Module 4 - Neoplasia Flashcards
1
Q
Neoplasia
A
Cancer
2
Q
Cell Cycle
A
Orderly sequence of events (usually) during which duplicated chromosomes align appropriately and results in cell proliferation
3
Q
Body tissues are divided into three types based on ability to undergo regeneration, what are the 3 types?
A
- Continuously dividing/Labile
- Stable
- Permanent Tissue
4
Q
Labile Tissue
A
Continuously dividing tissue that can regenerate easily and do so constantly
ex: skin, cervix, epithelium of the GI tract, fallopian tubes, bone marrow
5
Q
Stable Tissue
A
These cells stop dividing once growth ceases, but can undergo regeneration in response to a stimulus
ex: Solid organs, fibroblasts, endothelial cells
6
Q
Permanent Tissue
A
These cells stop dividing once growth ceases, and have no further regeneration
When damaged, they are replaced with scar tissue, and this tissue lacks the cell’s functional characteristics
ex: Neural cells, cardiac cells, etc
7
Q
Proliferation
A
Process of increasing cell numbers via mitotic division
It is the mechanisms for replacement when old cells die or additional cells are needed
8
Q
What triggers proliferation?
A
Growth Factors (increase cell size and cell division)
Hormones
Cytokines
9
Q
Growth cells stimulate proliferation usually, but they can also…
A
inhibit cell cycling or gene expression for other cells
ex: Erythropoietin, Granulocyte Colunate, Cytokines (All GH Examples)
10
Q
Differentiation
A
Process by which the structure and function of a cell becomes more specialized
The new specialized cells get structural, microscopic, and functional characteristics of cells they replace.
Once the cell picks a line, they differentiate into mature cells of that line and stick to that line
11
Q
Stem Cells
A
Undifferentiated cells that differentiate based on need in continuously dividing tissue
12
Q
Examples of Differentiated Cells
A
Granulocytes
Agranulocytes
Platelets
Erythrocytes
13
Q
Stem Cell division includes what 3 processes?
A
Self Renewal
Asymmetric Replication
Differentiation
14
Q
Self Renewal
A
Process where stem cells undergo numerous mitotic divisions in an undifferentiated state
More stem cells are made
15
Q
Asymmetric Replication
A
Stem cell divides and one daughter cell remains an undifferentiated stem cells, but the other daughter cell will become a progenitor cells that differentiates based on progenitor lines
This is how we maintain stem cells in the body while having cells that go on to differentiate
16
Q
Apoptosis
A
Programmed cell death in multicellular organisms that keeps the number of total cells constant in death
Macrophages will recognize the “not you” cells and remove them as well as cell lyses
17
Q
The rate of proliferation is = to the rate of ____ in health
A
Apoptosis
18
Q
Hypertrophy
A
enlargement or overgrowth of an organ due to an increase in the size of the cells
19
Q
Neoplasia
A
Unregulated/Dysregulation of cell differentiation and growth
Autonomous, Unregulated, and Lacks Physiologic Control
process of formation or presence of a new abnormal growth of tissue that is not under physiologic control
“Cancer”
20
Q
Neoplasm
A
New Growth; Swelling that is caused by different etiologic factors (ex: Inflammation, trauma, etc)
A “Tumor” - Benign or Malignant
21
Q
Neoplasm
A
New Growth; Swelling that is caused by different etiologic factors
A “Tumor” - Benign or Malignant
22
Q
What about Neoplasia leads to the formations of Neoplasms?
A
Proliferation forms new growths, and cells do not die off (apoptosis) to keep the number of total cells constant –> therefore a neoplasm occurs
23
Q
Benign Neoplasms are ___ Differentiated
A
Well Differentiated
24
Q
What sort of factors determine if a tumor will be Benign or Malignant?
A
Characteristics of the cell (ex: Differentiation)
Local Invasion
Rate of Growth
Ability to Metastasize
25
What sort of factors determine if a tumor will be Benign or Malignant?
