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principles of disease > tumour pathology > Flashcards

tumour pathology Flashcards

1
Q

whats a tumour

A

abnormal growing mass of tissue

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2
Q

what are the two groups of tumours

A

benign and malignant (cancer)

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3
Q

whats cancer

A

ability to invade into adjacent tissue and to metastasise (spread) and grow at other sites within the body”

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4
Q

what is the benign form of glandular

A

adenoma

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5
Q

what is the benign form of squamous

A

squamous papilloma

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6
Q

what is the malignant form of glandular

A

Adeno- Carcinoma

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7
Q

what is the malignant form of squamous

A

squamous carcinoma

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8
Q

what are the benign and malignant forms of bone

A

B- osteoma

M- osteo-sarcoma

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9
Q

what are the benign and malignant forms of fat

A

lipoma

lipo-sarcoma

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10
Q

what are the benign and malignant forms of fibrous

A

fibroma

fibro-sarcoma

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11
Q

what are the malignant forms of lymphoid tissue

A

lymphoma

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12
Q

what are the benign and malignant forms of melanocyte

A

naevus

melanoma

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13
Q

whats the tumours in central nervous system

A

Astrocytoma

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14
Q

whats the tumours in peripheral nervous system

A

Schwannoma

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15
Q

are Ovarian teratomas usually benign or malignant

A

benign

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16
Q

are Testicular teratomas usually benign or malignant

A

malignant

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17
Q

what are fetures of benign and malignant tumours 1

A

Growth pattern
Presence of capsule
Invasion
Presence of metastases

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18
Q

what are fetures of benign and malignant tumours 2

A

Differentiation
Appearance of tumour cells
Function
Behaviour

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19
Q

Features Of

Benign Tumours 1

A

Non-invasive growth pattern
Usually encapsulated
No evidence of invasion
No metastases

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20
Q

Features Of

Benign Tumours 2

A

Cells similar to normal
Benign tumours are “well-differentiated”
Function similar to normal tissue
Rarely cause death

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21
Q

Features Of

Malignant Tumours 1

A

Invasive growth pattern

No capsule or capsule breached by tumour cells

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22
Q

Features Of

Malignant Tumours 2

A 
Cells abnormal
Cancers often “poorly differentiated”
Loss of normal function
Often evidence of spread of cancer
Frequently cause death
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23
Q

what are the Properties Of Cancer Cells 1

A

Loss of tumour suppressor genes
Adenomatous polyposis (APC)
Retinoblastoma (Rb)
BRCA1

Gain of function of oncogenes
B-raf
Cyclin D1
ErbB2
c-Myc
K-ras, N-ras
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24
Q

what are the Properties Of Cancer Cells 2

A 
Altered cellular function
Abnormal morphology
Cells capable of independent growth
But no single feature is unique to cancer cells
Tumour biomarkers
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25
Q

Tumour Angiogenesis

A

New blood vessel formation by tumours
Required to sustain tumour growth
But provides route for release of tumour cells into circulation
More blood vessels in a tumour equals poorer prognosis

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26
Q

Invasion And Metastasis

A

Multi-step process
Increased matrix degradation by proteolytic enzymes
Altered cell-to-cell and cell-to- matrix adhesion

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27
Q

Modes Of Spread Of Cancer

A

Local spread
Lymphatic spread
Blood spread
Trans-coelomic spread

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28
Q

what is Trans-coelomic Spread

A

Special form of local spread
Spread of tumour cells across body cavities e.g. pleural or peritoneal cavities
Tumours of lung, stomach, colon and ovary show trans-coelomic spread

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29
Q

what are common sites of metastasis

A 
Liver
Lung
Brain 
Bone
Axial skeleton
Adrenal gland
Omentum/ peritoneum
30
Q

what are Uncommon Sites

Of Metastasis

A

Spleen
Kidney
Skeletal muscle
Heart

31
Q

Local Effects Of

Benign Tumours

A

Pressure

Obstruction

32
Q

Local Effects Of

Malignant Tumours 1

A 
Pressure
Obstruction
Tissue destruction
Ulceration/infection
Bleeding
Anaemia
Haemorrhage
33
Q

Local Effects Of Malignant Tumours 2

A 
Pain
Pressure on nerves
Perineural infiltration
Bone pain from pathological fractures
Effects of treatment
34
Q

