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NUR 339 ( LATEST 2024 / 2025 ) EXAM 2 | COMPLETE ANSWERS 100% CORRECT $15.99
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NUR 339 ( LATEST 2024 / 2025 ) EXAM 2 | COMPLETE ANSWERS 100% CORRECT

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NUR 339 ( LATEST 2024 / 2025 ) EXAM 2 | COMPLETE ANSWERS 100% CORRECT

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NUR 339 EXAM 22

1. What is proliferation?


Orderly process that provides body with means for re- placing cells as needed

- Usually number of cells dying = number of cells proliferating

2. What is differentiation?


Process by which proliferating cells are transformed into specialized cell types, which
determines cell function

- The more highly specialized a cell, the more likely it will lose its ability to reproduce and
divide
- Stem cells remain incompletely differentiated throughout life
- Highly specialized cells that don't reproduce and divide ->> nerve cells, heart cells

3. What is Anaplasia?


Lack of cell differentiation

4. What are the Cell Cycle Phases and what happens in each?


G0- resting phase (becomes mitotically dormant)

G1- Gap 1. Cell prepares to make DNA
S phase- DNA synthesis actually takes place (most mutations occur in this phase) G2- Prepares
for mitosis (cell division)
M phase- mitosis occurs

5. What is Neoplasms?


Do not obey normal tissue growth/adaption laws






- Do not occur in response to appropriate stimulus
- Continue to grow after stimulus has ceased
- Function independently of body's needs (faster growth rate, increase in size at expense of rest
of body's needs, great variation in cell size, shape, arrangement)

6. What is Benign Neoplasm?

Composed of well-differentiated cells that resemble cells of tissues of origin

- Slow growth rate
- Remain localized to site of origin without capacity to infiltrate, invade, or metasta- size
- May become encapsulated
- Less blood supply than malignant neoplasm
- Usually do not cause death unless interfere with vital functions because of their location
- Can cause alterations in body function through abnormal alternation of hormones

7. What is Malignant Neoplasm?


Atypical cell structure; abnormal nucleus & chromosomes

- Lose differentiation or resemblance to origin cell--more anaplastic (lack cell differ- entiation)
- Not cohesive, irregular growth pattern, no capsule formed, not distinct from sur-

rounding tissue
- Invade adjacent cells rather than pushing aside
- Varying growth rates and do not die within normal timeframe
- More blood supply than normal tissue (angiogenesis)

- Hallmark Sign of malignancy


ability to metastasize or spread to distant sites

8. What is Metastasis?


Ability of cancer cells to spread to distant sites




- Clumps of malignant cells break off and travel through blood (hematogenic spread) or lymph
(lymphatic spread) to new site - most are killed by body's defense mecha- nisms
- To survive in a tumor you need a host. To metastasize, you need to travel.

9. Metastasis in lymph nodes


- In lymph nodes, cancer may die, grow into mass, or remain dormant

Sentinel node

initial lymph node to which primary tumor drains (used to determine spread to lymph system)

- Cells in a primary tumor develop that ability to escape and travel in the blood or lymph
- Surviving cancer cells leave lymph nodes and enter venous blood and are carried to major
organs (bone, liver, lungs, brain)
Original tumor= primary neoplasm
Metastatic site= secondary neoplasm (retains characteristics or primary tumor)

10. What is Growth fraction (GF)?


Ratio of dividing cells / G0 cells

- A tissue with a large % of proliferating cells and few cells in G0 has a high growth fraction.
- Chemotherapeutic drugs are much more toxic to tissues that have a high growth fraction than
to tissues that have a low growth fraction

11. What is Doubling Time (TD)?


Time to double total mass of cancer cells

- GF and TD are very fast until tumor outgrows blood supply, then slows
- May be influenced by hormones
- High TD is good (takes longer to double in size)

12. What are Proto-oncogenes?


Normal genes that regulate cell growth & differentiation & are active for only a short time in

, с


cell cycle

13. What are Oncogenes?


Gene mutations which become cancer-causing genes; are active continuously & promote
unregulated, abnormal & disordered growth

14. What is Oncogenesis?


Mechanism by which a normal cell is transformed into cancer cell by random genetic mutation
or mutation induced by exposure carcinogens

- Is a monoclonal origin

15. What are Tumor Suppressor Genes?


Anti-oncogenes

- Normally inhibit inappropriate cell growth - start senescence and crisis or cell

growth
Senescence- cells stop dividing. In response to growth inhibiting proteins like P53 Crisis- cells
death
- Abnormal tumor suppressor genes are inherited or mutant genes

16. Describe the stages of cancer growth


Initiation

Exposure of cells (especially those actively synthesizing DNA) to enough carcinogens that alter
cell's genome-ir- reversible mutation

Promotion

Induction of unregulated accelerated growth by some agent, chemical, or endogenous hormone

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