Characteristics of the cell (ex: Differentiation)
Local Invasion
Rate of Growth
Ability to Metastasize
26
Benign Tumors
Contain cells that look like normal tissue cells and may perform the normal function of that type of tissue (ex: secrete hormones which can lead to over secretion)
Grow slowly
Have a fibrous capsule
Do NOT infiltrate, invade, or metastasize
27
What about a benign tumor makes it easier to surgically remove?
It has a fibrous capsule
28
How can a benign tumor potentially damage nearby organs?
It could grow large and compress the organ thus damaging it
29
Malignant Tumors
Contain cells that do not look like normal adult cells and do not perform normal functions of that type of tissue
May secrete signals, enzymes, toxins, etc
Grow rapidly (rate depends on level of differentiation)
Can infiltrate, invade, and metastasize to distant sites via blood and lymph
No fibrous capsule
Can compress and/or destroy the surrounding tissues and organs - leads to injury and ischemia
30
Most common new male cancer? Most deadly male cancer? Most common new female cancer? Most deadly female cancer?
Most Common Male - Prostate
Most Deadly Male - Lung and Bronchus
Most Common Female - Breast
Most Deadly Female - Lung and Bronchus
31
Tumor Types
Solid
Hematologic Cancer
Cancer in Situ
32
Solid Tumors
Initially confined to specific tissue or organ but then detach and invade surrounding tissue, blood and lymph
Allows Metastasis to occur
33
Hematologic Cancer
Blood and lymph contain the cancer cells initially
These cancers are considered disseminated diseases from the beginning
34
Cancer in Situ
Cancer cells that are localized in the organ of origin
Considered preinvasive lesions, they can be surgically removed or treated MORE EASILY and have a smaller chance of recurrence
EX: Cervical cancer is so localized it is almost 100% curable
35
Anaplastic Cells
poorly differentiated or non differentiated tumor cells
they have numerous morphologic changes and vary in size and shape
these cells have a high proliferation rate, but do NOT resemble the tissue of origin
These are Malignant Tumor cells
36
Pleomorphism
cells that vary in size and shape
37
What is the basis for grading tumors?
It is based on how differentiated the cells are and the number of proliferating cells on a grade of I to IV
38
A Grade I tumor means...
the cells are well differentiated
39
A Grade IV tumor means...
the cells are Anaplasia/Anaplastic - poorly differentiated or not differentiated
40
Hypoplasia (Cells)
Fewer cells than what is deemed a normal amount
Usually benign
41
Hyperplasia (Cells)
Increased cell number.
Occurs due to a stimulus and is similar to the surrounding tissue and cells are the same relative to each other
ex: Callus formation on skin when exposed to pressure
42
Neoplasia (Cells)
Cells that are similar to hyperplasia, but there is NO stimulus that triggers this (it is loss of normal proliferation regulation) and the cells are all different from one another
Increased cell number
43
Dysplasia (Cells)
Cells with a change in normal shape, size or organization, usually d/t chronic irritation
ex: Cigarette smoke and inflammation
Changes are reversible if stimulus is removed, otherwise the cells eventually turn metaplastic
44
Metaplasia (Cells)
A change in the actual TYPE of cells
ex: Ciliated Columnar Epithelium of resp. surface turning into Stratified Squamous Epithelium after prolonged smoking
Changes are reversible if stimulus is removed, if not they will turn anaplastic
45
Anaplasia (Cells)
A reversal in differentiation (dedifferentiation) OR loss of structural and functional differentiation of normal cells
These cell changes are NOT reverisble
These cells are cancerous tumor cells
46
What is the hallmark of cancer
Genetic Instability
47
Genetic Instability
defined as the presence of a high frequency of mutations in cells that change the sequences of nucleic acid and arrangement of chromosomes
growth reg. genes and genes involved in the cell cycle are altered or arrested and lead to gross chromosomal abnormalities
48
What is the result of Genetic Instability
Aneuploidy
49
Aneuploidy
incorrect number of chromosomes
50
How do Cancer Cell growth properties differ from normal cells?
