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principles of disease > tumour pathology 1-5 > Flashcards

tumour pathology 1-5 Flashcards

1
Q

what is a benign glandular epithelium called

A

adenoma

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2
Q

what is a malignant glandular epithelium called

A

adeno-carcinoma

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3
Q

what is a benign squamous epithelium called

A

squamous

papilloma

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4
Q

what is a malignant squamous epiyhelium called

A

squamous carcinoma

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5
Q

what is a benign bone cancer called

A

osteoma

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6
Q

what is a malignant bone cancer called

A

osteo-sarcoma

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7
Q

what is a benign fat tumour called

A

lipoma

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8
Q

what is a malignant fat tumour called

A

lipo-sarcoma

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9
Q

what is a benign fiborous tumour called

A

fibroma

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10
Q

what is a malignant fibtous tissue called

A

fibro-sarcoma

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11
Q

is there a benign white blood cell tumour

A

no

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12
Q

what’s the name of a malignant WBCs cancer (more specificly bone marrow)

A

leukaemia

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13
Q

what are the types of tumour in lymphoid tissue

A

no Benign

malignant = lymphoma

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14
Q

what are the cancers associated with melanocytes

A

naevus - benign

melanoma - malignant

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15
Q

what are the tumours in the central nervous system

A

Astrocytoma

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16
Q

what are the tumours in the peripheral nervous system

A

Schwannoma

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17
Q

what are germ cell tumours called

A

Teratomas

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18
Q

what are teratomas made off

what is the difference between ovarian and testicular

A

various tissue

ovarina teratoma is benign

testicular teratoma is usually malignant

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19
Q

what are the features and ‘‘break out’’ of a malignant tumour

A

invasive
can have the presence of a capsule however BREACHING will ocur

poorly differentiated
loss of normal function

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20
Q

what are the type of tumours that are well differntiated

A

benign

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21
Q

what is the top 3 cancers overall

A

breast then lung then prostate

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22
Q

what are the top - 5yr survivable cancers

A

melanoma - 90
breast - 85
prostate - 85
uterus - 80

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23
Q

what are the properties of cancer cells releated to genes

A

loss of suppressor genes

gain of function of oncogenes

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24
Q

what are some of the suppressor genes

A

APC
Retinoblastoma
RAC1

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25
Q

what are some of the oncogenes

A

B-raft

Cyclin D1

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26
Q

what are the other properties of cancer

A

altered function
independent/unregulated growth
tumour biomarkers

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27
Q

what is important to remember about cancer cell properties

A

no single feature is unique to cancer cells

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28
Q

how is cell function altered

A

loss of cell to cell adhesion

cell to extracellular matrix is lost

production of tumour biomarkers

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29
Q

what are tumour bio markers used for

A

Screening
Diagnosis
Prognostic
Predictive - response to therapy

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30
Q

what dose the biomarker kras detect

A

colorectal cancer

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31
Q

what dose braf detect

A

melanoma

‘bra your skins messed up’

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32
Q

what dose EGFR detect

A

lung cancer

EGs Fucking Resps

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33
Q

what dose Her 2 detect

A

BREAST CANCER, gastric cancer

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34
Q

what dose a Carcino-embryonic antigen (CEA)

suggest

A

colorectal cancer

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35
Q

what dose the presence Alpha-fetoprotein

A

Hepatocellular carcinoma

Teratoma of testis(malignant)

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36
Q

what happens to the morphology of a cancer cell

A

cellular and nuclear pleomorphism

variation in shape and size

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37
Q

what are the two factors that control tumour growth

A

angiogenesis

apoptosis

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38
Q

what is tumour angiogenesis

A

new blood vessel formation by tumour

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39
Q

why is tumour angiogenesis important

A

required to sustain tumour growth
route of metastasis

more blood vessel = poorer prognosis

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40
Q

what is apoptosis

A

Mechanism of programmed single cell death

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41
Q

what dose it regulate and what is it involved in

A

regulates tumour growth

involved in chemotherapy and radiotherapy

42
Q

what is the basic out line of tumour spread

A

normal tissue – tumour – metastasis

43
Q

what is trans-coelomic spread

A

type of local spread

across body cavities
pleural/peritoneal cavities

44
Q

what are the modes of spread

A

local
lymphatic
blood
trans-coelomic

45
Q

what is local spread

A

invasion into the connective tissue

46
Q

they site of metastasis is..

A

not related to tissue blood flow

47
Q

what is a metastatic niche

A

the role played by a tumour depending on its characteristics and tissue

48
Q

what are the most common metastasis locations

A

Liver
Lung
Brain

49
Q

where are the least like spread

A

Spleen
Kidney
Skeletal muscle

50
Q

where dose breast and prostate canner commonly metastasise

A

in the bone

51
Q

what are the local effects of a benign tumours

A

pressure and obstruction

52
Q

what dose a benign tumour usually put pressure on

A

the GI tract

blood vessels

53
Q

what are the local effects of malignant tumours

A

pressure
obstruction

tissue destruction
bleeding

Pain

54
Q

what dose the bleeding caused by malignant tumours do

A

lead to haemorrhage

lead to anaemia

55
Q

what does the tissue destruction caused by malignant tumours lead to

A

ulceration and infection

56
Q

what can the pain of a malignant tumour be down to

A

pressure on nerves

perineural infiltration bone fractures

57
Q

what tumours have systemic effects

A

malignant tumours

58
Q

what are the systemic effects of a malignant tumour

A

weight loss
secretion of hormones
paraneoplastic syndromes

EFFECTS CAUSED BY TREATMENT

59
Q

how dose cancer effect hormone secretion

A

normal hormones produced - however volume is all over the place (endocrine)

