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Pathophysiology Exam 2 > Lecture 15 > Flashcards

Lecture 15 Flashcards

1
Q

Benign epithelial tumor

A

-oma

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2
Q

Malignant epithelial tumor

A

-carcinoma

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3
Q

Benign glandular tumor

A

-adenoma

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4
Q

Malignant glandular tumor

A

-adenocarcinoma

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5
Q

Benign mesenchymal tumor

A

-oma

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6
Q

Malignant mesenchymal tumor

A

-sarcoma

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7
Q

Blastoma

A

malignant tumors of embryonic primordia/cells

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8
Q

Glioma

A

malignant tumor that arises from glial cells in CNS

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9
Q

Seminoma

A

malignant tumor for germ cells (testes)

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10
Q

Ewing’s Sarcoma

A

rare type of bone cancer (children and adolescents)

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11
Q

Kaposi’s Sarcoma

A

cancer that causes lesions in skin, lymph nodes (immunosuppression- HIV/AIDS)

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12
Q

Teratoma

A

Benign germ cell tumor

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13
Q

Teratocarcinoma

A

Malignant germ cell tumor

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14
Q

Anaplasia

A

Loss of differentiation and return to more embryonic state

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15
Q

What is staging of tumors based on?

A

Clinical exam, x-ray, biopsy, surgical exploration

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16
Q

International TNM

A

Method for staging: tumor size, lymph node involvement, metastasis

17
Q

What is grading based on?

A

Histological exam (benign or malignant nature)

18
Q

Grade I

A

Well-differentiated

19
Q

Grade II

A

Moderately well differentiated

20
Q

Grade III

A

Undifferentiated

21
Q

What are the hallmarks of cancer?

A
  1. Sustaining proliferative signaling
  2. Evading growth suppressors (genomic instability -> genetic diversity -> expedites acquisition and inflammation)
  3. Activating invasion and metastasis
  4. Enabling replicative immortality
  5. Inducing angiogenesis (formation of new blood vessels from existing ones)
  6. Resisting cells death
22
Q

Tumor Suppressor Genes (TSGs)

A

Provide varied normal inhibitory mechanisms in cell proliferation or apoptosis in defective cells (both copies of TSG must be inactive to eliminate its function)

23
Q

p53

A

Cell damage -> p53 inhibits cell cycle (allows for DNA repair) and induces apoptosis of unwanted cells

24
Q

Proto-Oncogene

A
  • normal cell counterpart of oncogene (regulate growth activating pathway
  • overactivity predisposes to cancer development
25
Q

Burkitt’s Lymphoma

A
  • C-Myc (t(8:14))
  • Non-hodgkin lymphoma
26
Q

C-Myc (t(8:14))

A

-C-Myc proto-oncogene
- Overexpression of c-Myc oncogene
- Myc codes for transcription factor that binds to DNA of other gene
- Immunoglobulin gene on chromosome 14 increases activity of translocated C-Myc gene (if adjacent) -> lymphoma

27
Q

Carcinogenesis

A
  1. Conversion of potentially harmful substance (procarcinogen) to carcinogen
  2. INITIATION: Carcinogen formed induces irreversible changes (DNA mutations)
  3. PROMOTION: initiated cells stimulated to proliferate (continuous exposure to carcinogen or to another non carcinogen growth promoter)
  4. CONVERSION: Promoters must be applied until cells acquire ability to proliferate on own and convert to new cell type
  5. PROGRESSION: converted cells acquire new genetic features, expand and progress to form clones that do not regress even after promoter or carcinogen removed
  6. CLONAL EXPANSION: clones rapidly grown (identical)
  7. Proliferation of divergent clones that arise by mutation of unstable tumor cells genome (tumor cell heterogeneity)
  8. Selection favors most vital clone that adapts to adverse condition and outgrows all others
28
Q

What are the three pathways of metastasis?

A
  1. Lymphatics
  2. Blood (hematogenous)
  3. Seeding surface of body cavity
29
Q

Autocrine motility factors

A

signaling molecules produced by cancer cells that promotes their own movement and invasiveness

30
Q

What are the steps of metastasis?

A
  1. Primary tumor
  2. Metastatic clone evolves
  3. Proliferation of clone and invasion of vessel
  4. Transport by circulation
  5. Embolization
  6. Invasion
  7. New tumor formation

Pathophysiology Exam 2 (8 decks)

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