1. They secrete growth factors and/or have receptors
2. Lack cell density dependent or contact inhibition
3. Anchorage independence (decreased anoikis; Shed into body fluids d/t loss of cohesiveness and adhesiveness)
4. Faulty cell to cell communication
5. They are immortal
51
What is Cell Density Dependence/Contact inhibition
in normal cells, the cells will cease to divide after cells become a certain density
ex: after a wound closes they will stop growing, but cancerous cells lack this and will continue
52
What does it mean if a cancer cell has anchorage independence?
They will grow when not anchored to the ECM, which is abnormal as normal cells need to be anchored or else they undergo anoikis
53
Anoikis
a version of apoptosis that occurs for normal cells when they detach from the ECM
54
How can faulty cell to cell communication lead to cancer?
If the cells signals for recognizing growth "short circuit" and do not signal inhibition they can lead to overgrowth and tumors
55
What does it mean that cancer cells are "Immortal"?
They can divide an infinite number of times unlike normal cells
They only end up having the functions of survival and proliferation though
56
What happens if a cell detaches in a normal cell versus a cancer cell?
Normal cell --> Cell shedding --> Cell is free from ECM --> Anoikis
Cancer cell --> cell shedding --> cell is free from ECM --> Metastasis
57
Mesenchymal Stem Cells (EMT)
Multipotent stem cells that can differentiate into different kinds of myocytes (muscles), adipocytes (fat), Osteoblasts (Bone cells), Chondrocytes (Cartilage cells) - and a lack of anoikis will lead to metastasis commonly with these cells if they shed
58
Normally, the number of cells produced is equal to ...
the number of cells that die, such that the total number of cells in the body remains constant
59
In cancer, the cell cycle is ___ ___ than healthy cells
not shorter (d/t immortality, allowing for increased growth fraction)
60
What are some reasons cancer cells are so prolific?
Cells do not die on schedule
Cells respond to growth factors that keep the cancer cells actively dividing in the cell cycle
61
Growth Fraction
Ratio of dividing cells to resting cells
62
What is the growth fraction in healthy cells versus cancerous cells?
Healthy - equilibrium is established between cell birth and death
Cancer - growth factor increases since the cell cycle is far longer
63
Doubling Time
the length of time it takes a mass of cells in a tumor to double (for the tumor to double in size)
64
When does doubling time begin to decrease in cancerous cells?
Once blood supply and nutrients fail to support growth
So they divide slower
65
What does the tumor growth rate look like on a graph?
Tumor growth rate will be very fast initially but after a while they do not have the nutrients and blood supply needed so the doublings stabilize out and doubling slows down
It ends up looking like a massive and quick jump in number of cells from only a small increase in doublings, and eventually slows down considerably once nutrients are not enough
66
How many doublings are required, and how many cells that is, to detect a tumor on a scan?
30 doublings - 1 billion cells
This tumor would be about 1 centimeter in size (some scans can see smaller tumors - like MRI though)
67
At what amount of doublings and cell among can a tumor kill the host?
35 doublings - over 1 Trillion cancer cells
68
What is different about malignant cancer cells that make them able to shed and lead to metastatic spread?
Benign growth occurs via expansion in a capsule, but malignant cells invade other tissue d/t not having a capsule and seed in cavities thus leading to spread/metastasis
69
Where is the most common cavity for malignant spread/seeding?
Perineal Cavity
70
What allows malignant cells to invade and penetrate other surrounding tissue?
A lack of a capsule and having "legs" (similar to crab like projections) that allow penetration (and a lack of demarcated boundaries because of these)
71
Malignant cells ___ into body cavities
seed
72
Cells in a primary tumor develop the ability to do what?
escape, travel, and survive in the blood. They then are able to exit the blood and develop a secondary tumor
73
What are some pathways for malignant tumors?
Lymph Channels (Lymphatic Spread)
Blood Vessels (Hematogenous Spread)
74
Sentinel Node
Initial lymph node to which the tumor drains
75
What can metastatic/secondary tumors do relative to the primary tumor?
because of different patterns of metastasis (early or late) they can potentially be larger than the primary tumor
76
What are the two main subgroups of malignant tumors?
