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Pase 2a Notes > Oncology > Flashcards

Oncology Flashcards

1
Q

What is a carcinoma

A

Malignant tumour of epithelium
E.g. basal cell carcinoma = skin

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2
Q

What kind of cancer is leukaemia?

A

White blood cell

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3
Q

Types of treatment

A

Chemotherapy
Local excision
Radiotherapy
Anti oestrogen therapy for breast cancer
Herceptin for certain genes in breast cancer

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4
Q

What is adjuvant therapy?

A

Extra therapy given after surgical excision e.g. radiotherapy

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5
Q

Where may carcinomas spread?

A

To lymph nodes that drain site
Bone
Other organs
(So need to check for micrometastases before treatment)

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6
Q

Define carcinogenesis

A

The transformation of normal cells to neoplasticism cells through permanent genetic alterations or mutations
= applies to malignant neoplasms

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7
Q

Tumour vs neoplasm

A

Oncogenesis causes tumours = abnormal swelling e.g. neoplasm
Carcinogenesis causes neoplasms = a lesion resulting from autonomous abnormal growth of cells after intimidating stimulus has been removed

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8
Q

3 Problems identifying environmental risks of cancer

A

Long interval may last decades
Complexity of environment
Ethical constraints when testing

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9
Q

How do we identify carcinogens?

A

Epidemiology evidence - look at where cancer is common and see common exposures

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10
Q

Some examples of occupational/ behavioural risks

A

Lung cancer - smoking
Bladder cancer - aniline dye and rubber
Scrotal cancer - chimney sweeps

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11
Q

Some example of direct evidence where environment has caused cancer

A

Chernobyl nuclear reactor exploded = radioactive iodine irritated thyroid

Radio graphic contrast medium thorotrast with very long half life caused liver cancer

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12
Q

Classes of carcinogen

A

Chemical - no common structure, may act directly or require enzyme metabolic conversion from pro to ultimate carcinogen
Viral
Ionising radiation - Long term effect
Non ionising radiation - UV A/B
Biological agents - hormones, mycotoxins and parasites
Miscellaneous

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13
Q

Common chemical and viral carcinogens

A

See week 2 notes!!

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14
Q

Host factors affecting carcinogenesis

A

Ethnicity
Constitutional factors - inherited, age, gender
Lifestyle - exercise, alcohol
Premalignant conditions - e.g. polyps
Trans placental exposures - drugs

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15
Q

Define carcinoma in situ

A

Hasn’t breached the Basement membrane or spread

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16
Q

Define micro-invasive carcinoma

A

Has breached basement membrane, but so little has left that risk of spreading is low

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17
Q

Invasion of basement membrane and Extracellular matrix via

A

Proteases
Collagenases
Cathepsin D
Cell motility

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18
Q

List 7 steps of metastasis

A

(Detachment)
1. Invasion of basement membrane
2. Tumour cell motility and breakdown of matrix
3. Intravasion of venules and lymphatics via collagenases
4. Adhesion protects cells in a ball and evades host defence
5. Extravasation
6.Growth (arrest)
7. Angiogenesis promotes growth

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19
Q

3 routes of hematogenous metastasis

A
  1. Metastases to lungs and grows in capillaries
  2. Blood from gut filtered in liver
  3. Adhesion molecules take to bone
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20
Q

Define invasive carcinoma

A

A carcinoma that has breached the basement membrane

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21
Q

What does in-situ neoplasia only apply to?

A

Epithelial neoplasm (basement membrane is intact)

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22
Q

3 routes of metastasis

A
  1. Haemaogenous - by blood
  2. Lymphatic - channels drain
  3. Trans-coelomic - pericardial and peritoneal cavities
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23
Q

Conventional chemotherapy is better for faster or slower growing tumours?

A

FASTER!!

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24
Q

Is conventional chemotherapy selective to tumour cells?

