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Medicine Year 2 > Scenario 32 > Flashcards

Scenario 32 Flashcards

1
Q

What is fine needle aspiration?

A

technique for obtaining cells for cytological diagnosis directly for palpable masses and radiologically guided for deep seated lesions

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2
Q

What are the two options for a tumour?

A

Malignant or benign

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3
Q

What is the 1-5 rating of lumps?

A

1- benign 5-cancer definite

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4
Q

What % of women at diagnosis have no overt metastatic disease?

A

95

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5
Q

What are the stages in the cell cycle?

A

G1 (G0)–>S–>G2–>M

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6
Q

What happens in G1?

A

Double internal structurees

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7
Q

What happens in G0?

A

Leave the cell cycle (eg neurones and cardiac muscle)

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8
Q

What happens in S?

A

Doubling the chromosomes

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9
Q

What happens in G2?

A

Check that things are copied correctly

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10
Q

How long does it take to go round the cycle?

A

Vaies- tumours take longer (24-72 hours)

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11
Q

What is the role of cyclin?

A

The activator present at different stages in the cycle (how it moves around the cycle)

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12
Q

What keeps cells in homeostasis?

A

The differentiation and specialisation that they have underfone, constraints by neighbouring cells, availability of metabolic substrates and the finite speed at which their internal metabolic pathways can function

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13
Q

What is hypertrophy?

A

Increase in cellular mass to maintain the higher levels of metabolic activity bought about by increasing the numbers of sub cellular organelles

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14
Q

What is hyperplasia?

A

Increase in number of cells in an organ or tissue which may lead to an increase in volume
Physiological- hormonal (breast), compensatory (liver)
Pathological- excessive hormonal stimulation of target cells (endometrium from oestrogen)

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15
Q

What is metaplasia?

A

Reversible change where one adult cell type is replaced by another
Eg- squamous metaplasia in the reap tract of smokers and at the cervix and glandular metaplasia in lower oesophagus

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16
Q

What are the morphological features of malignancy?

A

Increased cell proliferation and incomplete differentiation (irreversible change in the genome)

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17
Q

What is a neoplasm?

A

Abnormal mass of tissue, the growth of which exceeds and is coordinated with that of normal tissues and persists in the same excessive manner after the cessation of the stimuli which evoked the change
Arises from just one cell

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18
Q

What are the basic components of a tumour?

A

Proliferating neoplastic cells that constitute the parenchyma and supportive stroma made up of CT, BV and lymphatics

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19
Q

What are malignant neoplasms of epithelial cell origin called?

A

Carcinomas

eg. squamous, adeno (glandular), basal cell

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20
Q

What are cancers arising from mesenchymal tissue called? (connective tissue)

A

Sarcomas

eg. lipo, fibro, osteo, chondro

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21
Q

What is the mechanism of cancer invasion?

A

Physical invasion, reduced adhesiveness and cohesiveness of tumour cells, increased motility of tumour cells, loss of ‘contact inhibition’ (2 layers of cells should touch and stop proliferating) and release of destructive enzymes

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22
Q

What is the difference in differentiation of benign and malignant neoplasm?

A

Benign are well differentiated and malignant range from well to un

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23
Q

What is the difference in rate of growth of benign and malignant tumours?

A

Most benign grow slowly where most malignant grow rapidly. Growth rate of tumours correlates with the level of differentiation.

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24
Q

How do tumours spread?

A

Benign tumours are encapsulated but malignant are never encapsulated are are characterised by infiltrative, erosive growth and extend crab like feel into adjacent tissues (invasiveness)

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25
Q

What are the two most reliable features to distinguish malignant from benign tumours?

A

Invasiveness and metastases

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26
Q

What is a cancer starting in a blood forming tissue called?

A

Leukaemia

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27
Q

What is a cancer that starts in cells of the immune system calles?

A

Lymphoma/myeloma

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28
Q

What is a cancer that starts in the brain or spine called

A

Glioma

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29
Q

How can a benign tumour be dangerous?

A

If it compresses things or releases hormones

30
Q

What can a pit adenoma cause?

A

hypopituitarism and blindness

31
Q

What can a glioma cause?

A

Increased intra cranial pressure, hemorhhage in brain stem that knocks out CV system

32
Q

What are the 4 mechanisms of metastases formation?

A

Direct seeding, transplantation (surgeon cuts into tumour), lymphatic permeation, embolisation through blood vessels

33
Q

What are the steps in metastases formation?

A

Primary neoplasm, progessive growth, vascularisation, invasion, detattchment, embolisation, survival in the circulation (avoid NK cells, lymphocytes, monocytes etc), arrest, extravasion, evasion of host defences, progressive growth, metastasis

34
Q

Is metastasis episodic or continuous?