Carcinoma
Sarcoma
77
Carcinoma
Derived from epithelium
Always Malignant
Common
Mostly lymphatic spread
May have a pre-malignant (or in situ phase)
Common in older patients
78
Sarcoma
Derived from connective tissue
Always malignant
Less common than a carcinoma
Spread by blood
Not believed to have a pre malignant phase unlike carcinoma
More often seen in younger patients
79
Describe how lymphatic spread occurs for a metastatic carcinoma?
Cancer cells spread --> Lodge in the first node to receive drainage from tumor (sentinel node) --> Cells either die from lack of nutrients or non-good growth environment, remain dormant, or become a discernible mass (assuming the immune system did not already attack it) --> cells then can move to other nodes and go through ducts to enter blood cells or enter vessels providing tumors with blood.
80
Why is Hematogenous spread more difficult than lymphatic spread?
Hematologic spread is selective and has many steps
In circulation the tumor cells are vulnerable to destruction by host immune cells d/t recognition of the different MHC1
Thicker walled arterials and arteries are resistant to invasion so they must invade via capillaries or venules
81
Hematogenous spread involves cancer invading what?
Capillaries and Venules
82
In order to metastasize via hematogenous spread, what must occur?
Cancer cell must break loose and invade the ECM (enzymes give it access to a blood vessel) --> They must get through the blood vessel alive --> find a favorable site in the vessel to invade tissue --> Begin growth
83
How might a cancer cell gain protection in the blood vessels?
they sometimes aggregate and adhere to circulating blood components (especially platelets) to form tumor emboli which can then allow them to exit circulation by binding to the endothelium to form secondary tumors
84
In order for a metastatic/secondary tumor to grow after traveling the blood, it must have what?
Angiogenesis (new vessels formed for it)
Growth factors that promote proliferations
Have its own blood supply
85
Only select cancer cell clones have the right what, to perform all steps of metastasis to form a secondary tumor?
Right combination of gene products
86
Common Metastatic Sites for Secondary Tumors
1. Portal vein from venous blood of GI, pancreas and spleen going to the liver
2. Vena cava blood heading to the lungs
3. Preferential spread of cancer based on type?
!SO, Live and lungs are common sites from hematogenous spread to have metastasis
87
Prostate cancer tends to have metastasis to ___
bone
88
Bronchogenic cancer tends to have metastasis to ___ and ___
adrenals and brain
89
Neuroblastomas tend to have metastasis to ___ and ___
liver and bones
90
In health, proto-oncogenes code for what?
Normal cell division proteins
ex: Growth factors, growth factor receptors, transcription factors, cell cycle proteins, apoptosis inhibitors
91
When proto-oncogenes mutate into oncogenes, what can occur?
Overactivity and gene activation
They mutate from insertions, deletions and translocations into increased or activated oncogenes
This can lead to cancer
92
ras Oncogene
transmits signals to the cell nucleus to increase proliferation (cancer levels)
93
Philadelphia Chromosome oncogene
oncogene commonly seen after translocation in chronic myeloid leukemia
it is from translocation of a gene on chromosome 9 to 22
94
HER-1/neu oncogene
Multiple copies of this gene occur leading to overexpression and increased cell proliferation
This oncogene is seen in 30% of breast cancer cases when the cancer is considered AGGRESSIVE and with a POOR PROGNOSIS
95
Antioncogenes
in health, these tumor suppressor genes inhibit cell division
When inactivated, there will be unregulated growth leading to cancer
96
How can an antioncogene become inactivated?
