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Pathophysiology > Chapter 5 - Neoplasia > Flashcards

Chapter 5 - Neoplasia Flashcards

1
Q

What is neoplasisa?

A
  • “new growth”
    • implies abnormality of cellular growth/tumor
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2
Q

What is malignant neoplasm?

A
  • cancer
  • associated with altered expression of cellular genes
  • not always surviveable
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3
Q

True or false: benign growths are generally easily cured.

A

true

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4
Q

A ____ tumor has few mitosis, a slow growth rate, strictly local, no metastasis, rare tumor necrosis, rare recurrence, good prognosis.

A

benign

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5
Q

A ______ tumor is anaplastic with abnormal cell shape and size, has many mitoses, rapid growth rate, frequent metastases, common tumor necrosis, common recurrence.

A

malignant

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6
Q

What does this picture show?

A
  • anaplastic tumor cells showing variation in cell size, shape, and large hyperchomatic nuclei
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7
Q

____ suffix indicates benign tumor (adenoma)

A

-oma

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8
Q

true or false: carcinoma and sarcoma are malignant tumors

A

true

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9
Q

What is the origin of a carcinoma?

A

epithelial (i.e. adenocarcinoma)

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10
Q

What is the origin of a sarcoma?

A

mesenchyma (i.e. nerve, bone, muscle)

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11
Q

What is the origin of leukemia?

A

white blood cells

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12
Q

Lymphomas, hepatomas, and melanomas are all (benign/malignant) forms of tumors.

A

malignant

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13
Q

How do you decipher between a benign and malignant tumor?

A
  1. asymmetry
    • beningn = symmetrical
    • malignant = asymmetrical
  2. border
    • benign = even edges
    • malignant = uneven edges
  3. colour
    • benign = one shade
    • malignant = two or more shades
  4. diameter
    • benign= < 6 mm
    • malignant = > 6 mm
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14
Q

_____ allows the malignant cells to ignore growth controlling signals

A

malignant phenotype

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15
Q

What is the 2nd leading cause of death in the U.S.?

A

cancer

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16
Q

___% of cancer deaths occur in individuals over age 55

A

77%

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17
Q

True or false: men have a 1 in 2 risk of developing cancer; women have a 1 in 3 risk.

A

true

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18
Q

What is the 5-year cancer survival rate?

A

68%

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19
Q

______ of cancer-related deaths may be attibutable to lifestyle factors (i.e. tobacco use, nutrition, obesity, sun exposure, sexual exposure to HPV)

A

1/3

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20
Q

What is the leading cause of cancer related death in men and women?

A

lung cancer

  • worst survival rate
  • death rate increased
  • second-hand smoke increases risk
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21
Q

What are the two types of carcinogens found in tobacco smoke?

A
  • initiator (genetic damage)
  • promoter (promotes tumor growth)
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22
Q

Which 4 dietary factors are believed to be related to cancer risk?

A
  1. fat
  2. fiber
  3. alcohol
  4. antioxidants
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23
Q

What are the dietary suggestions with regards to reducing cancer risk?

A
  • limit excessive calorie and alcohol intake
  • increase dietary fiber, fruit and vegetables
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24
Q

What is a carcinogen?

A
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25
Q

potential cancer causing agent

A
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26
Q

What is a proto-oncogene?

A
  • enhance growth-producing pathways
  • normal cellular genes that can be transformed into oncogenes by activating (gain-of-function) mutations
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27
Q

What is an oncogene?

A

a proto-oncogene in its mutant overactive form

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28
Q

What is a tumor suppressor gene?

A
  • inhibits cell proliferation
  • cancers may arise when tumor suppresor gene function is lost or abnormally inhibited
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29
Q

What do gain-of-function mutations code for?

A
  • growth factors
  • receptors
  • cytoplasmic signaling molecules
  • nuclear transcription factors
30
Q

What are growth factors (mitogens)?

A

manufactured peptides secreted into extracellular space –> diffuse to nearby cells –> interact with recepters on target surface –> activate signaling cascade –> produce autocrine signaling

31
Q

What are growth factor receptors?

A
  • transmembrane proteins
    • mitogen-binding on area outside of cell
    • enzyme-activating area on inside of cell
  • binding activates cell proliferation
32
Q

What happens when there is a mutation of growth factor receptors?

A
  • expression of receptors that should not be there
  • excessive amount of normal receptors
  • receptors with abnormally high affinity
33
Q

What are cytoplasmic signalling pathways?

A
  • numerous enzymes and chemicals that transmit signals from receptors at cell surface to nucleus
  • mutant proto-oncogene can activate pathway even when no signal is at the cell surface
    • ras gene: mutations lead to cancer
      • RAS protein stimulates growth in presence of GTP but turned on in malignant cells
34
Q

What are transcription factors?

A
  • proteins that must be assembled at the promoter area to begin gene transcription
    • normally sequestered and prevented from discriminate activity until appropriate signals cause their release
    • mutations cause overproduction of transcription factors which interfere with normal functions
      • mvc gene: mutations lead to cancer
35
Q

True or false: mutations in the ras and mcv genes can lead to cancer

A

true

36
Q

When do proto-oncogenes become activated?

A

when mutations alter their activity so that prolifeation-promoting signals are generated inappropriately

37
Q

What are the 4 general ways for proto-oncogenes activation?

