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pathophysiology > neoplasia > Flashcards

neoplasia Flashcards

1
Q

neoplasia aka

A

new growth

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2
Q

tumour aka

A

neoplasm

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3
Q

neoplasm definition

A

a disorder of cell growth that is triggered by a series or acquired mutations affecting a single cell and its clonal progeny

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4
Q

The causative mutations give the neoplastic cells a …

A

survival and growth advantage, which then results in excessive proliferation that is independent of physiologic growth signals

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5
Q

parenchyma

A

a collection of neoplastic cells. Allows us to classify the tumor and its biologic behaviour

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6
Q

reactive stroma

A

comprised of CT, blood vessels, and cells of the immune system. Allows us to determine the rate of growth and its willingness to form metastases

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7
Q

if a tumour has a large proportion of parenchyma cells

A

the tumour will be soft and fleshy

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8
Q

if a tumour is abundant in collagenous stroma

A

the tumour will be stony and hard

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9
Q

benign tumour characteristics

A
  • relatively hard to distinguish between healthy tissue and tumour tissue from a microscopic level
  • the remain localised and do not metastasise
  • are often enclosed in a capsule
  • mostly harmless (but still have potential to be lethal)
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10
Q

benign tumours nomenclature

A

benign tumours are designated by attaching the suffix ‘-oma’ to the name of the cell type from which the tumour originates

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11
Q

chondroma

A

a benign tumour made of hyaline cartilage

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12
Q

osteoma

A

a benign tumour made of bone

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13
Q

lipoma

A

a bengin tumour made of adipose tissue

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14
Q

fibroma

A

a benign tumour originating from fibrous tissues

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15
Q

adenoma

A

a benign epithelial tumour derived from glands

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16
Q

papilloma

A

a benign epithelial tumour producing microscopically or macroscopically visible fingerlike projections

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17
Q

polyps

A

a neoplasm that produces a macroscopically visible projection above a mucosal surface and projects into the lumen of a hollow organ

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18
Q

malignant tumours

A
  • microscopic appearances are not innocent
  • invade and destroy adjacent structures and spread to distant sites (can metastasise)
  • have no capsule
  • if not treated, cause death
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19
Q

malignant tumours nomenclature

A

malignant tumours arising in solid mesenchymal tissues are usually called sarcomas

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20
Q

fibrosarcoma

A

a malignant tumour originating from fibrous tissues

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21
Q

chondrosarcoma

A

a malignant tumour originating from chondrocytes

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22
Q

rhabdomyosarcoma

A

a malignant tumour with mesenchymal origin and showing skeletal muscle differentiation

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23
Q

lymphoma

A

a malignant tumour of lymphocytes or their precursors (in the blood)

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24
Q

carcinomas

A

malignant tumours of epitheial cell origin

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25
Q

squamous cell carcinoma

A

the tumour cells resemble stratified squamous epithelium

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26
Q

adenocaarcinoma

A

the neoplastic epithelial cells grow in a glandular pattern

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27
Q

malignant tumours with term ‘-oma’

A

lymphoma, mesothelioma, melanoma

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28
Q

cell differentiation

A

the extent to which neoplastic parenchymal cells resemble the corresponding normal parenchymal cells, both morphologically and functionally

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29
Q

anaplasia

A

lack of differentiation

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30
Q

pleomorhpism

A

variation of cell size and shape

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31
Q

the likelihood of a primary tumour metastasising correlates with..

A

lack of differentiation, aggressive local invasion, rapid growth, large size

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32
Q

pathways for malignant cells to spread

A
  • direct seeding of body cavities or surfaces
  • lymphatic spread
  • haematogenous spread
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33
Q

sentinel lymph node

A

the first node in a regional lymphatic basin that receives lymph flow from the primary tumour

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34
Q

displasia

A

a disordered growth of cells, often considered a doorstep towards developing cancer.

35
Q

carcinoma in situ

A

when dysplastic changes are marked and involve the full thickness of the epithelium, but the lesion does not penetrate the basement membrane

36
Q

proto-onco genes

A

genes encode proteins that stimulate cell proliferation

37
Q

tumour supressor genes

A

thes genes encode proteins that inhibit cell division and/or repair dna errors

38
Q

clonal evolution of tumour cells

A

an accumulation of complementary mutations in a stepwise fashion over time

39
Q

driver mutations

A

mutations that contribute to the development of the malignant phenotype

40
Q

passenger mutations

A

mutations that have no phenotype consequence

41
Q

the initiating mutation

A

the first driver mutation that starts a cell on the path to malignancy

42
Q

genomic instability

A

loss-of-function mutations in genes that maintain genomic integrity. leads to driver and passenger mutations

43
Q

self-sufficiency in growth signals

A

a hallmark of cancer. capacity to proliferate without external stimuli

44
Q

autocrine loop

A

some cancer cells acquire the ability to synthesize the same growth factors to which they are responsive

45
Q

oncoproteins

A

promote cell growth in the abscence of normal growth-promoting signals

46
Q

insensitivity to growth-inhibitory signals

A

tumours may not respond to molecules that inhibit the proliferation of healthy cells

47
Q

tumour suppressor proteins

A

form a network of checkpoints that prevent uncontrolled growth and may force cells to lose their replicative ability

47
Q

Retinoblastoma (RB)

A

inhibits cell proliferation and controls cellular differentiation

48
Q

familial form retinoblastoma

A

frequent and bilateral blastoma, as it is quit easy for the second hit to occur when born with an already unfunctional allele

48
Q

TP53 protein

A

Considered the ‘Guardian of the genome’ it regulates many cell functions such as:
- cell cycle progression
- DNA repair
- Cellular senescence
- Apoptosis
This gene is only induced in response to cell stress or DNA damage etc.