Through either inherited or acquired mutations
But most mutations are acquired
97
p53 Tumor Suppressor Gene
Autosomal Recessive Antioncogene (named after its molecular weight) that usually senses DNA damage and initiates repair or apoptosis
When mutated in cancers like colon, lung, and breast occur
You are more likely to respond to chemotherapy if your P53 gene is intact and activated
98
RB Tumor Suppressor Gene
Autosomal Dominant or Sporadic Antioncogene
Hereditary form occurs 40% of the time with the rest acquired
If both RB genes are inactivated, the development of a retinoblastoma (malignant eye tumor) occurs
If only one gene is inactivated, that person is a carrier
Sporadic version of RB gene is non-inherited and is a result in both mutations occurring in one of the genes and inheritance of inactivation from parent in the other gene
99
Lynch Syndrome (r/t Tumor Suppressor Genes)
Autosomal Dominant
Inherited cancer d/t mutation - "Hereditary Polyposis Colorectal Cancer"
It is associated with a genetic predisposition to acquiring other types of cancer, so there is an increased risk for bowel, colon, uterine, and ovarian cancer in the person
There is no cure for this syndrome as it is genetic and no symptoms associated with it early on, but early detection of colon cancer is 90% curable
100
BRCA 1 and BRCA 2 (Tumor Suppressor Genes)
Autosomal Dominant Antioncogenes
Inactivation of these genes leads to a higher risk for breast cancer
101
What is the growth pathway for oncogenesis occurance?
Carcinogenic Agent + Normal Cell --> DNA damage --> Failure to repair DNA leads to activation of growth promoting oncogenesis, inactivation of antioncogenes, and alterations in genes that control apoptosis --> unregulated cell differentiation and growth occur as a result --> A malignant neoplasm occurs
Normal Cell
102
What is the pathway for growth regulation?
Stimulation of normal cells by growth factors will lead to growth factor receptor activation and signaling of proteins that promote growth promoting signals to the nucleus --> Nucleus modulates gene transcription and progression through the cell cycle and many of the signaling proteins exert their effects through proteins called kinases which controls regulation and growth
103
3 Stages of Carcinogenesis
1. Initiation
2. Promotion
3. Progression
104
Initiation
First carcinogenesis stage which leads to an initial mutation occurring
This occurs when cells are exposed to appropriate doses of carcinogenic agents like physical, chemical, or biological and mutations occur
These changes are irreversible in the genome, the cells most vulnerable are actively making DNA at the time of exposure, and if these cells become latent they can move onto promotion (even for a long latency time)
105
Promotion
Second stage of carcinogenesis where mutated cells are stimulated to divide
They do so in an unregulated and accelerated manner
Can be reversible if the substance stimulating the cells to do this are removed
106
Progression
Third stage of carcinogenesis where tumor cells compete with one another and develop more mutations, which make them more aggressive and spread
Cells quickly are gathering malignant phenotypic changes and cells can proliferate autonomously, invade, or metastasize in this phase
107
What are some etiologic factors for Cancer?
Cellular Level Factors
External and Host Factors
*commonly both are working together when cancer develops and progresses over time*
108
Examples of Cellular Level Etiologic Factors for Cancer
Genetic damage
Mutation
epigenetic factors that silence a gene or genes
Role of cancer stem cells
ECM, cytokines, growth factors, and other cell types
109
Examples of External and Host Factors for Cancer?
Age
Heredity (Mendelian inheritance of genes)
Hormonal Factors (from tumors, mutated hormones, etc)
Obesity
Immunologic Mechanisms
Environmental agents: chemical carcinogens, radiation, microorganisms
110
Why can hormone therapy be concerning when the patient has cancer?
The hormones could be closely related to what the tumor uses and could cause further proliferation - there is an unknown link between hormones and cancer
111
How can obesity lead to cancer?
Insulin resistance, increase in estrogen/androgen hormones, and lower insulin levels all lead to inhibition of apoptosis and increases in chronic inflammation and malignant cell transformation rate
112
Evidence supports the idea that the lower the immune response ...
the greater the incidence of cancer
113
Types of Chemical Carcinogens
Direct
Indirect
114
Direct Reacting Agents
Inherently carcinogenic (ex: charcoal smoke on meats)
115
Indirect Reacting Agents
Only actively carcinogenic after metabolic conversion (Ex: chemicals in red meat)
Includes Procarcinogens which are initiators
116
Promoters
chemicals that alter gene expression, enhance the # of copies of cells made, and alter intracellular communication
They alone are NOT carcinogenic, but act in the presence of carcinogens like cigarette smoke
117
The longer the dose and longer the exposure and difference in age...
the greater the risk of cancer from radiation(ex: sunlight)
118
UV exposure is more dangerous for what age group?
