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
Bone, Connective Tissue, Cartilage:
all elastic, fibrous, and collagenous tissue ex) sarcomas
26
Nerve:
brain, spinal cord, and nerves – named for the type of nerve cell Astrocytomas (astrocytes – cells in brain and spinal cord)
27
Lymphoid:
lymphoid tissue – lymph nodes, spleen ex) lymphomas
28
Hematopoietic:
bone marrow ex) Leukemias, multiple myeloma
29
Degree of Differentiation:
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
30
Grading of Neoplasms
Well differentiated = I Moderately differentiated = II Poorly differentiated = III Nearly anaplastic = IV
31
Anaplasia vs benign
Anaplasia: lacks differentiation Benign: Well differentiated
32
anaplasia =
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
33
Cancer: Differentiation
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
34
Hyperplasia:
an increase in the number of cells in tissue, resulting in increased tissue mass = often initial stage in the development of cancer
35
Metaplasia:
initial change of normal cell to a different cell type = It is a reversible and benign but abnormal
36
Dysplasia:
progression of cellular disorder with tissue = not always malignant = dysplasia can be reversed
37
Low grade dysplasia ->
High grade dysplasia -> carcinoma
38
Stage 0 - 4: describes the spread, size of the tumor, and differentiation of cancer cells
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
39
There is disagreement over whether CIS should be classified as cancer
The term "pre-cancer" has also been used These abnormal cells grow in their normal place, thus "in situ"
40
Physiologic hyperplasia:
change in breast size with lactation, formation of a bone callus during bone healing
41
Neoplastic hyperplasia:
increase in cell mass due to tumor formation, uncontrolled proliferation in which the dividing cell invades normal tissue
42
Metaplasia: early phase of dysplasia –
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
43
Dysplasia:
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
44
Hyperplasia & Metaplasia ->
Dysplasia -> Carcinoma in Situ -> Stage 1-3 -> Metastatic once it gets to CIS it becomes irreversible
45
primary differentiation =
tumor that develops from a local structure  named for the original tissue type
46
secondary differentiation =
tumor that develops from cells that have metastasized
47
Rate of Growth:
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
48
Malignant VS Benign
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
49
Lung cancer highest mortality in:
males and females
50
Males most frequent diagnosis
Carcinomas: prostate, lung, colon
51
Females most frequent diagnosis
Carcinomas: breast, lung, colon
52
Endogenous Origin:
Genetic Factors
53
Exogenous Origin:
Environmental Factors
54
Cumulative Effect:
Suspected that most cancers develop from multiple factors in combination with an aging immune system
55
Hereditary Predisposition (Endogenous): Secondary Prevention: Screening & Early Detection
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
Carcinogens (Exogenous): Primary Prevention: Behavior Change
Tobacco, viruses, chemical agents, physical agents, drugs, alcohol, hormones
57
Non-Modifiable Risk Factors
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
Modifiable Risk Factors
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
ACS best clinical practice includes diet and exercise before, during, and after cancer dx however research is needed to support
> 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
Risk Factors: Ethnicity
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
Risk Factors: Stress
Evidence growing for link between biobehavioral and psychological factors such as stress, depression, and social isolation Depression: Immune system dysregulation
62
Hereditary Cancer:
mutation passed from one generation to the next Mutations associated with development of malignancies Mutation is not equal to development of a neoplasm
63
Autosomal dominant neoplasia syndromes
Mutated gene inherited from one parent
64
Defective DNA repair syndromes
repair defects can cause an accelerated aging disease &/or an increased risk of cancer
65
Familial Neoplasm:
associated with specific inherited mutations that are seen in many generations in the same family – likely caused by genetic and environmental factors
66
Familial Neoplasm Characteristics:
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
carcinogens and associated neoplasms
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
Viruses associated with neoplasms
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
Effects of Tumors: Location
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
Examples of tumor in different locations & Clinical Manifestations
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
Cachexia =
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
Paraneoplastic syndromes
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
Paraneoplastic syndromes examples =
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
Carcinogenesis =
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
Carcinogenesis Characteristics
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
Carcinogenesis Phases
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
Proto-oncogene
