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MAD Exam 1 > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

neoplasia

A

abnormal tissue mass with uncoordinated, excessive growth; 3 defining criteria:
1) autonomous
2) clonal
3) proliferative

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2
Q

autonomous characteristic of neoplasia

A

growth independent of physiological signals

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3
Q

clonal characteristic of neoplasia

A

series of acquired mutations affecting a cell and ALL of its progeny

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4
Q

proliferative characteristic of neoplasia

A

mutations give neoplastic cells survival/growth advantage

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5
Q

benign neoplasms

A

1) localized and well-defined (may be encapsulated)
2) do NOT spread to other sites
3) growth usually recapitulates normal structures (cells look normal, relative to the tissue they are in)

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6
Q

benign neoplasms - nomenclature

A

-oma added to the cell of origin
*adenoma = benign glandular epithelial tumor
*fibroma = benign fibroblast tumor
*chondroma = benign cartilage tumor
*osteoma = benign bone tumor

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7
Q

papillary

A

visible fingerlike projections

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8
Q

polyp

A

visible projection above mucosa with a stalk

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9
Q

cystic

A

cyst/cavitary centers

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10
Q

malignant neoplasms

A

1) ill-defined growth
2) invasive (spread to and destroy adjacent structures)
3) metastasize (spread to non-contiguous, distant sites)
*requires interventional therapy

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11
Q

malignant neoplasm - nomeclature

A

*carcinoma = epithelial origin
(ex. adenocarcinoma, squamous cell carcinoma)
*sarcoma = mesenchymal origin
(ex. fibrosarcoma, liposarcoma)

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12
Q

differentiation of benign neoplasms

A

well-differentiated (close resemblance to normal)

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13
Q

differentiation of malignant neoplasms

A

*wide range of differentiation:
-well differentiated = closest resemblance to normal
-moderate = some resemblance to normal
-poor = little resemblance to normal
-undifferentiated = anaplasia, NO resemblance to normal

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14
Q

pleomorphism

A

variation in size/shape of cells (all cells look different from each other)

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15
Q

anaplasia characteristics

A

-pleomorphism
-abnormal nuclear morphology
-mitoses (increased and atypical)
-loss of polarity
-ischemic necrosis

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16
Q

metaplasia

A

replacement of one differentiated tissue with another
-chronic stress leads to reprogrammed stem cells
-typically reversible cell change
*precursor to malignancy

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17
Q

dysplasia

A

-“disordered growth”
-increased pleomorphism and increased mitotic activity
-may be reversible
*precursor to malignancy

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18
Q

typical sequence from normal to neoplastic

A

normal <-> hyperplasia <-> dysplasia <-> carcinoma

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19
Q

invasion

A

infiltration or destruction of surrounding tissues
(ex. mucosal layer invading the serosa of a tissue)
-sign of malignant (benign are non-invasive)

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20
Q

metastasis

A

spread of a tumor to physically distant, discontinuous sites
*unequivocally marks a neoplasm as malignant
*most reliable feature distinguishing malignant from benign

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21
Q

pathways of dissemination of metastasis

A
  1. seeding of body cavity or organ surfaces
  2. lymphatic spread
  3. hematogenous spread
22
Q

seeding & metastasis

A

*involving an open body cavity
*peritoneal cavity is most common, but could also be pleural, pericardial, subarachnoid, etc

23
Q

lymphatic spread & metastasis

A

*invade lymphatics to involve draining lymph nodes
**most common pathway for CARCINOMA dissemination
*pattern of nodal involvement follows natural lymphatic drainage (breast cancer to axillary nodes; lung cancer to hilar/mediastinal nodes)

24
Q

hematogenous spread & metastasis

A

*direct invasion of blood vessels
**most common pathway for SARCOMA dissemination
*follow blood flow (veins more common than arteries; liver and lungs are most frequent sites of metastasis)

25
Q

radiation and oncogenesis

A

UV radiation: mutations in oncogenes, tumor suppressor genes, formation of thymidine dimers
ionizing radiation: depends on type, length of exposure, etc

26
Q

microbial agents and oncogenesis

A

-HPV & Epstein-Barre viruses (EBV)
-H. pylori

27
Q

HPV oncogenesis

A

HPV can induce expression of oncoproteins
-E6: degrades p53, preventing apoptosis; activates telomerase
-E7: allows progression in cell cycle (binds RB and displaces E2F; blocks p21 and p27)
OVERALL EFFECT: immortalizes epithelial cells

