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Test 2 Cancer Flashcards

1
Q

Cell cycle

A

Is designed to be an orderly sequence of events during which duplicated chromosomes align appropriately which results in cell proliferation

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2
Q

Three types of body tissue

A

Continuously dividing tissue
Stable tissue
Permanent tissue

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3
Q

Examples of continuously dividing tissues

A

Skin cells, uterus cells, bone marrow cells

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4
Q

Examples of stable tissue

A

Solid organs, smooth muscle cells

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5
Q

Types of muscle cells

A

Smooth muscle (stable)
Skeletal muscle (voluntary)
Stiade muscle cells (involuntary)

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6
Q

Examples of permanent tissue

A

Neurons, nerve cells, cardiac muscle cells

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7
Q

Proliferation

A

Process of increasing cell numbers by mitotic division
Mechanism for replacement when old cells die or additional cells are needed

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8
Q

What triggers proliferation

A

Growth factors (help grow and divide), hormones and cytokines

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9
Q

Differentiation

A

Process through which the structure and function of a cell becomes more specialized
- new cells acquire the structural, microscopic and functional characteristics of cells they replace

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10
Q

Examples of differentiated cells

A

Granulocytes, agranulocytes, platelets and erythrocytes

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11
Q

Stem cells

A

Undifferentiated cells that differentiate based on need in continuously dividing tissue

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12
Q

Stem cell division

A

Self-renewal - after division one new cells starts specializing, the other stays a stem cell
Asymmetric replication
Differentiation

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13
Q

Apoptosis

A

Programmed cell death
Occurs in multicellular organisms
Keeps the number of total cells constant in health because it helps keep destruction = creation

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14
Q

Neoplasia

A

Occurs with dysregulation of cell differentiation and growth
Process of formation of presence of of a NEW ABNORMAL growth of tissues that is NOT under physiologic control

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15
Q

Hypertrophy

A

Enlargement or overgrowth of an organ due to an increase in the SIZE of the cells

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16
Q

Hyperplasia

A

Enlargement or overgrowth of an organ due to an increase in the SIZE of the cells

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17
Q

Neoplasm

A

New growth, swelling that is caused by different etiologic factors
- commonly referred to as a tumor
- classified as benign or malignant

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18
Q

Problem of neoplasia

A

Proliferation to form new growth
Cells do not die off (apoptosis) to keep the number of total cells constant

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19
Q

Benign vs malignant

A

Benign - well differentiated
Malignant - less differentiated (more mixed with normal cells, harder to located and treat)
- cancer
- cells often do not mature normally (differentiate) to do the “job” the tissue is supposed to do

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20
Q

Benign tumors

A

Contain cells that look like normal tissue cells
- may perform the normal function of the tissues
Grow slowly
Surrounded by a fibrous capsule (gives it the differentiation)
Do not infiltrate, invade or metastasize
Can damage nearby organs by compressing them

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21
Q

Malignant tumors

A

Contain cells that do not look like normal adult cells
- do not perform normal functions of the tissue
- may secrete signals, enzymes, toxins, etc
Grow rapidly
Infiltrate, invade and metastasize (to distant sites)
Can compress and/or destroy the surrounding tissues

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22
Q

Metastasize

A

Metastatic cancer means it hit a transport system

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23
Q

More common cancer in men and women

A

Prostate in men
Breast in women
Lung/bronchus in both

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24
Q

Solid tumors

A

Initially confined to specific tissue or organ but then detach and invade surrounding tissue, blood and lymph
Allow metastasis to occur

