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Growth and Development > Neoplasia including classification of tumours > Flashcards

Neoplasia including classification of tumours Flashcards

1
Q

What is a neoplasm?

A

An abnormal mass of tissue, growth of which is excessive and is unco-ordinated with that of normal tissues. It persists after the provoking stimulus is removed

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2
Q

Define invasion

A

Uncontrolled growth into CT - defining feature of malignant tumours

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3
Q

Define metastasis

A

Spread distant from primary tumour

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4
Q

Define differentiation

A

The extent of resemblance of normal cells/ tissue is very variable

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5
Q

Define cytology

A

Features of individual cells - often very abnormal

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6
Q

Classification of neoplasms

A 
By clinical behaviour
-benign
-malignant
By histogenesis (tissue of origin)
-epithelial - lining or glandular
-mesenchymal - various types
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7
Q

Growth pattern of benign or malignant tumours

A

Benign: expansion, encapsulated, localised
Malignant: invasion, no capsule, metastasis

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8
Q

Growth rate of benign and malignant tumours

A

Benign: slow
Malignant: more rapid, but variable

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9
Q

Histology of benign and malignant tumours

A

Benign: resembles tissue of origin, uniform cell/ nuclear shape and size, few mitoses
Malignant: variable resemblance to tissue of origin, cellular and nuclear polymorphism, many mitoses, abnormal

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10
Q

Clinical effects of benign and malignant tumours

A

Benign: localised, local pressure, excision cures
Malignant: infiltration and spread, local pressure, excision may not cure

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11
Q

Components of benign tumour

A 
Tumour cells
Stroma (supporting CT) including fibroblasts and BVs
Capsule 
-most, but not all tumours
-may be incomplete
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12
Q

Effects of benign tumours

A 
Pressure
Obstruction
Function - especially hormone secretion
-these vary by site and tumour
-effect is not always 'benign'
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13
Q

Pathology of malignant tumours

A 
Tumour cells
-invade, underlying tissues
-cytologically abnormal
-differentiation varies (well, moderate, poor; anaplasia)
Stroma 
-angiogenesis
-immune response
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14
Q

Cytology of malignant cells

A 
> no. of irregularly shaped dividing cells
> variable shaped nuclei
< cytoplasmic vol. relative to nuclei
Variation in cell size and shape
Loss of normal specialised cell features
Disorganised arrangement of cells
Poorly defined tumour boundary
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15
Q

Classification of epithelial neoplasms

A 
90% of neoplasms
BENIGN
Lining: papilloma
Glandular: adenoma
MALIGNANT
Lining: Carcinoma
Glandular: Adenocarcinoma
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16
Q

Classification of mesenchymal neoplasms

A 
BENIGN
Depends on tissue
-e.g. fibroma, osteoma, lipoma, myoma, chondroma
-skeletal muscle: rabdomyoma
MALIGNANT
Sarcoma, depends on tissue
-osteo, -leiyomyo
17
Q

Classification of neoplasms: oddities

A

Melanoma (melanocytes - malignant)
Lymphoma (arise from WBC)
Leukaemia (arise from bone marrow precursor cells)
Terratoma (germ cell tumours)
-most in testes, most malignant (ovarian tend to be benign)
-can mimic any tissue incl. teeth!

18
Q

Why do benign tumours arise?

A

Little known, may be due to inherited factors

Carcinogenesis is multi-step process

19
Q

Inherited factors: genetic susceptibility to cancer

A 
Inherited cancer syndromes
-single mutant genes, often tumour suppressor genes
-retinoblastoma, some colon cancers
-likelihood of developing cancer extremely high
Familial
-family clusters of cancers (e.g. BRCA1)
-e.g. breast and ovarian cancer
-pattern of inheritance unclear
-lots of other contributing factors
-not only one single gene gives risk
Defective DNA repair
-> sensitivity to carcinogens
-DNA damage isn't repaired
-e.g. skin cancer at very young age
20
Q

Why do malignant tumours arise?

A 
Inherited factors
Environmental factors
-chemical agents
-physical agents
-viruses
21
Q

Two stages of chemical carcinogenesis

A
  • initaition: permanent DNA damage

- promotion: may be reversible, promotes proliferation

22
Q

Important concepts of chemical carcinogenesis

A

Pro-carcinogen often metabolised to ultimate carcinogen

Co-carcinogens

23
Q

Latent period of chemical carcinogenesis

A

Time from promotion to clinical tumour

24
Q

Direct chemical carcignogens

A

Tumour arises at site of carcinogen application

-e.g. smoking and lung cancer

25
Q

Indirect chemical carcinogens

A

Tumour arises at different site from carcinogen application
E.g. aromatic amines - industrial exposure
-inhaled - lungs
-metabolised in liver, excreted by kidney
-bladder enzymes release aminophenol
result is bladder carcinoma

26
Q

Examples of chemical carcinogens

A 
Smoking
-polycylic
-hydrocarbons
-including tars
Diet
-burnt hydrocarbons
Asbestos
-fibrous silicates
-inhaled (fibrosis, mesothelioma)
-synergy in smokers
27
Q

Physical carcinogenesis

A 
Ionising radiation
-damages DNA, causing mutations
-X-rays
-radioactive metals and gases (radium: bone and bone marrow tumours, radon: lung cancer)
-atomic bomb
UV light
-damages DNA
-skin (squamous cell &amp; basal cell carcinoma, malignant melanoma)
-xeroderma pigmentosum
28
Q

Radiation sensitivity

A

Most sensitive tissues are where cells rapidly renewed. Most to least sensitive:

  • embryonic tissues
  • haematopoietic organs (spleen, bone marrow)
  • gonads
  • epidermis
  • intestinal mucous membranes (variable)
  • CT
  • muscle tissue and nerve tissue
29
Q

Viral carcinogenesis

A 
DNA viruses
-> common
-viral DNA inserted into host DNA
RNA viruses
-reverse transcribed and then inserted
-may contain 'oncogenes'
-importance in many tumours not certain
-act with other factors
30
Q

Virus –> tumour (act with other factors)

A

Epstein-Barr virus –> Burkitt’s lymphoma, nasopharyngeal carcinoma
Hep B/ C –> hepatocellular carcinoma
HPV –> cervical carcinoma

31
Q

HPV and cancer

A 
HPV sexually transmitted
Some genotypes cause
-cervical cancer
-oro-pharyngeal cancer
Viral protein binds to and inactivates tumour-suppressor, p53
32
Q

Other influences on cancer

A 
Often act as 'promoters'
Hormones
-breast cancer: hormonal dependence, ovary and adrenal
-prostate cancer: testosterone
Drugs, including alcohol
Inflammation
33
Q

Epidemiology of cancer

A 
20% of deaths
2nd most frequent cause of death
30% of pop. will develop cancer
Highest in elderly
Type
-90% carcinoma
-10% lymphoma or sarcoma (more in young)
34
Q

How does cancer develop?

A

De novo - salivary gland tumours
Via benign tumour - adenocarcinoma of colon
Via premalignant lesion - HNSCC (in some cases)

35
Q

Premalignancy

A

Some of changes in cells & tissue architecture are seen before invasion occurs
This disorganisation of tissue is called dysplasia
Basis of cancer screening

36
Q

Cancer screening

A

Detection of ‘premaligcancy’

  • identification of changes in cells before invasion occurs
  • cervical smears
  • oral cancer?

Growth and Development (23 decks)

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