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PRINCIPLES OF FUN > tumour pathology > Flashcards

tumour pathology Flashcards

1
Q

what is a tumour (neoplasm)?

A

abnormal growing mass of tissue, the growth of which is uncoordinated with normal tissue

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2
Q

what will happen to the tumour growth if any stimulus which may have caused the tumour to form is removed?

A

it will continue

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3
Q

is tumour growth irreversible?

A

true

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4
Q

what two types of tumour are there?

A

benign

malignant

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5
Q

what separates malignant (cancer) tumours from benign ones?

A

malignant tumours have the ability to invade adjacent tissue and to metastasise to other sites within the body

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6
Q

what are the 3 most common cancers for males?

A

prostate
lung
colon

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7
Q

what are the 3 most common cancers for females?

A

breast
lung
colon

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8
Q

what are the 3 most common overall cancers?

A

breast
lung
colon

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9
Q

how are tumours classified?

A

based on tissue of origin

benign vs malignant

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10
Q

what are the names for benign and malignant glandular tumours?

A

benign: adenoma
malignant: adenocarcinoma

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11
Q

what are the names for benign and malignant tumours of squamous epithelium?

A

benign: squamous papilloma
malignant: squamous carcinoma

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12
Q

what are the names for benign and malignant tumours of the bone?

A

benign: osteoma
malignant: osteosarcoma

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13
Q

what are the names for benign and malignant tumours affecting fat tissue?

A

benign: lipoma
malignant: lipo-sarcoma

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14
Q

what are the names for benign and malignant tumours affecting fibrous tissue?

A

benign: fibroma
malignant: fibro-sarcoma

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15
Q

what is the name given to malignant cancer of the blood?

A

leukaemia

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16
Q

what is the name given to malignant cancer of the lymphoid tissue?

A

lymphoma

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17
Q

what are the names of tumours of the central and peripheral nervous system

A

CNS: astrocytoma
PNS: schwannoma

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18
Q

what is the difference between ovarian and testicular teratomas? (germ cell tumours)

A

ovarian usually benign, testicular usually malignant

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19
Q

what are the features of benign tumours?

A 
non invasive growth pattern
usually encapsulated
no evidence of invasion
no metastases
cells similar to normal cells
cells function similarly to normal tissues
well differentiated
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20
Q

what are the features of malignant tumours?

A 
invasive growth pattern
no capsule or capsule breached by tumour cells
cells are abnormal
poor differentiation
loss of normal function
evidence of spread of cancer
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21
Q

what are some properties of cancer cells?

A

altered genetics
altered cellular function
abnormal morphology
cells are capable of independent growth

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22
Q

what are some examples of the altered genetics of cancer cells?

A

loss of tumour suppressor genes

increased function of oncogenes

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23
Q

what are the examples of altered cellular function of cancer cells?

A

production of tumour related proteins
loss of cell-cell adhesion
altered cell-matrix adhesion

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24
Q

what are some biomarkers indicative of cancer cells?

A

onco-fetal proteins
oncogene products
growth factors and receptors

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25
Q

what is alpha-fetoprotein indicative of?

A

teratoma of testis

hepatocellular carcinoma

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26
Q

what is carcino-embryonic antigen (CEA) indicative of?

A

colon cancer

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27
Q

what is oestrogen receptor indicative of?

A

breast cancer

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28
Q

what is her2 indicative of?

A

breast cancer

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29
Q

what is prostate specific antigen indicative of?

A

prostate cancer

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30
Q

what is the histological appearance of cancer cells?

A

cellular and nuclear pleomorphism (marked variation in size and shape)
mitoses are present and often abnormal

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31
Q

what are the two processes relating to cell growth and cell death that occur in tumour growth?

A

angiogenesis

apoptosis

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32
Q

what is the pathology of tumour angiogenesis?

A

new blood vessel formation by tumours
required to sustain tumour growth
new blood vessels provide a route for release of tumour cells into circulation
the higher the number of blood vessels in a tumour the poorer the prognosis

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33
Q

what is apoptosis and what is its role in tumour pathology?

A

programmed single cell death
regulates tumour growth
involved in the reponse to chemo/radiotherapy

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34
Q

what is the major clinical problem associated with cancer?

A

formation of metastatic tumours

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35
Q

what are some modes of cancer spreading?

A

local spread
lymphatic spread
blood spread
trans-coelomic spread

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36
Q

how would a tumour manage to spread into the blood/lymphatic system?

A

invasion into the connective tissue is followed by invasion into the lymphatic system/bloodstream

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37
Q

describe the process of tumour metastasis via lymphatics

A

tumour cells adhere to lymph vessels
tumours invade lymphatic system and then invade lymph nodes
formation of metastasis in lymph node
clinical evidence of metastasis

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38
Q

describe the process of tumour metastasis via blood?

A

adherence of tumour cells to blood vessels, followed by invasion into blood vessels
invasion of tumour cells into tissue
formation of metastasis
clinical evidence of metastasis

39
Q

what happens in trans-coelomic spread?

A

spread of tumour cells across body cavities

40
Q

what are some example of tumours that show trans-coelomic spread?

A

lung
stomach
colon
ovary

41
Q

what are some common sites of metastasis?

A 
liver
lung
brain
bone (axial skeleton)
adrenal gland
42
Q

what are some uncommon sites of metastasis?

A

spleen
kidney
skeletal muscle
heart

43
Q

where do tumours of breast tissue commonly metastasis do?

A

bone and lung

44
Q

where do tumours of the prostate commonly metastasis to?

45
Q

where do tumours of the colon commonly metastasise to?

46
Q

what are some local effects of benign tumours?

A

pressure and obstruction

47
Q

what are some local effects of malignant tumours?