abnormal - a hormone that usually isn’t produce from the organ

60
Q

what are the two hormones that are abnormal for lung cancer

A

ACTH

ADH

61
Q

what are Paraneoplastic Syndromes

A

no one really knows

symptoms in tissues nowhere near the tumour site

immune mechanism

62
Q

why is it important to detect cancer early

A

Reduce/prevent morbidity/mortality

63
Q

what has been identified when a caner is detected at a pre-invasive stage

A

dysplasia

intraepithelial neoplasia

64
Q

what is Dysplasia

how is it graded

A

a pre-malignant change (earliest pin of detection)

high grade - develop into cancer sooner

low grade - develop into cancer later

65
Q

where is it identified and

A

Identified in epithelium
No invasion
But can progress to cancer

66
Q

what are its features

A

disorganisation of cells
Increased nuclear size

Increased mitotic activity

Abnormal mitoses

67
Q

what is a intra-epithelial neoplasia

A

is the development of a HIGH GRADE dysplasia

68
Q

what dose early detection require

A 
Requires effective test
Sensitive/specific
Acceptable
cheap 
political backing
69
Q

what is an example of early detection

A

Cervical Cancer Screening

reduce incidence of squamous carcinoma of cervix

detects dysplastic cells in that region

70
Q

what is the basic process of the cell cycle

A

inter phases
mitosis
cytokinesis

m1, s, m2 
P
M
A
T 
cytokinesis
71
Q

what is G0

A

a stage of dormancy

72
Q

how do CDKs work

A

cyclin binds and lets them phosphorylate subunit which allows the cycle to continue

73
Q

what are CKIs

A

inhibitor molecules that bind to the cyclin/CDK complexes

what are some examples p16/p21

74
Q

what is the Retinoblastoma gene

A

Encodes a phosphoprotein (pRb) expressed in almost every human cell

the breaks

75
Q

what happens when pRB is hypophosporlyated

A

it becomes active and

cell stays at G1

76
Q

how are the breaks turned off

A

when the cDK/cyclin complexes pRB

77
Q

what happens when pRB is phosphorylated

A

it looses affinity to E2F

78
Q

what is E2F

A

powerful signal for cell cycle activation

79
Q

what is the process of carcinogenesis

A

Uncontrolled proliferation of cells forms tumours

80
Q

what are the two frequently disrupted pathways in carcinogenesis

A

the cyclin/CDK complex—pRB–E2F pathway

p53 pathway

81
Q

what dose p53 detect

A

DNA damage

82
Q

what dose NORMAL p53 do

A

detects damage
and either repairs
activates p21 (CDK inhibitor)
or kills the cell

83
Q

what dose BAX do

A

cause cell death apoptosis

84
Q

what happens if p53 is mutated

A

leads to the DEREGULATED proliferation of cells that have damaged DNA

85
Q

how is the cyclin/CDK–pRB- E2F pathway stopped

A

the tumour suppressor gene turns off the production of pRB

86
Q

what do cells with mutated p53 proliferate to form

A

malignant neoplasms

87
Q

what factors can cause carcinogenesis

A

Environmental agents
Chemicals
Radiation
Oncogenic viruses

Inherited factors

88
Q

what are proto-oncogenes

A

a normal gene that codes for normal growth regulation

growth factors and their receptors

89
Q

what is the two hit hypothesis

A

in a video game everyone has two lives but some people only have one

its the hypothesis that certain mutations occur more often if people who have been given a copy of a mutated gene

90
Q

an example of the two hit hypothesis

A

inherited retinoblastoma

91
Q

what are tumour suppressor genes

how will cancer occur

example

A

anti-oncogenes
act as the emergency elevator breaks

Loss of both normal allelic copies

p53

92
Q

how may people inherit cancer

what will it look like

A

5-10%

early onset of multiple tumours

93
Q

what do p16s do

what cancer occurs if they mutate

A

inhibits CDKs

malignant melanoma

94
Q

what are oncogenes

A

Derived from proto-oncogenes with gain of function

alteration of structure - point mutation or translocation

overexpression

95
Q

what is BRAC1/2

A

a tumour suppressor gene

96
Q

what is an example of a proto-oncogene

what dose it do

how is it activated

A

Her2 -

EGF receptor
VEGF
amplification
lead to breast ovarian and gut

97
Q

how dose chemical carcinogenesis occur

A

DNA is critically damaged by oxidizing and alkylating agents - it binds to the DNA (adducts)

leading to the loss of anti-oncogenes and the mutation of proto-oncogenes

98
Q

what is Radiation carcinogenesis

A

as it says on the tin

DNA damage

99
Q

what are Viral carcinogenesis

examples

A

viruses insert genome with a oncogene
or something that mutates a proto-oncogene

HPV - genital
HEP B - liver

100
Q

how is tumour formation is a multi-step process

what is needed

A

sporadic cancers need
several oncogenes
loss of anti-oncogenes

happens with mutations over time

101
Q

what are examples of anti oncogenes

A

p16, cyclin D, CDK4, Rb

principles of disease (18 decks)

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