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Cell Pathology > Cell Pathology 3- Cancer > Flashcards

Cell Pathology 3- Cancer Flashcards

1
Q

Define tumour

A

Any kind of mass forming lesion.

May be neoplastic, hamartomatous or inflammatory (e.g. nasal polyps).

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2
Q

What are nasal polyps

A

A non-neoplastic tumour

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3
Q

Define neoplasm

A

The autonomous growth of tissue which have escaped normal constraints on cell proliferation. Abnormal growth- exceeds that of normal tissues- abnormal mass

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4
Q

What is lung cancer an example of

A

A neoplastic tumour

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5
Q

Describe the two types of neoplasms/tumours

A

Neoplasms may be either
benign (remain localised) or
malignant (invade locally and/or spread to distant sites).

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6
Q

What are cancers described as

A

malignant neoplasms.

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7
Q

How do we name benign tumours

A

given suffix -oma to cell of origin.
Adenoma (epithelial derivative)
Fibroma (mesenchymal derivative)

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8
Q

Do skin cancers metastasise

A

No

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9
Q

What are the two basic components of tumours

A

Proliferating neoplastic cells parenchyma

Supportive stroma

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10
Q

Describe the difference in death rates between benign and malignant neoplasms

A

Important to note that many malignant tumours rarely cause death (especially skin cancers) and that some benign tumours do kill (usually because of their location, e.g. the brain)
This effects how we analyse their severity in the population
Incidence/prevalence in skin cancers
Death rates in brain tumours

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11
Q

What are hamartomas/ dysplasia

A

These are localised benign overgrowths of one of more mature cell types e.g. in the lung.
They represent architectural but not cytological abnormalities.
For example: lung hamartomas are composed of cartilage and bronchial tissue.
Malformed normal tissue

Loss of uniformity of individual cells

Sever dysplasia is carcinoma in situ

Mild to moderate dysplasia may revert to normal

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12
Q

What are heterotopias/ metaplasia

A

These are normal tissue being found in parts of the body where they are no normally present.
For example: pancreas in the wall of the large intestine.
Cause of a tumour

Result from chronic stimulus, when withdrawn may resolve to normal

Is adaptive, not premalignant

Substituted mature cell is more suited to that environment
Smoking causes metaplasia of glandular bronchial epithelium to squamous epithelium

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13
Q

How do we classify neoplasms

A

The primary description of a neoplasm is based on the cell origin and the secondary description is whether it is benign or malignant.
For example, tumours of cartilage are either chondromas (if benign) and chondrosarcomas (if malignant.)

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14
Q

What are the 3 types of epithelium

A

Squamous, glandular, transisitional

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15
Q

What do we classify tumours of the squamous epithelium

A

Benign; Squamous epithelioma, papilloma
Malignant: Squamous cell carcinoma
Examples: Skin, oesophagus, cervix

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16
Q

How do we classify tumours of the glandular epithelium

A

Benign: Adenoma
Malignant: Adenocarcinoma
Examples: Breast, colon, pancreas, thyroid

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17
Q

How do we classify tumours of the transitional epithelium

A

Benign; Transitional papilloma
Malignant: Transitional cell carcinoma
Example: Bladder

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18
Q

What are two types of connective tissue

A

Smooth muscle and bone

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19
Q

How do we classify smooth muscle tumours

A

Benign: Leiomyoma
Malignant: Leiomyosarcoma
Examples: Uterus, colon

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20
Q

How do we classify bone tumours

A

Benign: Osteoma
Malignant; Osteosarcoma
Examples: Arm, leg

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21
Q

Describe the locations of the two types of haematological neoplasms

A

Lymphocytes and bone marrow

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22
Q

How do we classify neoplasms of the bone marrow

A

Benign: Uncommon
Malignant: Lymphoma

Example: Stomach

23
Q

How do we classify neoplasms of lymphocytes

A

Benign: Uncommon
Malignant: Leuakaemia

24
Q

What are teratomas

A

These are tumours derived from germ cells and can contain tissue derive from all three for 3 germ cell layers.
They may contain mature and / or mature tissue and even cancers.

25
Q

What are the 4 factors distinguishing between benign and malignant tumours

A

Invasion
Metastasis
Differentiation and anaplasia
Growth pattern

26
Q

What is meant by invasion

A

This means direct extension into the adjacent connective tissue and /or other structures e.g. blood vessels. This is what distinguishes dysplasia/ carcinoma in situ from cancer.
Most benign tumours grow as cohesive, expansile masses that remain localised to their site of origin (encapsulated)

Malignant tumours infiltrate and destroy the surrounding tissue, poorly demarcated

27
Q

What happens upon invasion

A

A response is elicited from the tissue it invades (lymphocytes)

28
Q

What is meant by metastasis

A

This means spread via blood vessels etc (see below) to other parts of the body.
NB: All malignant tumours have the capacity to metastasise although they may be diagnosed before they have done so

29
Q

Describe metastasis

A

Unequivocal evidence of malignancy
Formation of discontinuous tumour implants at a distance from the main tumour mass
Only gliomas and basal cell carcinomas cannot metastasise
30% of patients present with metastasis