A

Episodic- groups of different sized ones seen in a tissue

35
Q

Where does lung cancer commonly spread to?

A

Liver and adrenal

36
Q

Where does breast cancer commonly spread to?

A

Lymph, skeleton, meninges, brain

37
Q

Where does prostate cancer commonly spread to?

A

Obturator lymph nodes, lumbar spine

38
Q

What decides where the cancer spreads to?

A

Not blood- kidneys would always be affected, depends on cell adhesion molecules

39
Q

What are the local effects of a tumour on the host?

A

Pressure, destruction of tissue, hypercalcaemia , haemorrhage, infection

40
Q

What are the systemic effects?

A

Fever (cytokine mediated from tumour cells or infiltrating macrophages), cachexia (loss of appetite, malabsorptuon, metabolic processes of tumour), immune defences compromised, haemotological effects (anaemia, increased RBC production), endocrine effects (appropriate hormone production or ectopic), non metastatic changes- clubbing, skin changes etc

41
Q

What are the most common cancers in the UK?

A

Breast, lung, colorectal and prostate

42
Q

What cancers are babies and children most likely to get?

A

Leukemia, brain/cns

43
Q

What cancers are teens most likely to get?

A

First peak for hodgkins lymphoma

44
Q

What cancer is most likely 25-49?

A

Breast cancer

45
Q

What is the current breast, cervical and bowel screening?

A

Breast- every 3 years after 40, cervical every 3 years after 25, every 2 years after 60 for bowel

46
Q

What is oncogenesis?

A

The process of transformation into cancer cells

47
Q

What type of cancer are caused by nitrites in the soil

A

oesophageal carcinoma

48
Q

What type of cancer are caused by soot?

A

Scrotal carcinoma (least washed)

49
Q

What type of cancer are caused by viruses?

A

Hep B and C- hepatocellular carcinokma
Epstein-Barr virus- Burkett’s lymohoma
HHVH- Kaposi’s sarcoma

50
Q

What type of cancer are caused by hormone levels?

A

Androgen levels- prostate cancer, oestogen- endometrial and breast cancer

51
Q

What type of cancer are caused by mycotoxins and parasites?

A

Bile ducts and bladder?

52
Q

If the host has a genetic risk factor will they definitely get cancer?

A

No- multistep not just a single insult, need initiation promotion and persistance

53
Q

What are oncogenes?

A

Stimulate cell growth and division or inhibit apoptosis- normal gene is protooncogene
eg. philadelphia chronosome, RAS
Behave as a dominant trait- only need 1

54
Q

What are tumour suppressor genes?

A

Behave as recessive genes- need to lose both

eg. p53 in thryoid, colonic and breast and BRCA 1 and 2 in ovarian and breast cancers

55
Q

What changes occur in sporadic cancer?

A

Many DNA changes most environmental

56
Q

What changes occur in familiar cancer?

A

Few mutations and environment not as important

57
Q

When can surgery be used as a cancer treatment?

A

When detected early

58
Q

What type of radiation does radiotherapy use?

A

Gamma

59
Q

What cancer biology do we target using druga?

A

Target identification, oncogene actication, tumour suppressor genes

60
Q

What is chemotherapy?

A

Cytotoxic therapy

61
Q

Why does hair fall out and WBC count drop?

A

Because stem cell populations are damaged when cells are agents that damage DNA, target tubulin and antimetabolites

62
Q

When can chemotherapy not be used?

A

Breast cancer after metastasis have formed

63
Q

What non-cytotoxic therapies exist?

A

Inhibitors of tyrosine kinase, monoclonal antibodies to cell surface protein and immunotherapies

64
Q

Why do we want to inhibit tyrosine kinase?

A

It is a molecule which takes signals from outside of cell in leading to gene expression. Tumours switch these on unnecessarily

65
Q

How to tyrosine kinase inhibitors work?

A

Competitve to ATP binding site
Some people have a mutation around this site and in these cases the mutation responds very well but after 9 months become resistant- mutation
Can get rash/acne

66
Q

What are monoclonal antibodies to cell surface proteins?

A

Highly specific to cancer cell surface proteins eg Herceptin

67
Q

What immunotherapies could work?

A

APC activation of the CD28 signal is not good in cancer as they switch off T cells using PDL1 and CTLA4- need an autoantibody to these but problems with autoimmunity

68
Q

What does tamoxifen do?

A

bLOCK OESTROGEN

69
Q

What are the likely outcomes of different lymph node status’ in breast cancer?

A

Negative- 70% disease free in 10 years
1-3-40%
>10-10%

70
Q

How much does herceptin reduce risk of relapse by?

A

35-50%

Medicine Year 2 (19 decks)

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