Neoplasia (AKA Cancer) Flashcards

1
Q

Cell Cycle

A

orderly sequence - duplicated chromosomes resulting in cell proliferation

Body Tissue:

continuously dividing tissue:
cells divide, replicate in life ex. skin, oral cavity, vagina…generate after injury as long as we have stem cells

Stable tissue: Cells that stop dividing, but undergo regeneration in response to stimuli Ex: solid organs like liver or kidney

permanent tissue:
no further regeneration at all ex: nerve cells, muscle cells, cardiac cells (when they die, they die forever) replaced with scar tissue.

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2
Q

Proliferation

A

process of increasing cell numbers thru mitotic division

triggered by growth factors , hormone and cytokines.
ex: erythropoetien, stimulating factor

proliferation is the mechanism for replacement when old cells die and additional cells are needed

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3
Q

Differentiation

A

Process when structure and function of cell becomes SPECIALIZED

new cells acquire characteristics of cells they replace

ex: granulocytes, agranulocytes, platelets, erythrocytes

stem cells are UNDIFFERENTIATED cells that differentiate based on need in continuously dividing tissues

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4
Q

Stem Cell Division

A

self renewal > asymmetric replication> differentiation

see pic on slide

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5
Q

Apoptosis

A

Programmed CELL DEATH

IN HEALTH - rate of cell death = rate of cell life

occurs in multiceullular organisms

keeps the number of total cell sin constant health

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6
Q

Neoplasia

A

occurs when: cell differentiation and growth are NOT regulated

Hypertrophy: enlargement or overgrowth of an organ due to increase in the SIZE of the cells

Hyperplasia: an abnormal multiplication or increase in NUMBER of normal cells of a body part

Neoplasia: Process of formation or presence of a NEW abnormal growth of tissue that is not under physiologic control

Neoplasm: New growth, swelling that is caused by different etiologic factors (AKA TUMOR - benign or malignant)

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7
Q

Neoplasia Pt II

A

proliferation to form new growth

cells do not die off, to keep the number of total cells constant

benign: well differentiated
malignant: less differentiated (CANCER - cells often do not mature normally to do the “job” the tissue is supposed to do)

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8
Q

Benign Tumors

A

contain cells that look like normal tissue cell

perform normal function of tissue ex: secrete hormones, but may lead to over secretion

grow slowly
surround by a fibrous capsule
do not infiltrate, invade or metastasize
can damage nearby organs by compressing them

Generally NOT dangerous and can be removed easily

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9
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 ect…

grow rapidly

infiltrate, invade, metastasize (to distant sites)

can compress and/or destroy the surrounding tissues

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10
Q

Cancer Incidence

A

leading types (not on test)

Men - prostate, lung, colon, rectum, bladder, melanoma

Women - Breast, lung, colon, rectum, uterine, thyroid

Most deaths from LUNGS, breast and colon

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11
Q

Tumor Types

A

Solid tumors:
initially confined to specific tissue or organ but then detach and invade surrounding tissue, blood and lymph (then it gets worse)

Hematologic cancer:
Blood and lymph contain the cancer cells INITIALLY. These cancers are considered disseminated diseases from the beginning

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

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12
Q

Tumor Cell Characteristics

A

Poorly differentiated or non-differentiated tumor cells are described as ANAPLASTIC cells

cells contain numerous morphologic changes and vary in size and shape (PLEOMORPHISM)

cells have high rate of proliferation, do not resemble tissue of origin

Grading of tumors is based on how differentiated the cells are and the number of proliferating cells: Range from I-IV

Grade I are well differentiated

Grade IV are identified as anaplasia

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13
Q

Cells and -Plasia

A

Hypoplasia - too few cells that deemed normal (ex. under developed breasts, benign)

Hyperplasia - increase number of cells than normal, result of external stimuli (think of callus on skin after trauma)

Neoplasia - similar to hyperplasia, but denotes ABNORMAL multiplication due to loss of normal proliferation regulation