In childhood, so protect from sunburns prior to age 4!
119
Treatment radiation has lower risks associated with it unless.
it is done over and over - time and amount and length of exposure effects risk
120
HPV and Cancer
An oncogenic virus in humans leading to cervical and anogenital cancer and genital warts
121
H. Pylori and Cancer
This bacteria is associated with gastric cancer, but also we need it for the benefits in our normal flora
Growing opportunistically is when it is a problem
122
Local Effects of Tumor Growth
1. Compression of Adjacent Structures
2. Effusions
123
What can compression of adjacent structures lead to?
1. Hollow organs
2. Blood vessels bleeding and hemorrhaging
124
What can cancer related effusions lead to?
Fluid build up and interference with normal functions
This may cause the effusion to need mandatory removal
ex: build up in the lungs makes it so they cannot expand and could lead to atelectasis so it might need centesis removal
125
Cancer impact moves from ___ to ___ upon metastasis
local to systemic
126
Initially cancer affects ___ ___ only
target organs only
127
S/S of cancer can be ___ or ___, but this changes to the former when the cancer progresses regardless of type
systemic/widespread or local
128
Systemic Manifestations of Cancer
Anemia
Anorexia and Cachexia
Fatigue and Sleep Disturbances
Ectopic hormones or factors secreted by tumor cells (paraneoplastic disorders)
129
The systemic manifestations of cancer can be compounded onto through...
the use of chemo meds!
130
How does Anemia occur/impact in relation to cancer?
Commonly occurs, especially with medicines destroying cells
Bone marrow function and side effects (Nausea, vomiting, anorexia) of the medicine lead to nutritional deficiencies and iron deficiencies leading to anemia
Also, inflammation from tumors decreases erythropoietin synthesis so RBC maturation occurs less
Need to check WBC/RBC count since hypoxia in advanced solid tumors occurs - so we must make sure chemo therapy is safe
131
Cancer r/t Anemia can lead to what effects regarding treatment and prognosis?
reduces effectiveness of treatment and safety of treatments
contributes to the needs of blood transfusions
increases mortality
132
Why does Anorexia/Cachexia occur in Cancer and what can it lead to?
It occurs because it becomes difficult to eat d/t nausea from tumors and meds and also your tastes change
This can lead to wasting syndrome, and cancer progression causes anabolic processes to not be maintained leading to the body digesting muscle and fat leading to wasting and causing dramatic weight loss and decrease in strength
133
Wasting Syndrome
Wasting of muscles and fat from cancer d/t increased CNF leading to hypothalamus satiety center suppression and increased lipoprotein lipase (increases FA release to use in metabolism thus causing acidosis)
This cancer anorexia cachexia syndrome can be seen in most solid tumor cancers and is impacted by may factors like tumor necrosis, changes in food taste, inflammation, treatment, and especially cytokines in more aggressive cancer
134
Why does Fatigue and Sleep Disturbances occur with Cancer?
Most common cancer side effects
Resting/Sleeping does not resolve fatigue like in normal people
Cancer impacts both the central and peripheral levels:
1. Peripheral levels do not have enough ATP leading to acid build up and muscles not responding to central stimulation
2. Central levels have fatigue starting in the CNS and resulting in difficulty leading to voluntary activities and movement
135
Paraneoplastic Syndrome (Disorders)
A consequence of cancer in the body but not from the cells themselves, rather the ectopic hormones and factors they release
RARE
can occur in benign OR malignant tumors d/t hormone release
commonly one of the first manifestations of lung, breast, hematologic cancers
136
Manifestations of Paraneoplastic Syndrome
Encephalitis
Ataxia
Neuropathy
Body Jerking
Irregular Eye Movements
Psychiatric Disturbances
137
Is Paraneoplastic Syndrome a direct consequence of cancer cells?
