Heme and cancer Flashcards
What are undifferentiated cells called? and what happens when they die?
Stem cells. They tell new cells to proliferate
What is dynamic equilibrium
When cell death is equal to cell growth
What do normal cells do? 3
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
What things do cancer cells do? 7
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
Doubling time
Time it takes for the tumor to double in size
Apoptosis
Programmed cell death
What are protoncogogenes 4
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
Oncogene proteins
are located?
2 ex
and one more thing they produce
Located on the cell membrane
in blood tests
CEA and Fetalprot
produce hormones
What are tumor decreasing genes
What happens to them during cancer
Two examples and about them
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
What is ACP gene
Tumor suppressor gene that can have a Family mutation gene for adenomatous
polyposis- colorectal cancer
Model of development of cancer
Initiation- Inherited or acquired
Promotion- Reversible proliferation
Progression-possible metastasis tumor growth
Initiation
What is it?
What about inherited?
What about acquired- 3 examples
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
Latent period and when does it happen?
the time between genetic alteration and actual evidence of cancer can be yrs-decades
In promotion
When are cancer cells evide?
! cm palp
0.5 MRI
Promotion
What are some reversible promoters?
obesity, smoking, alcohol, dietary fat.
What is a complete cancinogen? example
they are capable of promoting and initiating cancer
cig smoke
What cancers does alcohol cause?
Recommended drinks for men and women
Heavy drinking
week for m and w
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
What are some common spots for mat of cancer 6
Brain, cerebral fluid, lung, liver, adrenals, bone
CEP
FP
Carcenoembryonic antigen is a tumor cell protein
Alpha fetoprotein
What do cytotoxic t cells do
Produce cytokine, interleukin 2 y interferon- stimulates other t interleukin cells
Monocytes
Release other cytokines, tumor necrosis factor
and colony stimulating factor- work on bone marrow to stimulate WBC
How do cancer cells evade immune response?
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
What are the oncofetal antigens and how do we use them what are they 2
Tumor antigens from cell in the fetal state
use them as tumor markers
CEA and AFP
Classification
Benign vs malignant
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
Why do we classify tumors?
To communicate, prepare and evaluate a tx plan, determine prognosis, compare groups, and stratify risk
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
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
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
TMN classification
T tumor-primary tumor size and extent
N- nodes
M- Metastasis
Not for leukemia or blood , brain, spinal cord, bone marrow, lymphoma
One nursing thing
Avoid high nitrate concentrations
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
What are the tx for cancer 6
Surgury, radiation, chemo, immunotherapy, targeted therapy, hormone therapy
What is personalized medicine
When genetic info to guide tx, diagnosis,
What is targeted therapy
Targets cancer specific genes or prots that contribute to growth
Risks for chemo 3
Venous access prob, infection, extraversion
What is regional chemo
Directly into tumor site and few side effects
What is intraarterial and intravesical
Through art that are supplying the tumor and into the bladder
What are the delayed issues with chemo
mucositis, radh, bone marrow suppression, neurotox, C/D, organ damage
cancer can become resistant
Brachytherapy
Internal radiation seeds or ribbon used chronic lesss harmful acute need to have care in place.
One thing about raditaion
CAn be PO attached to antibodies and attach to cell
ALARA
As low as reasonably achievable
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
Skin issues with radiation
no hot/cold
Dry-Aloe
Wet des- Infection risk! sailine or vaseline
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
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
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
Side effects of immunotherapy and target 4
Flu-like- fluids
Tachy and ortho
Capillary leak-pulm edema and edema
CNS, organ issues
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
Hormone therapy
Stops the hormones that cancer cell make
Hematopoietic growth factors and about eyrthropoietin
Help support patients using colony stimulating factors that help blood cells
Eyrthro- Only when treating anemia specifically chemo
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
Complications from stem cell
Infection, grapht vs host disease- T cells from donated marrow attack body
Gene therapy
Experimental therapy genetic material is placed into person cells
Fighting nutrition issues with cancer 3
weigh twice a week
nut counseling if losing more than 5 percent weight
watch albumin
Fighting dysgeusia 5
Plastic, it makes food bitter, oral care more water food they like
Cancer Cachexia
Anorexia and. unintentional loss of weight
One big thing to report
TEMP! 100.4
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
causes of superior vena cava syndrome
s/s that you don’t know
tx
Presences of venous cath or medialstinal radiation
HA, Seizure
raditation
What causes cardiac tamp
Radiation
Thrombocytopenia numbers
tcp-150,000
bleed risk prolonged- 50,000
spontaneous bleed 20,000
neutrophills mature vs immature
segmented-mature bands immature
spleen
Hematopoiesis, filtration-filteres RBC Storage of IRON and about 1/2 platelets
What cells do blood cell come from?
Myeloid and lymphoid
Values for blood
Plasma 55
eryth 45
What is an immature rbc called
reticulocyte
48 hours to mature
Where is iron stored? recycled?
Bone marrow, liver, spleen,
macrophages in liver and spleen
which cells are phagocytes
MEN
What cells are humoral response and cellular
B cell production- lymphocyte
monocyte
What cells are allergic
Basophils
clotting
platelet cell life
vascular injury Adhesion Activation Aggregation platelet plug formation clot dissolution 8-11
Spleen 4 things
Storage, immune, filtration, hematopoietic
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
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,
One lab difference between primary and secondary poly
Tx
Primary-Low to normal EPO
secondary- high
Phlebotomy to normalize Hematocrit
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-
S/S of thrombocytopenia 2
echymoses, buccal bleeding,
Care for Imune thrrombocytopenia -4
General Two
Coritosteroids or splenectomy immunoglobbin, immunosuppressants
Corticosteroids and replace platelets if emergent
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
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
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