30
Q

What is meant by differentiation

A

This means how much do the parenchymal cells of the tumour resemble the cells of the tissue it is derived from.
Benign tumours are well differentiated
Malignant tumours show various levels of differentiation

31
Q

What is meant by anaplasia

A

Lack of differentiation. Characterised by;
Hyperchromasia
Pleomorphism
Irregularity of nuclear membrane
Tumour cells tend to have larger nuclei (and hence a higher nuclear-cytoplasmic ratio) and more mitoses than the normal tissue they are derived from.
They may have abnormal mitoses (e.g. tripolar) and marked nuclear pleomorphism (variability in nuclear size and shape).
Basically the cytological features of malignant cells

32
Q

What is meant by growth pattern

A

This means how much does the architecture of the tumour resembles the architecture of the tissue it is derived from.
Rate of growth correlates with the level of differentiation
Benign tumours grow slowly
Malignant tumours grow rapidly

33
Q

How does the architecture of tumour cells differ

A

Tumours have less well defined architecture than the tissue they are derived from.

34
Q

What are all adenocarcinomas derived from

A

Adenomas

35
Q

How do benign tumours become malignant

A

Series of steps- genetic alterations, get bigger and may become cancerous

36
Q

What have studies on tumour cells demonstrated

A

Many tumour cells shed from the primary tissue daily yet only a few metastases are produced.
Series of steps
Cells must end up in favourable soil.

37
Q

List the routes by which tumours spread

A 
Direct extension. 
Haematogenous.
Lymphatic 
Transcoelomic
Perineural
38
Q

Describe direct extension

A

This is associated with a stromal response to the tumour.
This includes fibroblastic proliferation (“ a desmoplastic response”), vascular proliferation (angiogenesis) and an immune response.

Direct seeding of body cavities and surfaces(peritoneal,pleural, pericardial, subarachnoid, joint)

Most commonly from ovarian carcinomas which may cake the peritoneal surface

Also spread of lung cancer into pleural cavity.

39
Q

What is meant by haematogenous spread

A

This is via blood vessels.
The blood vessels usually invaded are the venules and capillaries because they have thinner walls.
Most sarcomas metastasise first via the blood vessels.
Liver and lungs are most common site due to venous drainage
Renal cell carcinoma can grow within renal vein to Inferior Vena Cava and into the right atrium.

40
Q

Describe lymphatic spread

A

This is via lymphatics to lymph nodes and beyond.
The pattern of spread is dictated by the normal lymphatic drainage of the organ in question.
Most epithelial cancers metastasise first via the lymphatics.
Regional nodes drain tumours (axillary then infraclavicular and supraclavicular from UOQ breast carcinomas)
Nodes may contain the spread locally
Evoke and immune response which causes nodal hyperplasia
Not every enlarged node in the region of a tumour contains metastatic spread

41
Q

Where do cancers of the testes spread to

A

Para-aortic lymph nodes

42
Q

Describe Transcoelomic spread

A

This is via seeding of body cavities.
The commonest examples are the pleural cavities (for intrathoracic cancers) and the peritoneal cavities (for intra-abdominal cancers)
Direct seeding of body cavities and surfaces(peritoneal,pleural, pericardial, subarachnoid, joint)

Most commonly from ovarian carcinomas which may cake the peritoneal surface

Also spread of lung cancer into pleural cavity.

43
Q

Describe perineural spread

A

This is via nerves.

This is an underappreciated route of cancer spread.

44
Q

How do we assess tumour spread (stage)

A

Clinically
Radiologically
Pathologically

45
Q

How do we describe tumour spread (stage)

A

T = Tumour: the tumour size or extent of local invasion( T1-T4)
N = Nodes: number of lymph nodes involved (1,2,3)
M = Metastases: presence of distant metastases (No,1,2)
This is called the “TNM” system and the details are different for each kind of cancer

46
Q

How do we grade a tumour

A

Histologically
Based on degree of differentiation and on the number of mitoses

Less useful than staging.

47
Q

List some of the other systems for staging cancers

A

FIGO for ovarian cancers

Ann Arbour for Hodgkins Lymphoma

48
Q

In terms of prognosis which is more important

A

Stage

49
Q

Describe the epidemiology of cancer

A

Age incidence of cancer increasing overall as the world lives longer, in general the incidence increases after 55.
Geography (stomach cancer higher in Japan than USA, melanoma higher in NZ than Iceland).

50
Q

Describe the environmental agents linked to cancer

A

UV light, occupational agents, diet and weight, alcohol, smoking, infections most notably viruses.

51
Q

Describe the genetic factors associated with cancers

A

For a large number of cancers there exists some hereditary predispositions. Lung cancer mortalities are four times higher in non-smoking relatives of lung cancer patients against controls)

52
Q

Explain the genetic hypothesis of cancer

A

The genetic hypothesis of cancer implies that a tumour mass results from the monoclonal expansion of a single progenitor cell.
Subsequent additional mutations allow progression and opportunity for heterogeneity.

53
Q

Describe the key types of genes involved in cancer

A

Oncogenes
Anti-oncogenes
Apoptosis regulating genes
DNA repair genes

Cell Pathology (6 decks)

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