cancer and heme important Flashcards

1
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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2
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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3
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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4
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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5
Q

CEP

FP

A

Carcenoembryonic antigen is a tumor cell protein

Alpha fetoprotein

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6
Q

What do cytotoxic t cells do

A

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

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7
Q

Monocytes

A

Release other cytokines, tumor necrosis factor

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

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8
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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9
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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10
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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11
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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12
Q

One thing about raditaion

A

CAn be PO attached to antibodies and attach to cell

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13
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

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14
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

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15
Q

Side effects of immunotherapy and target 4

A

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

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16
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

17
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

18
Q

Complications from stem cell

A

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

19
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

20
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

21
Q

Thrombocytopenia numbers

A

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

22
Q

neutrophills mature vs immature

A

segmented-mature bands immature

23
Q

What cells do blood cell come from?

A

Myeloid and lymphoid

24
Q

Where is iron stored? recycled?

A

Bone marrow, liver, spleen,

macrophages in liver and spleen

25
Q

which cells are phagocytes

A

MEN

26
Q

What cells are humoral response and cellular

A

B cell production- lymphocyte

monocyte

27
Q

clotting

platelet cell life

A
vascular injury 
Adhesion 
Activation 
Aggregation 
platelet plug formation
clot dissolution 
8-11
28
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

29
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,

30
Q

One lab difference between primary and secondary poly

Tx

A

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

31
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-

32
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

33
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