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Year 2: EMS > Cancer > Flashcards

Cancer Flashcards

(106 cards)

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1
Q

Cancer

A

uncontrolled cells that can grow and spread to different parts of the body

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2
Q

Tumour

A 
Abnormal swells (not necessarily cancer) 
same as neoplasm
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3
Q

Neoplasm

A

Lesion = autonomous growth or relative abnormal growth of cells that then persists in absence of stimulus

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4
Q

Histogenesis

A

The differentiation of cells into specialist tissues and organs

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5
Q

Histogenic Classification of Tumours (definition)

A

The cell, tissue or organ of origin - NOT the organ/ tissue it is now in (mets)

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6
Q

Most common cancers (4) in order

A

Breast/Prostate
Lung
colorectal

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7
Q

Most fatal (4) in order

A

Lung
Prostate/ breast
Colorectal

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8
Q

Classification of tumours - rate of growth (3 ways)

A

Doubling time (number of cells double)
% cells in replicating pool
Rate at which cells die/ shed

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9
Q

Differentiation

A

the extent that neoplasmic cells represent normal parenchymal cells
BOTH morphologically and functionally

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10
Q

Grade? = how differentiated?

A

Grade 1 = well differentiated
Grade 2 = moderate differentiated
Grade 3 = poorly differentiated
Grade 4 = anaplastic (not differentiated)

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11
Q

Pleomorphic

A

cells the vary in shape and size (from normal cells)

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12
Q

Abnormal nuclei

A

Can be too large

Vary in shape

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13
Q

Chromatin distribution variation (3)

A

Coarsely clumped
Along cell membranes
Hyperchromatism = stain darkly

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14
Q

Abnormal Mitosis? Mitosis = indicator of proliferation and turn over rate

1) asymmetrical bikaryokineses
2) Trikaryokineses
3) tetrapolar division
4) Multipolar

A

1) asymmetrical separation of condensed chromosomes
2) organisation of chromosomes into 3 groups
3) organisation of chromosomes into 4 groups
4) Multiply spindle fibres

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15
Q

Loss of polarization?

A

orientation of cells disturbed

disorganized growth

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16
Q

Classification of tumours by invasion? (stage)
Benign
Malignant

A

Benign = encapsulated expansible mass, no infiltration or mets

Malignant = local invasion into adjacent structures, no boundaries, mets

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17
Q

Metastasis? (staging)

A

Spread of tumour to site NOT physically attached to site of origin

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18
Q

Mets are associated with? (5)

A 
Poorer prognosis
Less differentiation
increased size
local invasion
rapid growth
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19
Q

Met pathways (3)

A

Direct seeding
Lymphatic drainage
Venous pathway

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20
Q

Direct seeding met process?
Transcoelomic
eg. Colonic cancers

A

Penetration natural open field (eg. Open cavity) and remain adhere to surface with in it - eg. peritoneal mets

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21
Q

Lymphatic spread mets process?

A

Follow lymph node drainage

Senital nodes –> distant nodes

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22
Q

Stroma ?

A

connective tissue framework the solid tumours are embedded in
Contains blood vessel, lymphatics, fibro and myofibroblasts

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23
Q

Desmoplasmic reaction?

A

stroma formation due to fibroblast proliferation by growth factors from tumours

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24
Q

Complications - local?

