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BSNC 3000 > Cell Regulation & Cancer > Flashcards

Cell Regulation & Cancer Flashcards

1
Q

Causes of anemia

A

hypoxia –> reduced erythropoietin response
nutritional deficiencies
bone marrow failure
iron deficiency
inflammation –> decreases erythropoietin synthesis

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2
Q

Cellular regulation

A

all functions carried out w/i a cell to achieve homeostasis
includes:
cellular response to extracellular signals (cytokines, hormones, neurotransmitters)
growth, proliferation, differentation

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3
Q

Growth

A

refers to physical growth of cells in terms of size

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4
Q

Proliferation

A

refers to increase in number of cells

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5
Q

Differentation

A

process of specialization wherein cells become functional through subsequent cell cycles

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6
Q

Cell adaptation

A

increases in growth and proliferation d/t increase in metabolic/functional demand
Ex: ventricular hypertrophy

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7
Q

Neoplasia

A

uncontrolled cell growth & proliferation

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8
Q

Apoptosis

A

programmed cell death of damaged, excess or old cells

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9
Q

Normal cell regulation

A

involves a balance between growth factors & growth controls

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10
Q

Factors promoting cell proliferation

A

growth factors
availability of open space in tissue
perfusion, oxygen and nutrients (requirements of cell growth)

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11
Q

Examples of growth factors

A

hormones
cytokines
growth actors (VGEF)

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12
Q

Growth factor MOA

A

binds to a membrane receptor triggering an intracellular pathway –> cell enters the cell cycle
message is carried towards the nucleus causing transcription factors to bind to DNA

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13
Q

Cell cycle

A 
divided into four stages. presents the life cycle of a cell
G1
S
G2
M
G0
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14
Q

G0

A

resting phase
cell is not actively dividing or preparing to divide
cell carrying out normal function in tissues

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15
Q

G1

A

physical growth –> cell duplicates organelles, produces proteins, molecules for division
growth & normal metabolism

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16
Q

S

A

DNA synthesis occurs –> cell duplicates DNA and condenses into a chromosome + duplicates the centrosome

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17
Q

G2

A

cell continues to grow producing proteins & organelles

growth & preparation for mitosis

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18
Q

M

A

mitosis phase –> cell divides and produces two daughter cells

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19
Q

Phases of mitosis

A

prophase
metaphase
anaphase
telophase

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20
Q

Cytokinesis

A

cytoplasm divides producing two new distinct cells

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21
Q

Factors inhibiting cell divison

A

growth inhibiting factors

contact inhibition

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22
Q

Contact inhibition

A

cells division depends on cell density
cells form intercellular junctions between cells –> intercellular contact inhibits cellular growth
contact blocks DNA replication & protein synthesis

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23
Q

Factors limiting cellular lifespan

A

apoptosis

telomeres

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24
Q

Telomeres

A

short nucleotide sequences found at the end of chromosomes
shorten each cell cycle –> when telomeres become too short cell division shortens
cells become senescence or chromosomes break apart –> cell dies

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25
Q

Apoptosis process

A

cell shrinks
enzymes released that digest proteins & DNA
nucleus fragments
cell breaks down into small membrane bound fragments
fragments are digested by phagocytosis

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26
Q

Senescence

A

functional cells that can no longer divide

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27
Q

Telomerase

A

enzyme that rebuilds telomeres

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28
Q

Cells containing telomerase

A

germ cells
stem cells
cancer cells** –> cancer cells are immortal

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29
Q

Neoplasia

A

uncontrolled cell proliferation that is permanent

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30
Q

Neoplasm

A

tumor made up of cancer cells

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31
Q

Types of tumors

A

benign

malignant

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32
Q

Characteristics of benign tumors

A

slow, progressive growth
encapsulated by connective tissue capsule
grow by expansion –> compress adjacent tissue
well-differentiated –> maintain normal tissue function
resemble local tissue cells
localized –> not capable of metassis

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33
Q

Characteristics of malignant tumors

A

rapid cell proliferation
poor differentiation –> look different/function differently from local tissue cells –> impaired tissue function
infiltrate/invade local tissue –> lack well-defined borders
compress blood vessels –> ischemia, necrosis
can secrete hormones, cytokines, toxins
can metastasize –> enter lymph/blood

