Heme and cancer Flashcards

1
Q

What are undifferentiated cells called? and what happens when they die?

A

Stem cells. They tell new cells to proliferate

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2
Q

What is dynamic equilibrium

A

When cell death is equal to cell growth

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3
Q

What do normal cells do? 3

A

They respect boundaries (increase contact inhibition)
neighboring cells inhibit cell growth-through the cell membrane
rate of growth in each cell is different depending on location
rapid areas include bone marrow, epithelial tissue, hair/skin/nails

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4
Q

What things do cancer cells do? 7

A

Proliferate at the same rate as the tissue they came from
Don’t respond to equilibrium-they are continuous
don’t listen to contact inhibition
no regard for cell boundaries
grow on top of, in-between not in order
Can produce more than two cells during mitosis
the growth=pyramid effect

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5
Q

Doubling time

A

Time it takes for the tumor to double in size

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6
Q

Apoptosis

A

Programmed cell death

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7
Q

What are protoncogogenes 4

A

Genes that regulate cell growth but can become unlocked from carcinogens or oncogenetic viruses
once they become unlocked they work like oncogenes-tumor inducing
this means the ability and properties that the cell had in fetal development are now active
it is immature, dedifferentiated, change from normal to make
and can make new proteins

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8
Q

Oncogene proteins
are located?
2 ex
and one more thing they produce

A

Located on the cell membrane
in blood tests
CEA and Fetalprot
produce hormones

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9
Q

What are tumor decreasing genes
What happens to them during cancer
Two examples and about them

A

They regulate growth by not letting cells go through the cell cycle
Are mutated or turned off
BRAC1 and BRAC 2 have inherited mutations for breast and cervical cancer

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10
Q

What is ACP gene

A

Tumor suppressor gene that can have a Family mutation gene for adenomatous
polyposis- colorectal cancer

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11
Q

Model of development of cancer

A

Initiation- Inherited or acquired
Promotion- Reversible proliferation
Progression-possible metastasis tumor growth

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12
Q

Initiation
What is it?
What about inherited?
What about acquired- 3 examples

A

Any change or mutation in usual DNA sequencing
if inherited -sm risk but high risk
carcinogens- Alkylating drugs or immunosuppressants can cause secondary leukemia that is resistant to chemo
Radiation- Atomic bomb and UV
Viral- Epstein barr, HIV, Hep B, HPV

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13
Q

Latent period and when does it happen?

A

the time between genetic alteration and actual evidence of cancer can be yrs-decades
In promotion

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14
Q

When are cancer cells evide?

A

! cm palp
0.5 MRI
Promotion

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15
Q

What are some reversible promoters?

A

obesity, smoking, alcohol, dietary fat.

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16
Q

What is a complete cancinogen? example

A

they are capable of promoting and initiating cancer

cig smoke

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17
Q

What cancers does alcohol cause?
Recommended drinks for men and women
Heavy drinking
week for m and w

A
breast, colon, oral, pharynx, larynx, esophagus 
2 or less for men 1 for women 
4 or more any day 
w-8 more a week
15 or more a week m
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18
Q

What are some common spots for mat of cancer 6

A

Brain, cerebral fluid, lung, liver, adrenals, bone

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19
Q

CEP

FP

A

Carcenoembryonic antigen is a tumor cell protein

Alpha fetoprotein

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20
Q

What do cytotoxic t cells do

A

Produce cytokine, interleukin 2 y interferon- stimulates other t interleukin cells

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21
Q

Monocytes

A

Release other cytokines, tumor necrosis factor

and colony stimulating factor- work on bone marrow to stimulate WBC

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22
Q

How do cancer cells evade immune response?

A

Factors that stimulate t cells are suppressed
weak surface antigens
I system can become tolerant to antigens
cancer can secrete products that decrease IS
tumors can decrease t cells
tumors can make blocking antibodies that bind to its antigen

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23
Q

What are the oncofetal antigens and how do we use them what are they 2

A

Tumor antigens from cell in the fetal state
use them as tumor markers
CEA and AFP

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24
Q

Classification

Benign vs malignant

A

Benign- well differentiated, it is rare for them to reoccur and better prognosis
Malignant- Range from well differentiated ti undifferentiated they are able to invade and metastasize

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25
Q

Why do we classify tumors?