A

No, hits normal cells as well causing hair loss, diarrhoea etc

25
Why is targeted chemotherapy more effective?
Exploits differences between cancer and normal cells so less side effects
26
What differences to cancer cells can be exploited?
Gene arrays Proteomics Tissue microarrays
27
2 examples of cancer cell processes that are different to normal cells
1. Over expression of growth factor A so more proliferation 2. Mutation for growth factor A receptor means its always switched on and increases proliferation
28
How can we exploit these differences?
1. Monoclonal antibody binds to and block growth factor A from binding to receptor 2. Small molecular inhibitor of growth factor A receptors (hard to screen)
29
Cetuximab physiology
Monoclonal antibody acts against epidermal growth factor receptor (An internal tyrosine kinase activity switch up regulates gees to proliferate and angiogenesis)
30
Herceptin physiology
Monoclonal antibody binds to HER2 protein which causes endocytosis of receptors and lymphocytes cause cell cytotoxicity
31
Nivolumab physiology
Block PD1 over expression which encourages body to mount an immune response to tumour
32
Benign vs malignant tumour behaviour
Benign - non-invasive localise bland cell morphology with low mitotic activity and absent necrosis Malignant - invasive abnormal cell morphology with high mitotic activity and necrosis
33
4 tumour type classifications
Cell of origin: Epithelial Connective tissue Haematopoetic Other
34
How might we acquire genetic changes?
Chance mutation Environmental exposures Heriditary Micro-organisms
35
2 genetic drivers of oncogenesis
Proto-oncogenes - promote growth Tumour suppressor genes - inhibit growth
36
How might we investigate a tumour?
Sputum Radiology-guided biopsy Bronchoscope Surgical methods
37
What is small cell carcinoma?
Appears as flat, smaller and grows faster, spreading to lymph nodes
38
Tumour grading vs staging
Grading - how much tumour cells resemble normal cells Stage - how much tumour has soread
39
Expand TNM staging
Tumour - size, extent, depth Nodes - extent of lymph node metastasis Metastases - extent of spread
40
Define neoplasm
A lesion resulting from autonomous abnormal growth of cells which persist after the initial stimulus is removed
41
3 most common cancer type deaths
Lung Prostate / breast Bowel
42
Structure of neoplasms
= Neoplastic cells From monoclonal nucleated cells = surrounded by fibrous stroma Connective framework for nutrient
43
What determines size of tumour?
Angiogenesis (Blood supply providing oxygen and nutrients)
44
Behavioural vs Histogenic classification of tumours
B - benign / malignant H - cell of origin
45
Benign vs Malignant neoplasms
B - localised, non-invasive, slow growing and low mitotic activity resembling normal tissue M - Invasive metastasis quickly with poorly defined border
46
Growth direction of benign vs malignant neoplasms
B - exophytic (up and out) M - endophytic (down and in)
47
How do benign vs malignant neoplasms cause morbidity and mortality
B - pressure on structures obstruct flow, produce hormones and transform to malignant M. - Destruction of adjacent tissue, metastases to brain obstructs flow and blood loss from ulcers
48
3 tissue neoplasms may arise from and suffix
Epithelial cells Connective tisssue Lymphoid / haematopoetic cells = oma
49
2 benign epithelial neoplasm types
Papilloma - non glandular, non secretory Adenoma - secretory, glandular Prefix with cell type of origin e.g. thyroid adenoma
50
Malignant epithelial neoplasms called
Carcinoma - prefix with epithelial type E.g. glandular epithelial is adenocarcinoma
51
Benign connective tissue neoplasms
Suffix is cell origin Adipocytes. - Lipoma Cartilage - chondroma Bone - osteoma Vascular - angioma Skeletal striated muscle - Rhabdomyoma Smooth muscle - leiomyoma Nerves - neuroma
52
Malignant connective tissue neoplasms
Cell of origin prefix - sarcoma
53
What is degree of differentiation?
Further classification of malignant neoplasms by how closely they resemble normal tissue
54
What is an anaplastic neoplasm?
Where cell type of origin cannot be determined
55
Exceptions
Granuloma, Mycetoma, Tuberculoma Malignant neoplasms: Melanoma Mesothelioma Lymphoma
56
Sarcomas generally metastasis to
Lungs
57
Cancers which metastasis to bone
Breast Lung Prostate Renal Thyroid
58
What are benign tumours that only grow when body grows called?
Hamartoma

Pase 2a Notes (6 decks)

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