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34
Q

Stem cells

A

undifferentiated cells that can produce a variety of different cells
one daughter cell remains a stem cell
second daughter cell –> progenitor cell

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35
Q

Progenitor cells

A

committed but not fully differentiated cells

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36
Q

Oma suffix

A

benign tumor

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37
Q

Carcinoma suffix

A

malignant tumor

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38
Q

Sarcoma

A

malignant mesenchymal tumor

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39
Q

Polyp

A

growth projecting from a mucosal surface

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40
Q

Characteristics of tumors

A

characteristic of tumor cells
rate of growth
local invasion
ability to metastasize

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41
Q

Characteristics of normal tissue

A 
specific morphology
well-differentiated
tight adherence to neighboring cells/ECM (anchorage)
orderly, controlled proliferation
euploidy (complete chromosomes
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42
Q

Clinical classification of tumors

A

Benign

Malignant

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43
Q

Histological classification of tumors

A

type of tissue
cell type
from which they arise

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44
Q

Do malignant cells divide faster than benign cells?

A

No.

malignant tumors have a higher # of cells that area actively dividing, less apoptosis and cells do not enter G0 phase

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45
Q

Mitotic index

A

ratio of actively dividing cells to resting cells

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46
Q

Factors causing cellular death

A

immune factors (WBC, antibodies, complement)
apoptosis
insufficient blood supply

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47
Q

Anaplasia

A

cells with poor differentiation “move backwards”

cells move backwards to an earlier more primitive state of cellular specialization

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48
Q

When are benign tumors removed

A

cosmetic
symptomatic –> begin to impair local tissue function
risk of malignancy (colon polyps)
functional endocrine tumors oversecrete hormones
prevent organ injury (d/t growth by expansion)
reduce anxiety

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49
Q

Tumor grading

A

histological and cellular characteristics of cancer cells
determines degree of differentiation
helps predict rate of growth & likelihood of metastasis

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50
Q

Tumor staging

A

extent and advancement of cancer
T = tumor size
N = lymph node involvement
M = metastasis

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51
Q

Colorectal cancer etiology

A

almost all start off as polyps

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52
Q

Polyp

A

growth projecting from mucosal surface –> grows into the lumen
benign tumor

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53
Q

Sessile polyp

A

flat

difficult to remove endoscopically

54
Q

Pedunculated polyp

A

forms a stalk w/ mucosal surface

easy to remove

55
Q

Most common type of colorectal cancer

A

adenocarcinoma

56
Q

Cancer grading

A 
G1 = well differentiated, slow growth 
G2 = moderately differentiated
G3 = poorly differentiated 
G4 = undifferentiated, rapid growth
57
Q

Growth properties of cancer cels

A

growth factor independence –> grow w/o being stimulated
loss of contact inhibition –> do not respond to inhibiting factors
loss of cohesiveness/adhesion –> allows shedding of cancer cells
anchorage independence –> grow w/o being bound to ECM
angiogenesis –> cancer develops its own vascular supply
activation of telomerase –> immortality

58
Q

Anchorage dependence

A

normal cells do not grow unless attached to a solid surface i.e. the ECM/other cells
detached cells programmed to die via apoptosis
**prevents growth of cells outside of local region

59
Q

Direct tumor spread

A

tumor cells spread into local tissue

60
Q

Mestasis spread

A

tumor cells break off from primary tumor and create a secondary tumor at a distal site

61
Q

Requirements of tumor motility

A

1) cancer cell becomes more loosely attached to ECM/other cells
2) cancer cells evade apoptosis after detachment (anchorage independence)
3) produce enzymes that degrade basement membrane –> invasion

62
Q

Secondary tumor characteristics

A

retain characteristics of the primary tumor despite being in a different anatomic region
**sometimes the secondary tumor is discovered first

63
Q

Routes of metastasis

A

lymphatic spread
vascular spread
seeding

64
Q

Seeding

A

tumor cells can shed and enter body cavities
spread along serous membranes of body cavities
spread into other organs within the body cavity
*risk of cancer spread during surgical removal

65
Q

Tumor cells in lymph nodes

A

1) destroyed by immune cells
2) pass thru lymph –> enter subclavian vein –> circulatory system
3) form a secondary tumor in the lymph node