Systemic Effects Of Malignant Tumours

A 
Weight loss-cancer cachexia
Secretion of hormones
“Normal”
“Abnormal”/inappropriate
Paraneoplastic syndromes
Effects of treatment
35
Q

Hormone Production

By Tumours 1

A

“Normal” - produced by tumours of endocrine organ

But abnormal control of hormone production/secretion

36
Q

Hormone Production

By Tumours 2

A

“Abnormal”/inappropriate

Produced by tumour from an organ that does not normally produce hormone

37
Q

what does the hormone ACTH link to what specific tumour

A

lung cancer

38
Q

what does the hormone ADH link to what specific tumour

A

lung cancer

39
Q

Dysplasia 1

A

Pre-malignant change

Earliest change in the process of malignancy that can be visualised

40
Q

Dysplasia 2

A

Identified in epithelium
No invasion
But can progress to cancer

41
Q

Features Of Dysplasia

A 
Disorganisation of cells
Increased nuclear size
Increased mitotic activity
Abnormal mitoses
Grading of dysplasia
High grade
Low grade
No invasion
42
Q

Early Detection Of Cancer

A

Requires effective test
Sensitive/specific
Acceptable
Cervical cancer screening

43
Q

what are external factors of cell cycle control

A

Hormones, growth factors, cytokines, stroma

44
Q

what are intrinsic factors of cell cycle control

A

critical checkpoints

prior to restriction point progress through G1 depends on external stimuli

after restriction point progression becomes autonomous

45
Q

what checkpoint is for cell size inadequate

A

G1 or G2 arrest

46
Q

what checkpoint is for nutrient supply inadequate

A

G1 arrest

47
Q

what checkpoint is for Essential external stimulus lacking

A

G1 arrest

48
Q

what checkpoint is for the DNA is not replicated

A

S arrest

49
Q

what checkpoint is for DNA damage is detected

A

G1 or G2 arrest

50
Q

what checkpoint is for Chromosome mis-alignment

A

M-phase arrest

51
Q

what are catalytic subunits called

A

cyclin-dependent kinases (CDKs

52
Q

regulatory sub-units are called …

A

cyclins

53
Q

what do Active CDK/cyclin complexes do

A

phosphorylate target proteins

54
Q

what does Phosphorylation results in

A

activation/inactivation of that substrate

55
Q

are cyclins destroyed aas the cycle progresses?

A

yes

56
Q

what is the function of CDK inhibitors (CKIs)

A

regulate cell cycle

57
Q

what bind to CDK4 and 6 and prevent association of these CDKs with their cyclin regulatory proteins

A

INK4A family

58
Q

what does The Retinoblastoma gene encode

A

110 kDa phosphoprotein (pRb)

59
Q

what is pRb

A

hypophosphorylated

60
Q

what is the most important target

A

E2F transcription factor

61
Q

how is E2F inactivated

A

Hypophosphorylated/active Rb

62
Q

whats the affinity between Phosphorylated/inactive pRb and E2F

A

low

63
Q

what causes a brake to the cell cycle

A

Active pRb

64
Q

how is carcinogenesis caused?

A

by mutation of genetic material that upsets the normal balance between proliferation and apoptosis (cell death)

65
Q

purine and pyrimidine bases in DNA are critically damaged by what

A

various oxidizing and alkylating agents

66
Q

what is produced from Chemical carcinogens or their active metabolites react with DNA

A

forming covalently bound products (DNA adducts)

67
Q

Adduct formation at particular chromosome sites causes what

A

cancer

68
Q

the primary defect in cancer is

A

Uncontrolled cell proliferation via

cell cycle dysregulation

69
Q

whats the importance of cyclins/CDK/CDKIs

A

Many genes mutated in cancer regulate the cell cycle

Two regulatory pathways frequently disrupted -

The cyclin D-pRb-E2F pathway

  1. p53 pathway
70
Q

what happens when pRb is abscent or inactive

A

releases the cell cycle brake

71
Q

whats the function of p53

A 
Maintains genomic integrity
 p53 levels increase in damaged cells 
 induces cell cycle arrest at G1
 facilitates DNA repair 
 severe damage: p53-induced apoptosis (programmed cell death)
72
Q

what happens when p53 is mutated

A

can not repair dan and prliferates malignant cells

principles of disease (39 decks)

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