NO
the cancer cells themselves do not cause this, rather the ectopic hormones and factors they release do
138
Syndromes Related to Cancer (Paraneoplastic Syndromes/From Hormones/Hormone like protein production)
Endocrinologic Syndromes
Hematologic Syndromes
Paraneoplastic Neurologic Disorders
139
Endocrinologic Syndromes
Primarily occur from Lung Cancer
1. ADH - SIADH Syndrome
2. ACTH - Cushing Syndrome
3. PTH-related protein - Hypercalcemia (from bone cancer breaking bones down)
140
The 2 most common cancer syndromes are?
SIADH
Cushing Syndrome
141
Hematologic Syndromes
Primarily occur in pancreatic and lung cancers
1. Venous Thrombosis
2. Non Bacterial Thrombolytic Endocarditis
Cancer cells produce proteins that impact clotting !
142
Paraneoplastic Neurologic Disorders
Primarily occur in lung cancer
Leads to encephalitis, ataxia, neuropathy, progressive numbness and weakness of the hands and feet, myoclonus, and myasthenia gravis and lambert-eaton syndrome
143
Ataxia
loss of balance
144
Myoclonus
body jerks and irregular rapid eye movements and psychiatric disturbances
145
Myasthenia Gravis
Progressive muscle weakness that begins in the mouth and eyes
146
Lambert-Eaton Syndrome
Opposite of myasthenia gravis
Progressive muscle weakness beginning in the limbs
147
What is the origin of a paraneoplastic neurologic disorder?
It occurs from an altered immune response and production of onconeural antigens normally expressed in the nervous system - but they are made by cancer cells and are attacked by the nervous system for being ID'ed as foreign (self attack/autoimmune)
148
When do Paraneoplastic Disorders commonly appear?
Early and commonly lead to clinical challenges
149
What can paraneoplastic disorders mimic?
Metastatic Disease
150
The effects of paraneoplastic disorders can compound with ...
drug side effects
151
Cancer Screening is ___ Prevention
Secondary
152
Is there a screening method for every type of cancer?
no
153
Methods of Cancer Screening
Observation (type dependent, i.e. skin)
Lab Tests
Procedures
154
Effective Screening Tests are available for what types of cancer?
Breast
Cervical
Colon
Rectal
Prostate
Skin
155
How do we make a Cancer Diagnosis
the location and type of cancer determines the diagnosis - So TUMOR MARKERS, antigens on tumor surfaces, as well as hormones and enzymes being overexpressed need to be screened, staged, detected,, etc to diagnose cancer
example of tumor markers: CEA, hCG, calcitonin, catecholamines, monoclonal immunoclobulin, PSA, CA-125 and 19-1, CD Antigens
156
What are some methods to gather the information needed for a cancer diagnosis?
1. Cytologic Studies (ex: Pap smear)
2. Tissue Biopsy (ex: Fine needle aspiration)
3. Immunohistochemistry (ex: look at estrogen receptors)
4. Molecular Diagnostics like Microarray Technology/Gene Chips
157
Cytologic Studies
ex: pap smear
tissue and cells are taken to look for cancer
158
Tissue Biopsy
ex: fine needle aspiration
taking a tissue sample either via fine need, bronchoscopy, surgical incision, endoscopy, and cytoscopy to check for cancer
159
Immunohistochemistry
Uses antibodies to ID surface markers on cells and identification of the markers (i.e. estogen receptors) can facilitate more specific and effective treatment.
160
Molecular Diagnostics
Detects individual molecules by looking at DNA or RNA based assays to check for cancer
It can identify molecular targets to attack with drugs and tumor fragments that float in blood samples
161
What type of testing is very relevant when cancer is hereditary or treatment is based on characteristics of the tissue/tumor?
Molecular Diagnostics
162
With hereditary cancer, there is an increased risk for what things ...
secondary malignancy
early onset
multiple neoplasms
a recognizable histological pattern
163
Genetics does not have much play in what type of cancer?
