbalance in growth signals vs inhibitory signals
> Uncontrolled replication
> Avoid apoptosis

2) Defects in DNA repair

3) Initiators = original stimulus of cancer = mutations acquired

4) Promoters = support propagation of a cell with a mutation = region of the DNA that initiates transcription

5) Promote angiogenesis

6) Spread to surrounding tissue and distant tissue

76
Q

Carcinogenesis Phases

A

Initiation: alteration, change, or mutation spontaneously or exposure to a carcinogenic agent = stimulus

Promotion: considered reversible and can be lengthy; actively proliferating preneoplastic cells

Progression: genetic and phenotypic changes and cell proliferation continue

Metastasis: spread of cancer cells from primary site to other parts of the body

77
Q

Proto-oncogene

A

A healthy normal gene found in a cell = when altered by mutation, becomes an oncogene that can contribute to cancer = ‘high risk genes’

Proto-oncogenes may have many different functions in the cell = cell growth, cell division, and cell death

Mutation to proto-oncogene leads to oncogene = potential to lead to cancer

78
Q

Oncogene

A

Cause unregulated cell growth = results in spread of mutations

Mechanism: Normal DNA segment = exposure to cancer causing Agent = Mutation to Oncogene = Replication of mutation

79
Q

Tumor suppressor genes

A

Antioncogene

Help control cell growth = loss of TSG required to promote neoplasms

80
Q

Apoptosis gene

A

Inhibitor of apoptosis = mutation leads to promotion of neoplasms

81
Q

DNA repair gene

A

Responsible for defects in DNA replication and repair = mutation leads to decreased ability to repair DNA damage

82
Q

Tumor Antigens

A

Antigen substance produced by a tumor which provokes an inflammatory response

useful tumor markers in identifying tumor cells with diagnostic tests

used in the development of immunotherapy
- Immunotherapy uses the bodies immune system to target, recognize, and eliminate cancer cells

83
Q

Diagnosis of Neoplasms

A

Early detection and diagnosis are critical to improving prognosis

Physical Exam = subjective, observation, objective

Blood and Urine Analysis = CBC, inflammatory markers

Biopsy = Sample of tissue

Imaging = MRI, CT, PET, X-Ray

Metastatic tumors = challenging to diagnose and determine site of primary tumor
> Poorly differentiated – unorganized, grow fast

84
Q

Invasive Cancer =

A

Tumor growth through the epithelial basement membrane = stage 1, earliest stage

85
Q

Metastasize =

A

Spread from primary site to other locations in the body = must be invasive

Cancer cells travel through the body via the blood or lymphatic systems

Find a new area of the body to invade = in presence of promoters

Infiltrate a new organ/tissue and grow new tumors = secondary

86
Q

Different cancers have metastatic patterns

A

Common metastatic areas
Lymph nodes, liver, lung, bone, and brain

87
Q

Factors that slow metastatic changes

A

Radiation, chemotherapy, anticoagulants, steroids

88
Q

Incidence of Metastasis

A

30% of newly diagnosed cancer have clinically detectable metastases

30-40% of newly diagnosed cancer suspected to have micrometastases

30-40% of newly diagnosed cancer stage 1, 2 or 3

Metastatic colonization typically occurs early in the growth of a primary tumor

Early detection is key!

89
Q

Metastases can metastasize

A

Size, location, large numbers makes surgical removal of metastatic tumors impossible

90
Q

Metastatic Mechanism

A

Primary tumor = faster growing and larger = increased number of cancer cells released into vascular system

Vascular/Lymph system = research shows that 99% of tumorigenic cells are eliminated prior to initiation of metastatic tumor

91
Q

Metastases of remaining 1% is dependent upon success of the remaining cells finding a new host location and the right conditions

A

Metastases more likely to occur via veins vs arteries = cancer cells can not penetrate artery walls

92
Q

Early detection is key =

A

Treatment of a primary tumor is effective, treatment of metastatic tumors is very challenging

Characteristics and treatment of metastatic tumors is unique to each combination

93
Q

Metastatic Cascade:

A

a complicated series of tumor-host interactions resulting in a metastatic colony = success of 1%

It is estimated that 7-10 steps need to occur for successful metastatic colonization

94
Q

Tumor angiogenesis:

A

primary tumor invasion and support of local blood vessels

Tumor growth is dependent upon ability to gain access to an adequate blood supply

95
Q

Metastatic spread typically 3-5 years post initial diagnosis

A

Can occur up to 20 years later

Micrometasteses post cancer treatment

96
Q

Pulmonary System - Lungs

A

Common metastases secondary to hematogenous spread

Symptoms: Dry persistent cough, pleural pain, dyspnea (SOB)