A
  1. oncogenes introduced to host by retrovirus
  2. proto-oncogenes within cell suffers mutagenic event
  3. DNA sequence lost/damaged allowing oncogene to become abnormally active
  4. error in chromosome replication causes extra copies of proto -oncogene in genome
38
Q

What is a retrovirus?

A
  • composed of RNA
  • contains reverse transcriptase enzyme
    • direct synthesis of a DNA copy of viral RNA
    • DNA copy incorporates into host cell DNA
    • becomes part of host genome
39
Q

______ comes from the HIV retrovirus

A

Kaposi’s sarcoma

40
Q

______ comes from the epstein-barr virus

A

burkitt lymphoma

41
Q

______ comes from human t-lymphocyte virus type 1

A

adult t-cell leukemia/lymphoma

42
Q

What are tumor-suppressor genes?

A
  • “BRAKE” to regulate cell growth and prevent mutations
    • slow cell cycle
    • inhibit proliferation of cells due to GFs (growth factors)
    • stop proliferation if cells damaged
43
Q

Rb, BRMRE, and APC tumor all compromise:

A) proto-oncogenes

B) oncogenes

C) tumor-supressor genes

D) none

A

C

44
Q

What happens when tumor-suppressor genes are inactivated by mutations?

A

removes BRAKE on cell proliferation causing cell to proliferate uncontrollably

45
Q

What is the Rb gene?

A
  • “master brake” for cell cycle
  • blocks/stops cell division
    • binds TFs (transcription factors)
    • inhibits factors from transcribing genes that initiate cell cycle
46
Q

What happens when the Rb gene becomes inactivated?

A
  • removes brake that stops cell division causing replication to occur
47
Q

What is the p53 gene?

A
  • most common tumor-suppressor gene
  • normally inhibits cell cycling
    • accumulates after DNA is damaged and binds to DNA to stall division to allow DNA to repair itself
    • may direct cell to apoptosis
  • mutated or damaged p53 allows genetically damaged/unstable cells to survive and continue to replicate
48
Q

More than 1/2 of all types of human tumors lack functional ____.

A

p53

49
Q

true or false: cancer cells that lack functional p53 may be resistant to chemotherapy/radiation

A

true

50
Q

_____ and ____ are tumor suppressor genes associated with breast cancer.

A

BRCA1 and BRCA2

51
Q

Which BRCA gene is associated with family history and increase risk of breast cancer?

A

BRCA1

52
Q

What are the three steps involved in cancer development?

A
  1. initiation
    • via inappropriately active proto-oncogenes or inactive tumor suppresor genes
  2. promotion
    • stage during which mutant cell proliferates
      • activation of oncogene
      • inactivation of tumor suppressor gene
      • nutritional factors
      • infection
  3. progression
    • mutant cells exhibit malignant behaviouor
      • laminin receptors
      • lytic enzymes
      • anchorage independent
      • bizarre karyotype
53
Q

_____ carcinogens ar capable of initiating cell damage and promoting cellular proliferation

A

complete

54
Q

_____ carcinogens are promoters that stimulate growth but are incapable of causing genetic mutations sufficient to signly initiate cancer

A

partial

55
Q

How do cells become immortalized?

A
  • telomerase
    • telomeres cap the chromosomes
    • advanced cancer cells activate telomerase to stabilize and protect the telomeres, keeping the chromosome from fragmenting
56
Q

What is metastasis?

A
  • process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites
57
Q

How do cancer cells spread?

A

circulatory or lympathic systems

58
Q

______ help identify parent tissue of cancer origin

A

tumor markers

59
Q

Which of the following are typically used as tumor markers:

A) Enzymes

B) Proteins

C) Carbohydrates

D) All of the above

A

A, B

60
Q

What is angiogensis?

A
  • process by which cancer tumor forms new blood vessels in order to grow
    • does not develop until late stages
    • triggers not understood
    • inhibition of angiogenesis is important therapeutic goal
61
Q

What is the system most widely used when grading & stagint tumors?

A

TNM

T=tumor

N=nodes involved

M=metastasis

62
Q

What is cachexia?

A
  • overall weightloss and weakness
    • loss of appetite
    • increased metabolic rate
    • nausea/vomitting
  • immune suppression
63
Q

_______ contributes to anemia, leukopenia, and thrombocytopenia and is due to invasion and destruction of bone marrow, poor nutrition, annd chemotherapy

A

bone marrow suppression

64
Q

______ is deficiency in circulating red blood cells.

A

anemia

65
Q

What is leukopenia?

A
  • deficiency in circulating white blood cells
  • caused by malignant invasion of bone marrow via malnutrition and chemotherapy
  • may cause suspension of chemotherapy treatment until WBC count reovers
66
Q

What is thrombocytopenia?

A
  • deficiency in circulating platelets
    • important mediators in blood clotting
    • predispose to hemorrhage if count is below 20,000
67
Q

What are paraneoplastic syndromes?

A
  • tumor production of hormones or cytokines
    • hypercalcemia (excess calcium)
    • cushing syndrome via ACTH secretion
    • hyponatremia and water olverload due to ADH secretion (low sodium)
68
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69
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70
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71
Q
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72
Q
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Pathophysiology (6 decks)

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