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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
Tumour Angiogenesis
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
26
Invasion And Metastasis
Multi-step process Increased matrix degradation by proteolytic enzymes Altered cell-to-cell and cell-to- matrix adhesion
27
Modes Of Spread Of Cancer
Local spread Lymphatic spread Blood spread Trans-coelomic spread
28
what is Trans-coelomic Spread
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
29
what are common sites of metastasis
``` Liver Lung Brain Bone Axial skeleton Adrenal gland Omentum/ peritoneum ```
30
what are Uncommon Sites | Of Metastasis
Spleen Kidney Skeletal muscle Heart
31
Local Effects Of | Benign Tumours
Pressure | Obstruction
32
Local Effects Of | Malignant Tumours 1
``` Pressure Obstruction Tissue destruction Ulceration/infection Bleeding Anaemia Haemorrhage ```
33
Local Effects Of Malignant Tumours 2
``` Pain Pressure on nerves Perineural infiltration Bone pain from pathological fractures Effects of treatment ```
34
Systemic Effects Of Malignant Tumours
``` Weight loss-cancer cachexia Secretion of hormones “Normal” “Abnormal”/inappropriate Paraneoplastic syndromes Effects of treatment ```
35
Hormone Production | By Tumours 1
“Normal” - produced by tumours of endocrine organ | But abnormal control of hormone production/secretion
36
Hormone Production | By Tumours 2
“Abnormal”/inappropriate | Produced by tumour from an organ that does not normally produce hormone
37
what does the hormone ACTH link to what specific tumour
lung cancer
38
what does the hormone ADH link to what specific tumour
lung cancer
39
Dysplasia 1
Pre-malignant change | Earliest change in the process of malignancy that can be visualised
40
Dysplasia 2
Identified in epithelium No invasion But can progress to cancer
41
Features Of Dysplasia
``` Disorganisation of cells Increased nuclear size Increased mitotic activity Abnormal mitoses Grading of dysplasia High grade Low grade No invasion ```
42
Early Detection Of Cancer
Requires effective test Sensitive/specific Acceptable Cervical cancer screening
43
what are external factors of cell cycle control
Hormones, growth factors, cytokines, stroma
44
what are intrinsic factors of cell cycle control
critical checkpoints prior to restriction point progress through G1 depends on external stimuli after restriction point progression becomes autonomous
45
what checkpoint is for cell size inadequate
G1 or G2 arrest
46
what checkpoint is for nutrient supply inadequate
G1 arrest
47
what checkpoint is for Essential external stimulus lacking
G1 arrest
48
what checkpoint is for the DNA is not replicated
S arrest
49
what checkpoint is for DNA damage is detected
G1 or G2 arrest
50
what checkpoint is for Chromosome mis-alignment
M-phase arrest
51
what are catalytic subunits called
cyclin-dependent kinases (CDKs
52
regulatory sub-units are called ...
cyclins
53
what do Active CDK/cyclin complexes do
phosphorylate target proteins
54
what does Phosphorylation results in
activation/inactivation of that substrate
55
are cyclins destroyed aas the cycle progresses?
yes
56
what is the function of CDK inhibitors (CKIs)
regulate cell cycle
57
what bind to CDK4 and 6 and prevent association of these CDKs with their cyclin regulatory proteins
INK4A family
58
what does The Retinoblastoma gene encode
110 kDa phosphoprotein (pRb)
59
what is pRb
hypophosphorylated
60
what is the most important target
E2F transcription factor
61
how is E2F inactivated
Hypophosphorylated/active Rb
62
whats the affinity between Phosphorylated/inactive pRb and E2F
low
63
what causes a brake to the cell cycle
Active pRb
64
how is carcinogenesis caused?
by mutation of genetic material that upsets the normal balance between proliferation and apoptosis (cell death)
65
purine and pyrimidine bases in DNA are critically damaged by what
various oxidizing and alkylating agents
66
what is produced from Chemical carcinogens or their active metabolites react with DNA
forming covalently bound products (DNA adducts)
67
Adduct formation at particular chromosome sites causes what
cancer
68
the primary defect in cancer is
Uncontrolled cell proliferation via | cell cycle dysregulation
69
whats the importance of cyclins/CDK/CDKIs
Many genes mutated in cancer regulate the cell cycle Two regulatory pathways frequently disrupted - The cyclin D-pRb-E2F pathway 2. p53 pathway
70
what happens when pRb is abscent or inactive
releases the cell cycle brake
71
whats the function of p53
``` 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
what happens when p53 is mutated
can not repair dan and prliferates malignant cells

principles of disease (39 decks)

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