97
Q

Hepatic System – Liver

A

Among most ominous sign of advanced cancer

Filters blood from GI = metastatic to stomach, colorectum, and pancreas

Symptoms: abdominal and/or right upper quadrant pain, general malaise/fatigue, anorexia, early satiety and weight loss, sometimes low-grade fever, jaundice, edema

98
Q

Skeletal System – Bone

A

1 of 3 most favored sites of solid tumor metastasis

Bone microenvironment provides fertile growth opportunities

Primary sites include lung, breast, and prostate

Symptoms: Pain = deep and worsened by activity particularly in weight bearing (WB)

99
Q

Central Nervous System – Brain

A

Primary lung carcinomas account for ~1/2 of all metastatic brain lesions

Breast and malignant melanoma commonly metastasize to the brain

Symptoms: vary greatly dependent upon the location = motoric, sensory, intracranial pressure, psychological

100
Q

Lymphatic System =

A

Direct effect from cancer = primary or secondary

Symptoms: regional node bed enlargement

101
Q

Some primary site cancers exhibit symptoms that are cause for concern = help lead to earlier detection

A

Endometrial: abnormal bleeding
Laryngeal: hoarseness

102
Q

Cancer Pain

A

50%-70% of patients experience in the early phases of cancer

60%-90% of patients experience in late stages of cancer

Depression: may confound a patient’s perception of pain

103
Q

Nerve pain due to pressure and eventual displacement of nerves

A

Continuous, sharp, stabbing followed by pattern of nerve distribution

104
Q

Ischemic pain due to interference of blood supply

A

Throbbing

105
Q

Bone pain due to continuous breakdown and reabsorption

A

Deep bone ache

106
Q

Non-pharmacologic Pain Control

A

Massage: Evidence is sparse, no evidence that suggests the spread of cancer due to massage
> Direct pressure over a tumor is usually discouraged
> Indirect massage used to relieve secondary factors of cancer
> Promote postoperative healing, relieve stress and anxiety, improve immune system

Physical agents: ultrasound and electrical stimulation
> Contraindicated due to presumed increased risk of metastasis = increase blood supply

107
Q

Cancer-Related Fatigue (CRF)

A

One of the most common side effects of cancer and its treatments

Disproportionate level of fatigue as compared to activity or exercise level

Typically comes on suddenly = is not relieved by rest or sleep

May persist indefinitely for cancer survivors

80-90% of cancer survivors report CRF

Distressing, persistent, relentless feeling of exhaustion that is not proportional to recent activity

108
Q

Up to 30% of cancer survivors report fatigue years after treatment

A

Many patients rate fatigue as more distressing than pain or nausea

Physical therapy sessions
> All patients should be screened at initial visit, and monitored at every visit
> Patients and families educated on the management of fatigue

109
Q

Primary prevention:

A

Health promotion and specific prevention, healthy life-style choices, elimination of negative modifiable factors

110
Q

Secondary prevention:

A

Regular screening to detect high-risk people with subsequent behavior changes for modifiable risk factors

Tobacco, diet high in unsaturated fat and low fiber, radiation exposure, obesity

111
Q

Tertiary prevention:

A

Managing symptoms, limiting complications, and preventing disability associated with cancer

112
Q

Epigenetics =

A

study of how behaviors and environment can cause changes that impact gene function

> Newer science that has brought to light the control we have as individuals on whether or not cancer develops in our bodies

> Nutrigenomics can change our cells progression of cancer cells

113
Q

Nutrigenomics:

A

identifying ways to prevent cancer through the impact of nutrition on gene structure and stability = food, nutrition, obesity, and PA influence on the cancer process as DNA is translated

114
Q

Antineoplastic Treatment

A

surgery
radiation

115
Q

Surgery:

A

Typically used in combination with other therapies

Can be curative in localized cancer = Stage 0 or Stage 1

Can be palliative to relieve pressure or pain

70% of patients have potential micrometastases at the time of dx

Adjunct therapy used with surgery potentially eradicates any residual cells

116
Q

Radiation: RT or XRT

A

2 Types: used to destroy dividing cancer cells by destroying hydrogen bonds between DNA strands = dismantle the cells ability to replicate!