66
Q

Vascular spread

A

cancer cells usually enter through the veins/capillaries

67
Q

Common sites of metastasis

A

liver (hepatic portal vein)
lungs (pulmonary artery)
lymph nodes

68
Q

Bone metastases

A

occur in bones of high blood cell production (high in red bone marrow = higher blood supply)
ex: vertebrae, humerus, pelvis, ribs, femur, skull

69
Q

S/S of bone cancer

A

pain
fractures
hypercalcemia

70
Q

S/S of liver cancer

A

nausea
jaundice
RUQ pain
hepatomegaly

71
Q

S/S of brain cancer

A

headache

seizures

72
Q

S/S of lung cancer

A

SOB
cough
hemoptysis
wheezing

73
Q

S/S of lymph node cancer

A

enlarged (palpable) lymph nodes W/O pain

pain usually indicates inflammation/infection

74
Q

When does a polyp become malignant

A

genetic changes –> rapid growth
invasion thru GI tract wall alyers
spread to distant sites

75
Q

Factors causing DNA damage

A 
radiation (ionizing, UV)
chemical carcinogens
replication errors
viruses, bacteria
free radicals
76
Q

G1/S checkpoint

A

detects DNA damage BEFORE replication begins

77
Q

G2/M checkpoint

A

detects DNA replication errors BEFORE mitosis begins

78
Q

Outcomes of DNA damage

A

cell dies via apoptosis
cell cycle stops –> error is corrected
mutation survives and becomes part of cellular DNA

79
Q

Genetics of cancer

A

develops when control genes that regulate cell growth/proliferation become mutated

80
Q

Genes involved in cancer

A

proto-oncogenes
tumor suppressor genes
apoptosis regulating genes
DNA repair genes

81
Q

Proto-oncogenes

A

normal genes become PO when mutated

code proteins that PROMOTE cell division –> growth factors, receptors, transcription factors, apoptosis inhibitors

82
Q

Tumor suppressor genes

A

code for proteins that normally INHIBIT cell division
limits cell division
underactivity = uncontrolled proliferation

83
Q

Carcinogenesis stages

A

Initiation
Promotion
Tumor progression
Metastasis

84
Q

Initiation

A

cell exposed to carcinogen –> irreversible mutation

*actively dividing cells most susceptible

85
Q

Promotion

A

promoters enhance growth/proliferation of mutated cells

new colony of cells containing original mutation

86
Q

Tumor Progression

A

cells gain additional mutations

87
Q

Factors stimulating cancer growth

A

increase in proto-oncogenes
decrease in tumor suppressor genes
decrease in apoptosis

88
Q

Colorectal cancer RF

A 
carcinogen exposure (smoking, alcohol, abdominal radiation)
advanced age >50
genetics
chronic irritation/inflammation (IBS)
weak immune function
lifestyle
obesity
89
Q

Why is age (>50) a RF

A

longer exposure to carcinogens
time to accumulate mutations
decreased ability to fix replication errors
weakened immunity

90
Q

Acquired mutations

A

occur throughout life

more common

91
Q

Inherited mutations

A

received from mother/father

92
Q

Oncogenic viruses

A 
HPV
Hep B/C
Esptein Barr (mono)
Herpesvirus 8
Human T-cell lymphotropic virus
93
Q

Oncogenic bacteria

A

H. pylori

94
Q

Immune surveillance

A

malignant cells have tumor-specific antigens –> marked for destruction by lymphocytes/antibodies
can cause spontaneous regression

95
Q

Local Manifestations of cancer

A

palpable/visible lump
bleeding
obstruction
pain (mechanical compression)

96
Q

Changes in organ function manifestation

A

loss of function

hormonal effects

97
Q

Systemic Manifestation of Cancer

A 
anemia
anorexia/cachexia
non-specific
paraneoplastic syndrome 
fatigue, sleep disorders
98
Q

3 Endocrine syndromes assoc w/ cancer

A

SIADH
Cushing’s
Hypercalcemia

99
Q

S/S of colorectal cancer

A 
change in bowel habits --> constipation, narrow stools, incomplete evacuation 
abdominal pain
bloating
N/V
blood in stool (frank, fecal occult, melena)
palpable mass in rectum
fatigue
anorexia, weight loss
S/S of metastatic tumor
100
Q