A

To communicate, prepare and evaluate a tx plan, determine prognosis, compare groups, and stratify risk

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26
Q
Autonomic what is it?
Epithelial 
connective
nervous
lymph 
plasma
bone marrow
A
name that tumor. It is identified by the tissue of origin and behavior (benign or mal) 
b then m 
Epithelial- oma carcinoma 
connective oma sarcoma
nervous oma and oma 
lymph NA Hodg/nonhodg
plasma NA Multiple myeloma
bone marrow NA lymphocyte, myelogenous, leukemia
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27
Q

What is histologic grading

A

1-4 and x low to high looks to see how closely it resembles the tissue it is from
1- Mild dysplasia and well differentiated
2- Calls are more abnormal mod dys and diff
3 very abnormal severe dys and poorly diff
4. cells are immature, primitive, undefined- hard to tell what tissue it came from
x-Can’t be assessed

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28
Q

Cancer staging

and what we don’t use this for

A

0-4 use to show size, location, extent of spread, helps determine prognosis and tx
0-Cancer in situ
1-Tissue of origin-localized tumor growth
2-Limited local spread
3-Extensive local and regional spread
4- metastasis
Leukemia and blood

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29
Q

TMN classification

A

T tumor-primary tumor size and extent
N- nodes
M- Metastasis
Not for leukemia or blood , brain, spinal cord, bone marrow, lymphoma

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30
Q

One nursing thing

A

Avoid high nitrate concentrations

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31
Q

CAUTION

A
Change in bowel or bladder 
A sore that won't heal 
Unusual bleeding or discharge
Thickening lump 
Indigestion or difficulty in swallowing 
obvious change in wart/mole/mouth sore
Nagging cough or hoarseness
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32
Q

What are the tx for cancer 6

A

Surgury, radiation, chemo, immunotherapy, targeted therapy, hormone therapy

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33
Q

What is personalized medicine

A

When genetic info to guide tx, diagnosis,

34
Q

What is targeted therapy

A

Targets cancer specific genes or prots that contribute to growth

35
Q

Risks for chemo 3

A

Venous access prob, infection, extraversion

36
Q

What is regional chemo

A

Directly into tumor site and few side effects

37
Q

What is intraarterial and intravesical

A

Through art that are supplying the tumor and into the bladder

38
Q

What are the delayed issues with chemo

A

mucositis, radh, bone marrow suppression, neurotox, C/D, organ damage
cancer can become resistant

39
Q

Brachytherapy

A

Internal radiation seeds or ribbon used chronic lesss harmful acute need to have care in place.

40
Q

One thing about raditaion

A

CAn be PO attached to antibodies and attach to cell

41
Q

ALARA

A

As low as reasonably achievable

42
Q

Risks for patients for chemo and radiation

A

myelodecrease- decrease in blood cells more with chemo
Radiation one spot chemo all over 7-10day nadir
Neutrapenia- more common with chemo
Thrombocytopenia
Anemia-both
GI greatly affected-SITS bath work well no fruits veggies fiber
Mucosa irritation
Pulmonary- edema, fibrosis, hypersensitivity
Cardio- peri effusion- esp with CAD

43
Q

Skin issues with radiation

A

no hot/cold
Dry-Aloe
Wet des- Infection risk! sailine or vaseline

44
Q

What are secondary cancers

What are the high risk groups

A

leukemia, angiosarcoma, skin
Patients tx with alk agents or hogh dose raditation
does not CI risk

45
Q

What is immunotherapy
aka
what do they do
drugs?

A

Uses the bodies immune system
biological therapy
boost, or attack cancer using cytokines, vaccines, monocolonal antibodies-specific to antibodies mab drugs

46
Q

What is targeted therapy
EFGR?
One thing about target

A

interferes by targeting growth
it is specific
Transmembrane molecule that activates tyrosine kinase over expression of EFGR= unregulated cell growth we want drugs to inhibit EFGR. It is associated with high mortality
Works best with chemo to prevent resistance

47
Q

Side effects of immunotherapy and target 4

A

Flu-like- fluids
Tachy and ortho
Capillary leak-pulm edema and edema
CNS, organ issues

48
Q

Nursing care with target and immuno 3

A

effects are acute and dose dependent
Fear to talk about SE-stop tx
Stop TX on own because of SE

49
Q

Hormone therapy

A

Stops the hormones that cancer cell make

50
Q

Hematopoietic growth factors and about eyrthropoietin

A

Help support patients using colony stimulating factors that help blood cells
Eyrthro- Only when treating anemia specifically chemo

51
Q
Hematopoietic stem cell transplant 
aka 
1 ben 1 prob
types
For what cancer?
A
Bone marrow transplant 
 collection of stem cells 
even if no cure can cause remission- Lots of risks 
allogenic Donor- Usually family
Syngeneic -Twin
Autologous-self 
usually blood
52
Q

