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
Why do we classify tumors?
To communicate, prepare and evaluate a tx plan, determine prognosis, compare groups, and stratify risk
26
``` Autonomic what is it? Epithelial connective nervous lymph plasma bone marrow ```
``` 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 ```
27
What is histologic grading
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
28
Cancer staging | and what we don't use this for
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
29
TMN classification
T tumor-primary tumor size and extent N- nodes M- Metastasis Not for leukemia or blood , brain, spinal cord, bone marrow, lymphoma
30
One nursing thing
Avoid high nitrate concentrations
31
CAUTION
``` 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 ```
32
What are the tx for cancer 6
Surgury, radiation, chemo, immunotherapy, targeted therapy, hormone therapy
33
What is personalized medicine
When genetic info to guide tx, diagnosis,
34
What is targeted therapy
Targets cancer specific genes or prots that contribute to growth
35
Risks for chemo 3
Venous access prob, infection, extraversion
36
What is regional chemo
Directly into tumor site and few side effects
37
What is intraarterial and intravesical
Through art that are supplying the tumor and into the bladder
38
What are the delayed issues with chemo
mucositis, radh, bone marrow suppression, neurotox, C/D, organ damage cancer can become resistant
39
Brachytherapy
Internal radiation seeds or ribbon used chronic lesss harmful acute need to have care in place.
40
One thing about raditaion
CAn be PO attached to antibodies and attach to cell
41
ALARA
As low as reasonably achievable
42
Risks for patients for chemo and radiation
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
Skin issues with radiation
no hot/cold Dry-Aloe Wet des- Infection risk! sailine or vaseline
44
What are secondary cancers | What are the high risk groups
leukemia, angiosarcoma, skin Patients tx with alk agents or hogh dose raditation does not CI risk
45
What is immunotherapy aka what do they do drugs?
Uses the bodies immune system biological therapy boost, or attack cancer using cytokines, vaccines, monocolonal antibodies-specific to antibodies mab drugs
46
What is targeted therapy EFGR? One thing about target
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
Side effects of immunotherapy and target 4
Flu-like- fluids Tachy and ortho Capillary leak-pulm edema and edema CNS, organ issues
48
Nursing care with target and immuno 3
effects are acute and dose dependent Fear to talk about SE-stop tx Stop TX on own because of SE
49
Hormone therapy
Stops the hormones that cancer cell make
50
Hematopoietic growth factors and about eyrthropoietin
Help support patients using colony stimulating factors that help blood cells Eyrthro- Only when treating anemia specifically chemo
51
``` Hematopoietic stem cell transplant aka 1 ben 1 prob types For what cancer? ```
``` 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
Complications from stem cell
Infection, grapht vs host disease- T cells from donated marrow attack body
53
Gene therapy
Experimental therapy genetic material is placed into person cells
54
Fighting nutrition issues with cancer 3
weigh twice a week nut counseling if losing more than 5 percent weight watch albumin
55
Fighting dysgeusia 5
Plastic, it makes food bitter, oral care more water food they like
56
Cancer Cachexia
Anorexia and. unintentional loss of weight
57
One big thing to report
TEMP! 100.4
58
Oncologic emergencies
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
causes of superior vena cava syndrome s/s that you don't know tx
Presences of venous cath or medialstinal radiation HA, Seizure raditation
60
What causes cardiac tamp
Radiation
61
Thrombocytopenia numbers
tcp-150,000 bleed risk prolonged- 50,000 spontaneous bleed 20,000
62
neutrophills mature vs immature
segmented-mature bands immature
63
spleen
Hematopoiesis, filtration-filteres RBC Storage of IRON and about 1/2 platelets
64
What cells do blood cell come from?
Myeloid and lymphoid
65
Values for blood
Plasma 55 | eryth 45
66
What is an immature rbc called
reticulocyte | 48 hours to mature
67
Where is iron stored? recycled?
Bone marrow, liver, spleen, | macrophages in liver and spleen
68
which cells are phagocytes
MEN
69
What cells are humoral response and cellular
B cell production- lymphocyte | monocyte
70
What cells are allergic
Basophils
71
clotting | platelet cell life
``` vascular injury Adhesion Activation Aggregation platelet plug formation clot dissolution 8-11 ```
72
Spleen 4 things
Storage, immune, filtration, hematopoietic
73
What is polycythemia? | Two types and about them
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
S/S of primary polycythemia
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
One lab difference between primary and secondary poly | Tx
Primary-Low to normal EPO secondary- high Phlebotomy to normalize Hematocrit
76
Thrombocytopenia and drugs and types
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
S/S of thrombocytopenia 2
echymoses, buccal bleeding,
78
Care for Imune thrrombocytopenia -4 | General Two
Coritosteroids or splenectomy immunoglobbin, immunosuppressants Corticosteroids and replace platelets if emergent
79
Leukemia | Acute vs chronic
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
What are the acute vs chronic leukemias?
All-acute lyphoctic l. AML- acute myelogenous (granulocyte) CML Chromnic myeloid l CLL-chronic lymphocyte l Most common is AML
81
Lymphoma
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