Dysplasia - change in the normal shape and size and organization of cell, usually bc of CHRONIC irritation (ex. smoking)

Metaplasia - Change in cell type. ex. lung epithelium to squamous after prolonged smoking

Anaplasia - reversal in differentiation OR loss of structure and function of cell. Ex. cancerous tumors

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14
Q

Genetic Instability

A

HALLMARK OF CANCER

Defined as presence of high frequency of mutation fo cells that change sequences of nucleic acid and arrangement of chromosome

growth regulatory genes and genes involved in cell cycle progression are ALTERED or arrested, resulting in gross chromosomal abnormalities

end result is ANEUPLOIDY - an incorrect number of chromosomes

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15
Q

Growth properties: Cancer VS Normal cells

A

some cancers secrete growth factors and/or have receptors
ex. breast cancer cells - no estrogen receptor cells

Normal cells have a cell density dependent on inhibition. Ex. wound healing, when cells contact (contact inhibition) the cells respond and stop growing, but with CANCER, they KEEP growing (aka lack inhibition)

Cancer cells do not stick together and shed into surrounding body fluids.

cancer cells have anchorage independence

Anoikis - healthy cell apoptosis

cancer cells: faulty cell to cell communication also immortal (never die)

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16
Q

Tumor Cell Cycle

A

cancer: cell cycle is not shorter than healthy cells bc they DO NOT DIE

Growth fraction is the RATIO of dividing cells to resting cells:

  • in health, equilibrium is established btwn cell brith and death
  • growth fraction INCREASES in cancerous cells

Doubling time is the length of time it takes a mass of cells in a tumor to DOUBLE
-doubling time decreases in cancerous cells once blood supply and nutrients fail to support growth

17
Q

Malignant Invasion

A

Directly invade surround tissue, no capsule and seed in body cavities.

leads to metastatic spread as tumor erode and sheds cells

lack of capsules send “legs” into surrounding tissue

Malignant cells synthesize and secrete enzymes that break down proteins in HEALTHY cells

18
Q

Basal Cell Carcinoma

A

EX: Extra tissues needs to be excised in order to establish cancer free margins (See photo on slide)

19
Q

Metastasis

A

cells in a primary tumor develop the ability to escape, travel and survive in the blood, exit the blood and develop a secondary tumor

malignant tumor pathways:
Lymph Channels & Blood Vessels

Sentinel node: initial node to which the tumor drains

20
Q

Two Main sub ground of malignant tumors

A
Carcinoma:
derived from epithelium
always malignant
common
spread mostly by lymphatics
may have pre-malignant phase
older patients
Sarcoma:
Derived from connective tissue
always malignant
less common
spread by blood
not believed to have pre-malignant phase
younger patients
21
Q

Hematogenous Spread

A

Hema (think blood)
Cancer cells invade capillaries and venules

hematologic spread is selective and has many steps

Once in circulation, tumor cells are vulnerable to destruction by host immune cells

some cancer cells gain protection by aggregating and adhering to circulating blood components (esp. platelets) to from tumor emboli

22
Q

Metastatic Sites

A

Portal vein to the liver

vena cava blood to the lungs

preferential spread of cancer

prostate cancer to the bone

bronchogenic cancer to
adrenals and brain

neuroblastoma to the liver and bones

23
Q

Cancer- Associated Genes

A

These are classified on genes over activity or under activity increases risk of cancer.

IN HEALTH, proto-oncogenes code for normal cell division proteins. Growth factors, growth factor receptors, cell cycle proteins and apoptosis inhibitors

Proto-oncogenes MUTATE to oncogenes and gene amplification can occur:
-insertions, deletion, translocations are increased or activated
EX: RAS, philadelphia chromosome, HER-2/neu (30% of breast cancer)

IN HEALTH, tumor suppressor genes (antioncogenes) inhibit cell division.