A

Compression eg. pituitary on CN2 = visual defects

Destruction eg. ulceration on mucosal surfaces

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25
Complications - metabolic? General (4) Specific
General = cachexia (weaknes), Neuropathies and loss of endocrine function, myopathies (muscle fibers) Specific examples for neurological and endocrine
26
Histological classification of tumours
Make up the names include reference to: | Cell type - tissue type - benign or malignant
27
Pampilloma
Bengin non glandular surface epithelial tumour (cell type before)
28
Adenoma
Benign tumour of the Glandular endothelial (Tissue type before)
29
Carcinomas
Malignant non glandular surface epithelial tumour (add cell type before)
30
Adenocarcinomas
Malignant glandular epithelial tumour
31
Urothelial carcinoma
Malignant epithelial bladder cancer
32
Benign mesenchymal (connective tissue) tumour
__ oma (proceeded by tissue of origin)
33
Sarcomas
Malignant mesenchymal (connective tissue) tumour - proceeded by tissue of origin
34
Liposarcoma
Malignant tumour of adipose
35
osteoma
benign tumour of bone
36
Melanocytic lesions
pigment tumour of the epidermis
37
Benign Melanocytic lesion
Melanocytic naevi - freckles or patchy pigments of skin
38
Melanoma - Malignancy measured by ABC?
asymmetrical shape, irregular Boarders and inconstant Colour
39
Leukaemias
cancers of blood cells or in the bone marrow
40
Lymphomas
lymph nodes and solid organs BUT also lymphocytes in blood (cross over with leukaemias)
41
Myeloma
plasma cells tumour
42
Special features of brain tumours (3)
Can not break through basement membrane Can't metastasise BUT can have mets in it (from elsewhere) Benign tumours are very harmful due to increase ICP
43
Examples of Brain and CNS tumours (4)
Meningiomas astrocytomas oligodrendroglioma Pituitary tumours
44
Where do germ cell tumours normally arise
Gonades | Midline - due to germ cell migration
45
Ovarian Germ cell tumours
dysgerminoma
46
Sperm germ cell tumours
seminoma
47
Embryonal tumours - resembled? named after?
pediatric tumors of not fully differentiated cells | Resemble to embryonic cells of the organ it is destined to be BUT named after organ of origin
48
_blastomas
``` Emryonal tumours (due to not being fully differentiated) Preceeded with tissue of origin ```
49
Harmatomas
non neoplastic tissue overgrowth = benign Confused with tumours Insidious and idiopathic
50
Choristoma
heterotopic - tissue types in the wrong site. | Non neoplastic and benign
51
Primary
tumour is at site of origin
52
Secondary (met)
not at site of origin BUT still named after primary tissue type/ organ
53
Cancers of unknown primary source (3 reasons)
Occult primary - unknown or too small to see Migrating pre malignant stem cells Regressed primary tumour
54
Malignant tumours with benign names (4)
Melanoma (skin cancer) Mesothelioma (mesothelium) Myeloma (plasma) lymphoma (lymphocytes)
55
Exposure to carcinogens (3)
Geographic - environmental (UV light) Occupational - eg. silica dusts Accidental - lab tests or radiations
56
Types of carcinogens (6)
``` Chemicals infectious agents Radiation Minerals Physiological - hormones Chronic inflammation ```
57
Carcinogens
any agents the significantly increase the risk of developing cancer
58
Initiator carcinogens
Genotoxic | Damage/ modify the DNA = exasperating tendency for polymerases to make mistakes
59
Promotors carcinogens
non-genotoxic Induce proliferating and DNA replication = clonal expansion of mutated cells (after 2 rounds of replication = mutation is fixed)
60
Complete carcinogens
both promote and initiated
61
Result of mutations (2) - which genes altered
Gain of function - activation of proto-oncogenes | Loss of function - inactivation of tumor suppressor gene
62
CpG islands are associated with?
promotor regions that are methylation --> turns off the gene
63
Tumor suppress genes are associated with?
Famillia cancers
64
Procarginogens - how taken in? | example
carcinogens (usually ingested) that require enzymatic activation Benzopryene - found in meat, tobacco and fuel
65
3 examples of DNA repair - which carcinogen they repair
Nucleotide-excision repair (NER) = UV light, hydrocarbons Recombinantional repair = X-rays Mismatch repair = replication agent
66
Proto-oncogene - what do they do
promote cell cycle Proliferation, growth, survival and angiogenesis
67
How does mutation affect Proto-oncogenes?
activates them to oncogenes
68
Oncogenes - what do they do? (2) | Dominant - one mutated allele and one mutational 'hit' to be expressed
Increase expression of oncogenes = controlled growth and protein development Aberrent (diversion for normal cell type) proliferation
69
Mechanism of proto-oncogene activation (4)
Translocation = low to high transcriptional state Point mutation = hyperactive Amplification = more oncogenes --> increased expression Insertion - of a promoter sequence