Complications from stem cell

A

Infection, grapht vs host disease- T cells from donated marrow attack body

53
Q

Gene therapy

A

Experimental therapy genetic material is placed into person cells

54
Q

Fighting nutrition issues with cancer 3

A

weigh twice a week
nut counseling if losing more than 5 percent weight
watch albumin

55
Q

Fighting dysgeusia 5

A

Plastic, it makes food bitter, oral care more water food they like

56
Q

Cancer Cachexia

A

Anorexia and. unintentional loss of weight

57
Q

One big thing to report

A

TEMP! 100.4

58
Q

Oncologic emergencies

A

Life threatening emergencies caused by cancer or cancer tx
Obstructive-superior vena cava syndrome, spinal cord compression, third spacing, intestional obstruction
Metabolic- Ectopic hormones, syndrome of inapprop antidiuretc hormone, hypercalcemia, tumor lysis, septic shock, diss intravascular coagulation
infiltration- cancer infiltrates organ-cardiac tamp, carotid art rupture

59
Q

causes of superior vena cava syndrome
s/s that you don’t know
tx

A

Presences of venous cath or medialstinal radiation
HA, Seizure
raditation

60
Q

What causes cardiac tamp

A

Radiation

61
Q

Thrombocytopenia numbers

A

tcp-150,000
bleed risk prolonged- 50,000
spontaneous bleed 20,000

62
Q

neutrophills mature vs immature

A

segmented-mature bands immature

63
Q

spleen

A

Hematopoiesis, filtration-filteres RBC Storage of IRON and about 1/2 platelets

64
Q

What cells do blood cell come from?

A

Myeloid and lymphoid

65
Q

Values for blood

A

Plasma 55

eryth 45

66
Q

What is an immature rbc called

A

reticulocyte

48 hours to mature

67
Q

Where is iron stored? recycled?

A

Bone marrow, liver, spleen,

macrophages in liver and spleen

68
Q

which cells are phagocytes

A

MEN

69
Q

What cells are humoral response and cellular

A

B cell production- lymphocyte

monocyte

70
Q

What cells are allergic

A

Basophils

71
Q

clotting

platelet cell life

A
vascular injury 
Adhesion 
Activation 
Aggregation 
platelet plug formation
clot dissolution 
8-11
72
Q

Spleen 4 things

A

Storage, immune, filtration, hematopoietic

73
Q

What is polycythemia?

Two types and about them

A

The production on presence of increased numbers of RBC
Primary (vera) or secondary
P- chronic-all BC involved=viscosity and volume= meglys and clotting
S-hypoxia driven or independent
driven-Hypoxia stimulates EPO
S-independent- tumor is making EPO
There is no splenomeg with secondary

74
Q

S/S of primary polycythemia

A

HA, vertigo, tinnitus, visual changes
pruitus, paresthesia, erythromelagia-buring and red of hands and feet
angina, HF, intermittent claudication, clot issues hypoxia and stroke
Hyperuricemia, hemorrhage, ulcers, meylofibrosis, leukemia,

75
Q

One lab difference between primary and secondary poly

Tx

A

Primary-Low to normal EPO
secondary- high
Phlebotomy to normalize Hematocrit

76
Q

Thrombocytopenia and drugs and types

A

Accelerated platelet destruction or myelosuppressant- Chemo
Immune-Body sees themas a threat
Thrombic- hemolytic anemia, thrombocytopenia and neuro-fever w/o infection, renal problesms. TTp-von wil is not normal size it is big and clots- medical emerg
Heparin-

77
Q

S/S of thrombocytopenia 2

A

echymoses, buccal bleeding,

78
Q

Care for Imune thrrombocytopenia -4

General Two

A

Coritosteroids or splenectomy immunoglobbin, immunosuppressants
Corticosteroids and replace platelets if emergent

79
Q

Leukemia

Acute vs chronic

A

Gen term to describe cancer of blood and blood related areas -bone marrow, lymph, spleen.
all ages
Acute and chronic- cell maturity and nature of disease
Acute- Malignant transformation of HPO cell
chronic-more mature WBC- Gradual

80
Q

What are the acute vs chronic leukemias?

A

All-acute lyphoctic l. AML- acute myelogenous (granulocyte) CML Chromnic myeloid l CLL-chronic lymphocyte l
Most common is AML

81
Q

Lymphoma

A

Hodg-Hodg cells proliferate in the nodes age specific 15-30 Ebstein barr, HIV . reed sternberg cells
non hodg- Lrg group b t natural killers, no RSC b cell is most common type