Mutation are either inherited or acquired EX: P53, RB Genes, Brca1 or Brca2

24
Q

Oncogenesis

A

Stages: (see slide)

Normal cell > DNA Damage >activation of growth prompting oncogenes>unregulated cell differentiation and growth>malignant neoplasm

25
Q

Stages of Carcinogenesis

A

initiation: initial mutation occurs (exposure to agent)

Promotion: mutates cells are stimulated to divide (unregulated and accelerated)

Progression: Tumor cells compete with one another and develop more mutation, which make them more aggressive

26
Q

Etiologic Factors for Cancer

A
cellular level:
genetic damage
mutations
epigenetic factors that silence genes
cancer stem cells
extracellular matrix, cytokines, growth factors
External and host factors:
age, heredity
hormonal factors
obesity
immunologic mechanisms
environmental agents
27
Q

Host and Environmental Factors

A

Mendelian inheritance of

genes

reproductive hormones

obesity

immune surveillance and tumor antigens

Chemical carcinogens (cigarettes, alcohol) (contain pro-carcinogens - initiators)

Radiation

Viruses and bacteria that cause cancer

28
Q

Local effects of tumor growth

A

Compression of adjacent structures:

  • hollow organs
  • blood vessels
  • bleeding, hemorrhage

Effusions:

  • fluid builds and interferes with normal function
  • effusions may need to be removed
29
Q

Systemic Manifestations of Cancer

A

Anemia

Anorexia and cachexia (solid cancers)

fatigue and sleep disturbances

hypoxia (advanced cancers)

Ectopic hormones or factors secreted by tumor cells (paraneoplastic disorders - lung/ breast cancers)

30
Q

Cancer Syndromes

A

Cancer cells produce hormones or hormone-like proteins.

Endocrinologic syndromes (primarily lung cancer)

  • ADH problems
  • SIADH Problems
  • ACTH problems
  • PTH-related protein (hypercalcemia)

Hematologic syndrome (pancreatic and lung cancers)

  • Venous thrombosis
  • non-bacterial thrombolytic endocarditis
  • cancer cells produce proteins that affect clotting
31
Q

Cancer Syndromes Pt II

A

Paraneoplastic neurologic disorder (lung cancer) - show up early

Encephalitis (brain)

Ataxia

Neuropathy

Myasthenia gravis and lambert-eaton syndrome (mouth and eyes)

32
Q

Cancer screening

A

Screen tests are a type of secondary prevention

Methods:
observation, lab tests, procedures

Effective screening test are available for breast, cervical, colon, rectal, prostate and skin cancer

33
Q

Cancer Diagnosis

A

Looking at TUMOR MARKERS

specific antigens on tumor cells, hormones and enzyme over expressed as result of tumor

34
Q

Cancer Diagnosis Pt II

A

Cytologic studies (pap smear)

Tissue biopsy (fine needly aspiration)

Immunohistochemisty (estrogen receptor)

Molecular Diagnostics

Microarray technology (gene chips) (can see genes turned off or on in cells)

liquid biopsy (early detection)

35
Q

Grading VS Staging

A

Grading: Microscopic examination of differentiation
I= well differentiated, IV= poorly differentiated

Staging: Clinical, radiographic, surgical examination of extent and spread > treatment, prognosis

TNM: T1-4= tumor size
N0-3 = lymph node involvement
M0-1=Metastasis

AJC: Stages 0-IV = size of primary lesion and presence of nodal spread and metastasis

36
Q

Cancer treatment

A

Surgery

radiation therapy (many adverse effects)

chemotherapy (systemic treatment)

hormone and anti-hormone therapy (deprive cells chance to divide)

biotherapy (immunotherapy)

targeted therapy (agents that attack only malignant cells)

37
Q

Childhood Cancer

A

No discrimination - affect every socioeconomic and ethnic group

Usually hematologic - nervous , soft tissue or bone

Most common is leukemia

incidence in 1st years of life, no warning or signs

generally we don’t know why it occurs, treatment can cause a lot of cardio complication and risk for reoccurrence