70
Oncoproteins - coded for by oncogenes = functions (3)
Growth factor receptors Bind to DNA to stimulate transcription Secondary messenger that activates the cells cycle
71
Tumor suppressor genes (2 types + what they do)
'gatekeepers' - negative regulator of cell proliferation OR 'caretakers' - repair DNA so defect DNA doesn't replicate
72
Mechanism of Tumor suppressor deactivation? (3) | Recessive - two mutation 'hits' for mutated tumor supressor to be expressed
point mutations deletions epigenetic silencing - by methylation on CpG promoter regions
73
Example of TSG (3)
RB1 - retinoblastoma p53 - Li- Fraumai (Breast sarcomas) APC - Famillial adenomatous polyposis (colorectal)
74
Examples of Caretaker genes (2)
BRACA1 and BRACA2 = familliar breast caner | hMLH1 and hMLH2 = familliar non-polyposis colorectal cancer
75
Minimum number of mutations (germline or somatic) for carcinogenesis
3
76
Hallmarks of cancer - acquired functional capabilities (6)
Self sufficent growthpathways Insensitivity to antigrowth factors Immortality - talomeres on the end of chromosome never diminish in length = can replicate multiple times Resistant to apoptosis Sustained angiogenesis Local invasion (basement membranes) and mets
77
How do tumor cells self stimulate growth? (names of genes that mutate)
Over expression of EGFR (growth factor receptor) | RAS and RAF mutations = produces proliferating proteins
78
Mutation that causes resistance to anti-growth factors?
Rb (gatekeeper) = inactivated
79
Telomerase ?
Is over expressed in tumor cells so chromosomes always have telomere = replicate infinite number of times
80
Mutation that makes tumour cells resistant to apoptosis
T53 = normally cause cell cycle arrest followed by DNA repair OR apoptosis of faulty cells
81
Size of tumors that can sustain angiogenesis
2 mm
82
How do tumour cells invade and metastasis
Mutation in gene = loss of E-cadherin --> motile | Secrete proteases = pass through basement membranes
83
Genetic screening
Cancer predisposition
84
Tumor markers for diagnosis? - type of cancer
Raised PSA in the blood (prostate specific antigen)
85
Predictive markers for therapeutic response/ targeting drugs?
HER2 growth factor receptor over expressed in breast caner and responsive to Herceptin
86
Tumor markers for monitoring response to treatment?
CA-125 in ovarian cancer
87
5 clinical applications of tumor markers
``` screening diagnosis prognosis therapy monitoring ```
88
Dysplasia
abnormal differentiation
89
Anaplasia
no differentiation
90
Epithelial become _____ cells in tumors
Mesenchymal cells (as these are not adhered and able to move even in health)
91
Mutation in Ecaderhins Intergrin expression in epithelial cells Cause?
``` E-caderhins = loss of cell to cell adhesion Intergrin = loss of cell to matrix adhesion ```
92
Matrix Metalloproteinases | eg. gelatinases, stomolysins
degrade the basement membrane and collagen in the extra cellular matrix
93
Mechanical pressure and the effect on the behavior of the tumor (6 step process)
No contact inhibition | Mass = pressure = occlude vessel = ischemia and death --> tumor then moves along line of weakness
94
Cancer that metastasis via lymphatics firstly
carcinomas
95
Cancers that met via blood (firstly) + from where?
Sarcomas from liver, lungs, bone and brain
96
Process of Blood spread of Mets? (4 stages)
Tumor locally invades a blood vessel --> cells break off --> carried to narrower vessel --> embed and cause secondary tumor
97
Implantation spread of mets?
Accidental deposit of cells during resection/ other surgery
98
'seed and soil' theory
The idea that cancer cells have to find an ideal tissue environment to met is = organ selectivity for mets
99
Angiogenesis | - part of healing process (physiological)
New vessel formation (derived from existing vessels)
100
Growth factors released by tumor cells that control angiogenesis VEGF PDGF TGFBeta
Vascular endothelial growth factor platelet derived growth factor Transforming growth factor beta
101
Staging (3 components)
How big the primary tumor is How far its spread Any mets?
102
TMN staging? (all 1 - 4)
``` T = tumor - size of primary and how far spread M = mets - how many and how far N = nodes - how many and how far ```
103
Dukes staging? - what cancer?
Colon cancer
104
Ann arbor stages for Lymphoma | LN = lymph nodes
``` 1 = one lymph in isolation 2 = 2 physically unasocciated LN 3 = Multiple unassociated LN - at least one on the oposite side of the diaphragm 4 = multiple unassociated LN ```
105
Grade
How differentiated the cells are = how aggressive Less differentiated = more aggressive
106
Stage and Grade do what?
Diagnose and guide prognosis - surgery? chemo? years left?

Year 2: EMS (1 decks)

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