28
Q

EBV oncogenesis

A

-allows inappropriate expression of latency-phase genes
-EBNA and LMP

29
Q

oncogenes

A

mutations in oncogenes turn them on and endow cell with self-sufficiency in growth; genes that accelerate cells and tell them to proliferate; “gain of function” process
*ONLY ONE COPY NEEDS TO BE MUTATED

30
Q

growth factors

A

oncogenes that induce cellular growth
-some tumors induce autocrine loop, in which they synthesize the same growth factors to which the cell is responsive
-ex = PDGF (brain cancer)

31
Q

growth factor receptors

A

oncogenes that mediate growth factor signals
-activation by growth factors cause dimerization and phosphorylation signaling cascade substrates
*constitutively dimerized/activated mutant receptors can be on without growth factor
*overexpression of normal forms of growth factor receptors

32
Q

signal transducers

A

oncogenes that mediate signals to nucleus into different cascade events; mutations become “trapped” in active form

33
Q

transcription factors

A

oncogenes that orchestrate the mitotic cycle

34
Q

cell cyclers

A

oncogenes that orchestrate the cell cycle

35
Q

tumor suppressor genes

A

mutations that lead to failed response to growth inhibitory signals; “loss of function” process that stops cellular proliferation
*BOTH COPIES MUST BE MUTATED

36
Q

RB (retinoblastoma) gene

A

common tumor suppressor gene
-normal function = regulate G1-S transition
-mutations allow tumor cells to enter S phase unchecked
**require a DOUBLE HIT (both copies must be knocked out)

37
Q

TP53 gene

A

common tumor suppressor genes
-normal function = slow down cell cycling in response to DNA damage, allowing repair or apoptosis
-mutations lead to no cell cycle arrest in tumor cells
**requires a DOUBLE HIT (both copies must be knocked out)

38
Q

apoptosis regulators

A

disruption leads to immortalization of cells via evasion of cell death
-ex = BCL2 inhibits apoptosis; normally turned OFF in cells, but tumors can upregulate this gene and therefore they don’t undergo apoptosis

39
Q

other features of oncogenesis

A

-replicative immortalization via upregulated telomerase (allows cells to continue to proliferate over time)
-angiogenesis to supply nutrients to tumor cells (tumor upregulates angiogenic factors)
-escape of immunosurveillance (down-regulate MHC class I)

40
Q

warburg effect

A

tumor cells shift their metabolism to favor glycolysis, even with adequate oxygen, because it provides them a lot of other nutrients; provides a growth advantage in hypoxic tumor microenvironment; characteristic “glucose hunger” of tumor cells can be identified via PET scans

41
Q

local problems associated with neoplasms

A

-space-filling can lead to obstruction
-tissue compression can lead to dysfunction and destruction
-surface ulceration can lead to bleeding and secondary infection

42
Q

systemic problems associated with neoplasms

A

-cachexia
-paraneoplastic syndromes

43
Q

paraneoplastic syndrome

A

clinical signs/symptoms that result from substances produced by the tumor and occurring remotely
include:
-hypercalcemia
-endocrinopathies
-hypercoagulability

44
Q

tumor grade

A

pathology morphologic assessment (level of differentiation)
*low grade = well differentiated (better)
*high grade = poorly differentiated / anaplastic

45
Q

tumor staging

A

determines the extent of SPREAD using the TMN system

46
Q

TNM system

A

T = tumor size
N = node involvement
M = metastases

47
Q

T (tumor size) of TMN system

A

T0 = in situ (non-invasive)
T1-T4 = increasing tumor size

48
Q

N (node involvement) of TMN system

A

N0 = no regional lymph node involvement
N1 to N3 = increasing number of involved lymph nodes

49
Q

M (metastases) of TNM system

A

M0 = no distant metastases
M1 = distant metastases

50
Q

tumor markers

A

biochemical indicators of a tumor’s presence that are detectable in plasma

51
Q

examples of tumor markers

A

-mucins (CA125, CA19-9)
-oncofetal antigens (AFP, CEA)
-specific proteins (PSA, immunoglobulins)

MAD Exam 1 (20 decks)

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