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25
Hematologic cancer
Blood and lymph contain the cancer cells initially These cancers are considered disseminated diseases from the beginning (can move around from the start)
26
Cancer in situ
Cancer cells that are localized in the organ of origin Considered pre-invasive lesions, they can be surgically removed or treated more easily and have a smaller chance of recurrence
27
Tumor cell characteristics
Poorly differentiated or non-differentiated tumor cells are described as anaplastic cells - cells contain number our morphologic changes and cart in size and shape (pleomorphism) - cells have a high rate of proliferation, but do not resemble the tissue of origin
28
Grading tumors
Based on how differentiated the cells are and the number of proliferating cells - range from Grade I to Grade IV - grade I are well differentiated - grade IV are identified as anaplasia (loss of mature/specialized features of a cell)
29
Hypoplasia (type of plasia)
Fewer cells than what is deemed normal Usually benign Ex: female with under developed breasts
30
Hyperplasia (types of plasia)
Increased cell number Under control of normal proliferation regulatory mechanism Result of external stimuli Ex: calluses
31
Neoplasia (types of plasia)
Similar to hyperplasia but denotes abnormal multiplication due to loss of normal proliferation regulation Benign or malignant Ex: adenomas or polyps or fibroids
32
Dysplasia (types of plasia)
A change is the normal shape, size and organisation Usually a response to chronic irritation Changes are reversible if stimulus is removed (reverses to metaplasia) Can happen to lungs due to chronic irritation (smoking, aspectus, etc)
33
Metaplasia (types of plasia)
A change in the cell type Changes are reversible to stimulus is removed, otherwise cells become anaplastic Ex: caused by irritation
34
Anaplasia (types of plasia)
A reversal in differentiation OR loss of structural and functional differentiation of normal cells NOT reversible Ex: cancerous tumors
35
Genetic instability
The present of a high frequency of mutations in cells that change the sequence of nucleic acids and arrangement of chromosomes - growth regulatory genes and genes involved in cell cycle progression are altered or arrested, resulting in gross chromosomal abnormalities Results in aneuploidy
36
Aneuploidy
An incorrect number of chromosomes
37
Growth properties - cancer vs normal
Some cancer cells can secrete growth factors and/or have receptors Lack cell density (fail to stick together) - depended or contact inhibition Anchorage independence - decreased anoikis Faulty cell to cell communication Immortal - unlimited lifespan and division
38
Anchorage independence
Normal cells grow when attached to or organ, cancer cells travel and move
39
Anoikis
Type of apoptosis due to lack of attachment
40
Tumor cell cycle
Cell cycle is not short than healthy cell Cancer cells are very prolific Growth fraction increases in cancerous cells Doubling time decreases in cancerous cells once blood supply and nutrients fail to support growth
41
Reasons cancer cells are so prolific
Cells do not die on schedule bc they don’t follow anoikis Cells respond to growth factors that keep the cancer cells actively dividing in the cell cycle
42
Growth fraction
The ration of dividing cells to resting cells In health an equilibrium is established between cell birth and death
43
Doubling time
The length of time it takes a mass of cells in a tumor to double
44
Malignant invasion
Lack capsules - sends “legs” into surrounding tissue Malignant cells synthesize and secrete enzymes that break down proteins in healthy cells Cells “seed” into body cavities
45
Basal cell carcinoma
Large amounts of extra tissue needs to be excised in order to establish cancer-free margins
46
Metastasis
Cells in a primary tumor develop the ability to escape, travel and survive in the blood, exit the blood and develop a secondary tumor in a different site
47
Malignant tumor pathways in metastasis
Lymph channels and blood vessels
48
Sentinel node
Initial node to which the tumor drains (Point of reference)
49
Carcinoma
One of the two main sub groups of malignant tumors - derived from epithelium (surface of organ/tissue) - always malignant - common - spreads mostly by lymphatics - may have pre malignant phase - older patients
50
Sarcoma
One of the two main sub groups of malignant tumors - derived from connective tissue - always malignant - less common - spreads mostly by blood - not believed to have pre-malignant phase - younger patients
51
Lymphatic spread
Seen in metastatic carcinoma Cells can die due to lack of suitable environment, remain dormant OR create a mass