49
Q

what is the most frequently mutated gene in human cancers?

A

the TP53 gene

50
Q

Malignant transformation

A

an increased likelihood of the emergence of numerous cancer cell clones

51
Q

if a cancer patient is negative in TP53

A

the are relatively resistant to chemotherapy and irradiation

52
Q

altered cellular metabolism

A

a metabolic switch to aerobic glycolysis

53
Q

cancer cell metabolism differs to healthy cells as they

A

have a high glucose uptake, which can be identified in a PET scan

54
Q

warburg effect

A

cancer cells convert glucose to lactose following the fermentation pathway despite the availability of oxygen

55
Q

why do cancer cells undergo an aerobic glycolysis?

A

proliferative cells need both energy and lots of metabolic intermediates due to rapid cell division. thus aerobic glycolysis seems to be the sweet spot that is optimal for growth

56
Q

aerobic glycolysis

A

heavily biased toward aerobic fermentation with a bit of oxidative phosphorylation chucked in

57
Q

evasion of apoptosis

A

tumours are resistant to programmed cell death. cancer cells have found a limitless replicative potential

58
Q

angiogenesis

A

controlled by a balance between angiogenesis promoters and inhibitors

59
Q

sustained angiogenesis in tumours

A

the angiogenic balance in tumours is skewed in favour of the promoters, this allows a blood vessel growth within and around the tumour, supplying blood and therefore nutrients to the cancer cells, enabling the tumour to rapidly proliferate

60
Q

neoangiogenesis

A

when growing cancers stimulate vessels to sprout from previously existing capillaries

61
Q
  1. invasion of the extracellular matrix
A

A carcinoma must breach the underlying basement membrane, transverse the interstitial CT and gain access to the circulation by penetrating the vascular basement membrane

62
Q
  1. Vascular dissemination and homing
A

cancer cells may die in the circulatory system, as the consequence of mechanical shear stress, apoptosis stimulated by loss of adhesion, and innate and adaptive immune defences.

63
Q

How can cancer cells increase their survival whilst in the circulatory system?

A
  • formation of platelet-tumour aggregates
  • tumour cells may bind and activate coagulation factors
  • fibrin coating helps block immune response
64
Q

Immune evasion

A

Cancer cells can ‘hide’ their abnormal (onco-) proteins

65
Q

immune surveillance

A

the immune system constantly ‘scans’ the body for emerging malignant cells and destroys them (via cell-mediated immunity)

66
Q

Genomic instability

A

cancer cells are more prone to mutations

67
Q

cancer-promoting inflammation

A

infiltrating cancers are ‘wounds that do not heal’ and they provoke and maintain a chronic inflammatory reaction

68
Q

Inflammatory cells

A

can modify the local tumour microenvironment and enable many of the cancer hallmarks

69
Q

initiated cell

A

a cell is permanently altered, making it potentially capable of giving rise to a tumour, however it alone is not sufficient for tumour formation

70
Q

promoters

A

chemical agents that can induce tumours to arise from initiated cells and stimulate cellular proliferation, but they are nontumorigenic by themselves

71
Q

direct acting initiators

A

require no metabolic conversion to become carcinogenic

72
Q

indirect acting initiators

A

require metabolic conversion to become active carcinogens. certain metabolic pathways me inactivate the procarcinogen or it derivatives

73
Q

human oncogenic viruses

A

HPV and Hepatitis B Virus

74
Q

How can HPV lead to more genomic instability?

A

some HPV viral proteins interfere with the functions of TP53 and increase telomerase activity

75
Q

Hepatitis B virus

A

the dominant effect seems to be immunologically mediated chronic inflammation and hepatocyte death leading to regeneration and, over time, genomic damage.

76
Q

Helicobacter pylori

A

a bacterium which my induce cancer formation via increased increased epithelial cell proliferation in a background of chronic inflammation

77
Q

cachexia

A

progressive loss of body fat and lean body mass accompanied by profound weakness, anorexia, and anaemia

78
Q

cancer cachexia is associated with

A
  • equal loss of both fat and lean muscle
  • elevated basal metabolic rate
  • evidence of systemic inflammation
79
Q

TNF-α

A

a chemical leading suspect amoung several mediators released from immune cells that may contribute to cachexia

80
Q

malignancy

A

the presence of cancerous cells that have the ability to metastasize or to invade locally and destroy tissues

81
Q

atherosclerosis

A

a chronic inflammatory and healing response of the arterial wall to endothelial injury.
- causes more morbidity and mortality in the western world than any other disease

82
Q
A

pathophysiology (9 decks)

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