A 
pressure
obstruction
tissue destruction
bleeding (anaemia, haemorrhage)
pain
adverse effects of treatment
48
Q

why can malignant tumours cause pain?

A

pressure on nerves
perineural infiltration
bone pain from pathological fractures

49
Q

what are systemic effects of malignant tumours?

A

secretion of hormones ( can be normal or abnormal)
weight loss- cachexia
paraneoplastic syndromes
effects of treatments

50
Q

what are paraneoplastic syndromes?

A

a syndrome that is the consequence of cancer in the body but is not due to the local presence of cancer cells (such as inappropriate hormone secretion)

51
Q

what is “normal” hormone production from tumours?

A

when hormones are produced by tumours of endocrine organs (however there is abnormal control of hormone production/secretion)

52
Q

what is abnormal/inappropriate hormone production from tumours?

A

when hormones are produced by tumours of an organ that does not normally produce hormones (such as ACTH being produced in lung cancer)

53
Q

what is dysplasia?

A

pre malignant change which is the earliest stage that the process of malignancy can be visualised

54
Q

what are some features of dysplasia?

A

it is identified in the epithelium
no invasion
can progress to cancer
disorganisation of cells

55
Q

what would you see at a cellular level in dysplasia?

A

increased nuclear size
increased mitotic activity
abnormal mitoses

56
Q

what is the cell cycle?

A

time interval between mitotic divisions

57
Q

what are some external factors that control the cell cycle?

A

hormones, growth factors, cytokines, stroma

58
Q

what are some intrinsic factors that control the cell cycle?

A

critical checkpoints- restriction point (R)

59
Q

what is the significance of the restriction point?

A

prior to the restriction point progress through G1 depends on external stimuli
after the restriction point the cell cycle progresses autonomously

60
Q

what are the phases of the cell cycle?

A

quiescent - G0
interphase - G1, S, G2
cell division - mitosis (M)

61
Q

when would the cell cycle be arrested in G1?

A

if the cell size is inadequate
if the nutrient supply is inadequate
if an essential external stimulus is lacking
if DNA damage is detected

62
Q

when would the cell cycle be arrested in G2?

A

if the cell size is inadequate

if DNA damage is detected

63
Q

when would the cell cycle be arrested in S?

A

if the DNA is not replicated

64
Q

when would the cell cycle be arrested in M phase?

A

chromosome mis-alignment

65
Q

what are the checkpoints in the cell cycle composed of?

A

system of cyclically active and inactive enzymes

catalytic sub unit activated by a regulatory sub unit

66
Q

what are catalytic subunits of checkpoints called?

A

cyclin dependent kinases

67
Q

what are the regulatory units of checkpoints called?

68
Q

what is the name given to the active enzyme complex at a cell cycle checkpoint?

A

CDK/cyclin complex

69
Q

what do active CDK/cyclin complexes do?

A

phosphorylate target proteins

70
Q

what effect does phosphorylation of target proteins by CDK/cyclin complexes have?

A

activates/inactivates the substrate, substrates regulate events in the next cycle phase

71
Q

what form are CDKs expressed in?

A

inactive form

72
Q

what other group of compounds regulates CDK activity apart from cyclins?

A

CDK inhibitors

73
Q

what family of CKIs bind to CDK 4 and 6?

74
Q

what is carcinogenesis caused by?

A

mutation of genetic material that upsets the normal balance between proliferation and apoptosis

75
Q

mutations of what can cause a cell to lose control of proliferation?

A

cell division, apoptosis and DNA repair

76
Q

formation of what causes cancer at chromosome sites?

77
Q

what is a DNA aduct?

A

covalently bound product formed from when chemical carcinogens or their active metabolites react with DNA

78
Q

what is the primary defect in cancer?

A

uncontrolled cell proliferation via cell cycle dysregulation

79
Q

what are the two regulatory pathways that are frequently disrupted to cause cancer?

A

cyclin D-pRb-E2F pathway

p53 pathway

80
Q

what is the function of the retinoblastoma gene (pRb)

A

to activate or inactivate the E2F transcription factor

81
Q

what is the function of E2F?

A

potent stimulator of cell cycle entry

82
Q

what is the effect of absent or inactive pRb?

A

releases the “brake” on the cell cycle

83
Q

where are virtually all cancers dysregulated?

84
Q

what are the 4 genes that mutate to cause cancer dysregulation at G1-S?

A

Rb, CDK4, cyclin D p16

85
Q

what is the function of p53?

A

maintains genomic integrity:

86
Q

what is the effect of increased p53 in damaged cells?

A

induces cell cycle arrest at G1
facilitates DNA repair
in severe damage - p53 induced apoptosis

87
Q

what is the effect of mutated p53?

A

no G1 arrest and no repair of damaged DNA - leads to the proliferation of genetically damaged cells and the formation of malignant neoplasms

88
Q

what do Rb gene mutations favour?

A

cell proliferation

89
Q

what mutations can mimic the effect of pRb loss?

A

mutational activation of cyclin D or CDK4

mutational inactivation of CDKIs

90
Q

what are some genetic inherited characteristics of inherited retinoblastoma?

A

one defective copy inherited

somatic point mutation of the other copy

91
Q

what are some genetic characteristics of sporadic retinoblastoma?

A

both hits occur in a single cell

92
Q

what are some examples of inherited cancer syndromes?

A

familial retinoblastoma
familial adenomatous polyposis of colon
multiple endocrine neoplasia

93
Q

what are some characteristics of familial cancers?

A

family clustering of cancers but individual presdisposition unclear
multifactorial inheritance
early age of onset
multiple/bilateral tumours

94
Q

what are some examples of familial cancers?

A

some breast and ovarian cancers

PRINCIPLES OF FUN (29 decks)

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