Ionizing radiation
Particle radiation

Goal: ablate as many cancer cells as possible while sparing normal tissue

Treatment of localized lesions = Stage 1, 2, or 3

117
Q

Chemotherapy:

A

wide array of chemical agents to destroy cancer cells

Systemic treatment of widespread or metastatic cancer = Stage 1 - 4

Used to eradicate residual cancer cell circulation = disrupt DNA synthesis

118
Q

Risk: Benefit of Chemo

A

Life saving aggressive treatment

Cancer cells are unstable – they replicate rapidly and inaccurately = this process can produce chemical resistant versions that do not respond to chemotherapy

Microcirculation of chemo resistant cells can lead to tumor and metastases that will not respond to treatment

119
Q

Chemotherapy kills cancer cells by disrupting cell life cycle

A

Numerous chemical agents used – each work during a different phase of the DNA cycle – often used in combination to increase effectiveness

Administered: orally, subcutaneously, intramuscularly, intravenously, arterial infusion

120
Q

Immunotherapy:

A

biological response modifier

Changes the relationship between the tumor and the host by strengthening the host’s immune response

121
Q

Hematopoietic Cell Transplantation:

A

Bone marrow transplantation following high doses of chemotherapy

122
Q

Hormonal Therapy:

A

used with certain types of cancer shown to be affected by specific hormones

Example: tamoxifen = an antiestrogen hormonal agent used to block estrogen receptors in breast tumors

123
Q

Prognosis

A

Today = 17 million cancer survivors in the US

~70% of individuals in the US diagnosed with cancer have a 5-year survival rate
> 5 years survival rate in 1970 58%

Prognosis highly dependent upon stage, type, grade, availability of effective treatment

Major cause of death is metastasis that are resistant to treatment

124
Q

Exercise as a Cancer Prevention Strategy

A

Research indicates that PA greater than moderate level = reduce cancer risk

Moderate level PA = 55%-69% MHR

150-300 minutes of moderate intensity aerobic exercise or 75-100 minutes of vigorous intensity aerobic exercise

Resistance training at least 2x per week

Sedentary lifestyle: Risk factor for numerous types of cancer

Dose and mode of PA needed to decrease risk/prevent cancer is inconclusive

Research speculates that exercise boosts the immune system mechanisms

125
Q

Exercise for Cancer Survivors

A

Recommended at time of diagnosis, during treatment, and after completion of treatment

Exercise should be individualized to meet the patients baseline and willingness to comply

ACS recommends 150 minutes moderate and 75 minutes vigorous exercise post cancer diagnoses
> reduce the risk of cancer recurrence
> maximize function and QoL

126
Q

American College of Sports Medicine recommends survivors exercise the same amount as the general population

A

150 minutes of moderate exercise per week

Gradual progression of time, frequency, intensity

Progress resistive exercise

127
Q

Exercise Precautions for Cancer Survivors

A

Anemia – close monitoring - delay exercise if needed = SpO2, subjective report of fatigue and weakness

Suppressed immune system – avoid public places

Severe fatigue – passive is better than no exercise = cancer related fatigue disproportionate to activity

Irradiated Skin – avoid chlorine

Catheters – avoid water or microbial exposure; avoid exercise that can dislodge catheters

Peripheral neuropathies – stationary bike preferred over treadmill, patient education regarding skin check

128
Q

Staging - Invasive Cancer

A

Stage 0: Carcinoma in situ  non-invasive cancer
Stage 1: Localized to primary organ
Stage 2: Increased risk of regional spread because of tumor size or grade
Stage 3: Local cancer has spread regionally but may not be disseminated to distant regions
Stage 4: Cancer has spread and disseminated to distant sites

129
Q

TNM: Tumor, Node, Metastases primarily solid tumors

A

T: Size of primary tumor
N: Regional node involvement
M: Metastatic

0 = undetectable
T0-4, N0-3, M0-1 = progressive increase in size and node involvement

T1 N 1 M 0
T 4 N 3 M 1

130
Q

Grading

A

Differentiation Grading Performed by a pathologist

3 categories: Low, Intermediate, and High grade

Low: Most promising predictive and prognostic outcomes = well differentiated

High: Least promising predictive and prognostic outcomes = poorly differentiated

Results used to guide treatment plan

131
Q

A therapist is currently treating a 47 y/o type 1 diabetic patient in an outpatient physical therapy clinic. During treatment, the therapist begins to observe irritability, slurred speech, and profuse sweating. The therapist suggests that the patient check their blood glucose levels, which reveals a blood glucose reading of 60 mg/dl. What is the most appropriate course of action for the therapist to take FIRST?
a. Call 911 immediately
b. Call the patient’s physician immediately
c. Provide some fruit juice for the patient
d. Ask that the patient administer their prescribed insulin

A

C. Provide some fruit juice for patient

This question asks us to prioritize our response during a patient’s hypoglycemic reaction. While we may need to notify the patient’s physician and call 911 if symptoms worsen, the most immediate course of action should be to provide the patient with some type of hyperglycemic agent. If the patient is unable to take this agent then 911 should be called immediately. It is always a good idea to inform responders that your patient is a diabetic and experiencing low blood sugar so that they can plan accordingly.

Insulin would not be a good option in this scenario. Insulin lowers a patient’s glucose levels and therefore would make this hypoglycemic event much worse.