Lung Cancer
BRAC2 gene has a higher risk for lung cancer despite lung cancer not being a hereditary cancer, so sometimes genes play a role in history lung cancer, but genetics does not often play much into lung cancer specifically
164
Microarray Tech and Gene Chips
Gene chips are used to detect and quantify the expression of large numbers of genes at the same time, so we can see the extent that genes are turned off and in in tissues
This can ID tumors, make a prognosis, classify hereditary tumors, and check on response to therapy
165
Cancer Grading
Microscopic examination of differentiation
Comes up with either I, II, III, or IV with differentiation and prognosis becoming poorer the higher the number
166
Cancer Staging
Clinical, radiographic, surgical examination of extent and spread --> Treatment and Prognosis
System that can be used to decide the extent of cancer
Include TNM and AJC
167
What is the most common Staging system used?
TNM
168
TNM
Staging system that is based on tumor size, whether it is in lymph nodes, whether cancer has metastasized
The higher the stage the worse the prognosis
T1-4 = Tumor Size
NO-3 = Lymph node involvement
M0-1 = Metastasis
169
What would a T4N3M1 Cancer mean
It is a size 4 tumor, in 3 lymph nodes, and has metastasized
170
AJC
Staging method by American joint committee
Less commonly used than TMN but stages cancers from 0 to IV based on size of primary lesion and presence of nodal spread and metastasis
171
Methods for Cancer Treatment
Surgery
Radiation Therapy
Chemotherapy
Hormone and Antihormone Therapy
Biotherapy
Targeted Therapy
172
When is surgery used for cancer?
to make diagnosis, staging, do tumor removal, for relief of symptoms
most feasible when tumor is smaller, has well defined margins, and potentially a capsule (benign)
173
Radiation therapy
Ionizing radiation hurts and kills cancer cells - with cancer cells more likely to be hurt than healthy cells
However, rays can damage bone marrow and GI tract mucosal lining so adverse effects can occur like infection, bleeding, anemia, nausea, and vomiting
Given in small doses to prevent effects
174
Chemotherayp
Major systemic treatment for tumor and metastasis sites with multiple anti cancer chemicals given
Many side effects occur such as hair loss, bone marrow suppression, anorexia, and vomiting
Nurses must be chemo certified in order to give these drugs
175
Hormone and Antihormone therapy for Cancer
given to deprived cells that stimulate division
Mostly for breast, prostate, and endometrial cancers
Can be of concern if hormones can exacerbate tumor effects/growth
176
Biotherapy
Immunotherapy used to change the immune response (increase) and change tumor cell biology
177
Targeted Therayp
agents attack malignant cells but not healthy cells
It can disrupt molecular signaling pathways and inhibit cancer angiogenesis leading to deprivation of needed nutrients and blood and therefore death
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What is often needed regarding treatment for cancer?
use of more than one type of therapy to allow a longer life expectancy (even in poor prognosis)
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With chemotherapy, a constant progression of cancer cells are killed with each treatment, so what would happen if the last treatment was not given?
the cancer would return even if it was in clinical remission
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Why may targeted treatment become ineffective if a person has liver cancer that returns following treatment?
Liver cancer is not usually hereditary and hepatocellular carcinomas commonly mutate a lot
Once genes are mutated, the targeted treatments are unable to target the cancer and the treatment has become ineffective since the cancer cells are not the same
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Do childhood cancers have any discrimination in different groups?
No discrimination, it affects every socioeconomic group and ethnic group
every 2 minutes a child is diagnosed with cancer (300,000 annually)
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A childhood cancer can be hereditary or acquired, but when they are hereditary what occurs?
Occur at a very young age
Have a higher frequency of multifocal lesions in a single organ or both organs if that organ is paired
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Childhood cancer is not usually linked to ___ or ___ factors
environment or lifestyle factors
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The most common childhood cancers are?
Leukemia!
Usually childhood cancers are hematologic, nervous, soft tissue, or bone cancers
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There are no what for childhood cancers?
no early warning signs or screening tests
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Cancer treatment in children can cause what years after treatment?
cardiovascular complications
impaired growth
fatigue
cognitive problems
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What is critical for children who are cancer survivors?
Regular follow ups since there is a risk for recurrence of that type of cancer
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Why does it matter if a lump is painful or not?
Cancer masses are non-painful (and often moveable) while cysts are more commonly painful - So this matters a lot on palpation!