Goals of cancer therapy

A

cure –> remove all of cancer
control –> slow/stop spread
palliation –> relieve symptoms
prophylaxis –> individual high risk of cancer

101
Q

Cancer treatments

A

surgery
radiation
chemotherapy

102
Q

Radiation therapy

A

damages cellular DNA through the production of free radicals OR by breaking chemical bonds in DNA
*most effective against actively dividing cells

103
Q

Neoadjuvant therapy

A

shrink before BEFORE first-line therapy

stimulates cells to move from G0 –> cell cycle increasing effectiveness of radiation

104
Q

Adjuvant therapy

A

destroy cancer cells remaining AFTER first-line therapy

105
Q

Concurrent therapy

A

chemo & radiation used at the same time

106
Q

Types of radiation therapy

A 
External = radiation beam
Internal = brachytherapy & systemic radiation
107
Q

Brachytherapy

A

sealed radioactive source inserted into tumor or nearby tumor –> temporary or permanent
“radioactive seeds”

108
Q

Systemic radiation

A

small radioactive isotopes with short half life given by mouth/injected into tumor site

109
Q

External beam

A

x-rays
gamma rays
delivered in smaller, fractionated doses to minimize damage to healthy cells & allow for healing

110
Q

Chemotherapy

A

use of cytotoxic drugs to destroy cancer cells or slow growth
*systemic side fx

111
Q

Types of chemotherapy drugs

A

cell-cycle specific
non-cell cycle specific
*diff drugs can be combined d/t diff MOA, onset, etc.

112
Q

Cell-cycle specific drugs

A

act on a specific stage of the cell cycle

113
Q

Non-cell cycle specific

A

act on all stages of the cell cycle –> works on resting/dividing cells
cause DNA damage –> apoptosis

114
Q

Chemotherapy drug classifications

A

antimimotics –> M phase prevents formation of the mitotic spindle
antimetabolites –> S phase prevents replciation
antibiotics –> S/G phases –> inhibits replication & protein synthesis
alklylating –> any phase

115
Q

Chemotherapy hematologic side fx

A

decreased RBC –> anemia
decreased platelets –> bleeding
decreased WBC –> infection

116
Q

Chemotherapy GI side fx

A 
anorexia
nausea/vomiting (CTZ stimulation)
diarrhea
mouth sores 
changes in taste
117
Q

Chemotherapy skin side fx

A

alopecia

hair loss

118
Q

Chemotherapy reproductive side fx

A

changes in menstruation
amenorrhea
reduced sperm count, no sperm
teratogenic fx

119
Q

Secondary screening for colorectal CA

A

fecal immunochemical test (FIT)

120
Q

Diagnostics for colorectal cancer

A

colonoscopy

biopsy

121
Q

Biopsy

A

microscope examination of a tissue sample

used to grade tumors

122
Q

Tests to check metastasis

A

chest xray - lung metastasis

abdominal CT scan - liver metasis

123
Q

Tumor marker for colorectal cancer

A 
carcinoembryonic antigen (CEA) -> produced by cancer cells 
measured in the blood
124
Q

PET scan

A

positron emission tomography

detects changes in cellular metabolism `

125
Q

Cellular adapation

A

occurs in response to cellular stress –> hypertrophy, hyperplasia, metaplasia
reversible change in cells
if cells cannot adapt –> cell injury occurs

126
Q

Permanent cells

A

skeletal muscle cells
cardiac cells
neurons

127
Q

Permanent cells & hyperplasia

A

permanent cells DO NOT DIVIDE

these cells adapt by increasing in size (hypertrophy)

128
Q

Types of cellular adaptation

A

atrophy
hypertrophy
hyperplasia
metaplasia

129
Q

Metaplasia

A

reversible conversion of one cell type to another
causes loss of function in original tissue
ex; smoking causes epithelium to convert from ciliated pseudostratified –> stratified squamous

130
Q

Causes of atrophy

A

decreased functional demand
decreased stimulation
inadequate nutrition/perfusion

131
Q

Dysplasia

A

disordered cell growth

non-adaptive cellular change

132
Q

Characteristics of dysplasia

A 
cells vary in size, shape, organization
caused by persistent, severe irritation
primarily occurs in epithelial tissue & metaplastic squamous epithelium 
may be reversible
precursor to neoplasia

BSNC 3000 (11 decks)

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