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
Oncogene
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
Tumor suppressor genes
Antioncogene Help control cell growth = loss of TSG required to promote neoplasms
80
Apoptosis gene
Inhibitor of apoptosis = mutation leads to promotion of neoplasms
81
DNA repair gene
Responsible for defects in DNA replication and repair = mutation leads to decreased ability to repair DNA damage
82
Tumor Antigens
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
Diagnosis of Neoplasms
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
Invasive Cancer =
Tumor growth through the epithelial basement membrane = stage 1, earliest stage
85
Metastasize =
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
Different cancers have metastatic patterns
Common metastatic areas Lymph nodes, liver, lung, bone, and brain
87
Factors that slow metastatic changes
Radiation, chemotherapy, anticoagulants, steroids
88
Incidence of Metastasis
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
Metastases can metastasize
Size, location, large numbers makes surgical removal of metastatic tumors impossible
90
Metastatic Mechanism
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
Metastases of remaining 1% is dependent upon success of the remaining cells finding a new host location and the right conditions
Metastases more likely to occur via veins vs arteries = cancer cells can not penetrate artery walls
92
Early detection is key =
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
Metastatic Cascade:
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
Tumor angiogenesis:
primary tumor invasion and support of local blood vessels Tumor growth is dependent upon ability to gain access to an adequate blood supply
95
Metastatic spread typically 3-5 years post initial diagnosis
Can occur up to 20 years later Micrometasteses post cancer treatment
96
Pulmonary System - Lungs
Common metastases secondary to hematogenous spread Symptoms: Dry persistent cough, pleural pain, dyspnea (SOB)
97
Hepatic System – Liver
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
Skeletal System – Bone
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
Central Nervous System – Brain
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
Lymphatic System =
Direct effect from cancer = primary or secondary Symptoms: regional node bed enlargement
101
Some primary site cancers exhibit symptoms that are cause for concern = help lead to earlier detection
Endometrial: abnormal bleeding Laryngeal: hoarseness
102
Cancer Pain
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
Nerve pain due to pressure and eventual displacement of nerves
Continuous, sharp, stabbing followed by pattern of nerve distribution
104
Ischemic pain due to interference of blood supply
Throbbing
105
Bone pain due to continuous breakdown and reabsorption
Deep bone ache
106
Non-pharmacologic Pain Control
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
Cancer-Related Fatigue (CRF)
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
Up to 30% of cancer survivors report fatigue years after treatment
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
Primary prevention:
Health promotion and specific prevention, healthy life-style choices, elimination of negative modifiable factors
110
Secondary prevention:
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
Tertiary prevention:
Managing symptoms, limiting complications, and preventing disability associated with cancer
112
Epigenetics =
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
Nutrigenomics:
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
Antineoplastic Treatment
surgery radiation
115
Surgery:
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
Radiation: RT or XRT
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
Chemotherapy:
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
Risk: Benefit of Chemo
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
Chemotherapy kills cancer cells by disrupting cell life cycle
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
Immunotherapy:
biological response modifier Changes the relationship between the tumor and the host by strengthening the host’s immune response
121
Hematopoietic Cell Transplantation:
Bone marrow transplantation following high doses of chemotherapy
122
Hormonal Therapy:
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
Prognosis
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
Exercise as a Cancer Prevention Strategy
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
Exercise for Cancer Survivors
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
American College of Sports Medicine recommends survivors exercise the same amount as the general population
150 minutes of moderate exercise per week Gradual progression of time, frequency, intensity Progress resistive exercise
127
Exercise Precautions for Cancer Survivors
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
Staging - Invasive Cancer
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
TNM: Tumor, Node, Metastases primarily solid tumors
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
Grading
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
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
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.