52
Hematogenous spread
Cancer cells invade capillaries and venues Selective and has many steps Once in circulation, tumor cells are vulnerable to destruction by host immune cells
53
How cancer cells face protection in hematogenous spread
By aggregating and adhering to circulating blood components (especially platelets) to form tumor emboli What makes people with cancer more prone to clots
54
Metastatic sites
Portal vein to the liver Vena cava blood to the lungs
55
Metastatic sites preferential spread of cancer
Prostrate cancer to bone Bronchogenic cancer to adrenals and brain Neuroblastomas to the liver and bones
56
Proto-oncogenes
Cancer associates genes In heath proto-oncogenes code for normal cell division proteins These mutate to oncogenes and gene amplification can occur - insertions, deletions, translocations > increased or activated
57
Antioncogenes
Cancer associated gene In health, tumor suppressor genes (antioncogenes) inhibit cell division proteins - mutations are either inherited or acquired Examples: p53, RB gene, Lynch syndrome, BRCA1 and BRCA2
58
Pathway of oncogenesis
Carcinogenic agent > normally cell > DNA damage > failure of DNA repair > activation of prosthetic promoting onogenes, inactivation of tumor suppressor genes, alterations in genes that control apoptosis > unregulated cell differentiation and growth > malignant neoplasm
59
Growth regulation
Normal pathway for regulation of gene expression, cellular growth and survival Where there is abnormal MAP kinase signaling, there is uncontrolled cell proliferation and resistance to apoptosis
60
Stages of carcinogenesis
1) initiation - initial mutation occurs 2) promotion - mutated cells are stimulated to divide - reversible if the stim substance is removed 3) progression - tumor cells compete with one another and develop more mutations, which make them more aggressive
61
Cellular level etiologic factors for cancer
Genetic damage Mutations Epigenetic factors that silence a gene or genes Role of cancer stem cells Extracellular matrix, cytokines, growth factors, and other cell types
62
External/host etiologic factors for cancer
Age Heredity Hormonal factors Obesity Immunologic mechanisms Environment agents: chemicals, radiation, microorganisms
63
Local effects of tumor growth
Compression of adjacent structures - hollow organs - blood vessels: bleeding, hemorrhage Effusion - fluid builds and interferes with normal function - effusion may need to be removed
64
Systemic manifestations of cancer
Anemia - limits bone marrow function Anorexia and cachexia - meds cause lack of desire to eat and loose muscle tissue bc body digesting itself Fatigue and sleep disturbances - lack of ATP, building of acids Ectopic hormones or factors secreted by tumor cells
65
Paraneoplastic disorder
Syndrome is consequence of cancer in the WHOLE body Variety of manifestations
66
Endocrinologic syndrome
Cancer syndrome Primarily comes from lung cancer - ADH (SIADH) - ACTH (cushing’s) - PTH-related protein (hypercalcemia) Bone cancer > hypercalcemia bc bones break down
67
Hematologic syndrome
Cancer syndrome Comes from pancreatic and lung cancers - Venous thrombosis - Non-bacterial thrombolytic endocarditis - cancer cells produce proteins that affect clotting
68
Paraneoplastic neurologic disorders
Cancer syndromes Comes from lung cancer - encephalitis (inflammation of the brain) - ataxia (loss of balance) - neuropathy (numb feet and hands) Myasthenia gravis: muscle weakness starting in the mouth and eyes Lambert-Eaton syndrome (thymoma): muscle weakness starting in limbs
69
Cancer syndromes
Can develop with cancer BUT don’t mean cancer
70
Cancer diagnosis tumor markers
antigens on the surface of the tumor cells that help with identification and staging
71
Cancer diagnosis types
Cytologic studies - Pap smear Tissue biopsy - fine needle aspiration Immunohistochemisty - looks at receptor and antibodies in body Molecular diagnostics Microarray technology (gene chips) - what genes are turned on/off
72
Grading vs Staging
Grading - microscopic examination of DIFFERENTIATION - I = well differentiated, IV = poorly differentiated Staging - clinical, radiographic, surgical examination of EXTENT AND SPREAD, prognosis - T1-4 = tumor size - N0-3 = lymph node involvement - M0-1 = metastasis - AJC: 0-IV = size of primary lesion and presence of nodal spread and metastasis
73
Cancer treatment
Surgery Radiation Chemotherapy Hormone and anti hormone therapy Biotherapy Targeted therapy
74
Surgery Radiation Chemotherapy Hormone and anti hormone therapy Biotherapy Targeted therapy

Patho 2 (6 decks)

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