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Pathology > More disorders of tissue growth > Flashcards

More disorders of tissue growth Flashcards

1
Q

How do benign and malignant tumours compare in terms of growth rate?

A

Benign - slow

Malignant - fast

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2
Q

How do benign and malignant tumours compare in terms of demarcation (growth limits)

A

Benign tumours may reach limit

Malignant have no limit

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3
Q

How do benign and malignant tumours compare in terms of invasion?

A

Benign - no invasion

Malignant - invasion

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4
Q

How do benign and malignant tumours compare in terms of resemblance to original architecture?

A

Benign resemble original tissue

Malignant may or may not resemble original tissue

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5
Q

How do benign and malignant tumours compare in terms of anaplasia?

A

Benign have no anaplasia

Malignant may or may not have anaplasia

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6
Q

Give 5 examples of how malignant and benign tumours differ

A

Benign - localised, expansile growth, stroma produced by neighbouring cells, growth limit, resemble original tissue, no metastasis
Malignant - infiltrative growth, produce own stroma, may not resemble original tissue, metastasise, no growth limit

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7
Q

What are tumour associated macrophages?

A

Macrophages present in tumours
M1 = tumoricidal (better prognosis)
M2 = relevant role

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8
Q

What is an oncogene?

A

A gene that drives neoplastic transformation

drive tumour development

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9
Q

What is a proto-oncogene?

A

Normal cellular gene that regulates the cell cycle

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10
Q

What is a viral-oncogene?

A

Oncogene in virus DNA/RNA

Infection with virus causes it to become an oncogene

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11
Q

What are carcinogenic agents? What type of agents are they?

A

Agents that cause malignant neoplasia in cells

Chemicals, irradiation, infectious agents

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12
Q

Carniogenic agents can be direct or indirect. What do these terms mean?

A

Direct - need no chemical transformation (ultimate carcinogens)
Indirect - need chemical transformation, usually metabolised in the liver (pro-carcinogens)

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13
Q

Both indirect and direct carcinogenic agents are highy reactive what? What do they do?

A

Electrophiles

Bind to DNA/RNA/protiens to form covalent bond

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14
Q

Chemical carcinogenesis requires 2 steps. What are these?

A

Initiation - irreversible genetic change

Promotion - damaged DNA replicates so change becomes fixed

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15
Q

What are promoters? What do they do?

A

Regions of DNA that initiate transcription of a gene

Stimulate division of mutated cells

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16
Q

Give examples of promoters

A 
Carcinogens 
Radiation 
Viruses
Hormones 
Parasites
Dietary factors
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17
Q

Give an example of a direct carcinogen and an indirect carcinogen

A

Direct - anticancer drug

Indirect - tobacco

18
Q

How do different doses of radiation damage cells?

A

Low dose - DNA damage
Mild dose - repair or tumor
High dose - apoptosis

19
Q

Radiation can be ionising or non-ionising. What do these terms mean? Give an example of each

A

Ionising - not enough energy to displace electrons from atoms e.g. UV
Non-ionising - enough energy to displace electrons from atoms e.g. X-rays

20
Q

Give an example of a hormone that increase risk of tumours.

A

Oestrogen - increased risk of mammary tumours

21
Q

Mutated cells can lead to increased function of loss or function. What type of genes cause each of these?

A

Non-functioning - by tumour or suppressor gene

Functioning - by growth promoting or normal gene

22
Q

When are cells checked for damage or unduplicated DNA?

A

Only if proliferating

23
Q

Tumours have a limitless reactive potential. What is this?

A

Normal cells stop replicating after certain time length due to shortening of telomeres at end of chromosome
Tumour and stem cells have telomerase - maintain normal telomere length and allow continued replication

24
Q

Which individuals are more susceptible to tumours?

A

Immunocompromised

25
Q

What cells are tumour specific antigens found on?

A

Antigens found on restricted tumour cells

26
Q

What cells are tumour associated antigens found on?

A

Antigens found on both normal and tumour cells

Tumour = overexpressed

27
Q

What can be used as a non-invasive way of diagnosing cancer, when they have been released into the bloodstream?

A

Tumour specific antigens

Tumour associated antigens

28
Q

Why are tumour associated antigens not good targets for therapeutic purposes?

A

On both normal and tumour cells

29
Q

What are the 4 ways tumour evade the immune system response?

A

Reduce expression of MHC
Antigen masking - hide tumour associated/specific antigens
Immunosuppression
Tolerance

30
Q

What are the direct effects of malignant or benign tumours?

A 
Obstruction 
Pressure
Replacement of normal tissue (malignant)
Dyshaematopoiesis 
Bone fracture
Malabsorption 
Haemorrhage
Infection
31
Q

Tumours can cause mural or extra mural obstruction. What do these mean? What does obstruction use?

A

Mural - against cavity wall
Extra mural - outside cavity wall
Disruption of arterial, venous and lymphatic flow

32
Q

Tumours can induce pressure on surrounding tissue. What might this cause the tissue to do if in a non-expandable cavity?

A

Atrophy

33
Q

How can tumours cause dyshaematopoiesis?

A

Invade myeloid tissue

34
Q

What are secondary tumours?

A

Tumours caused by metastasis from the original tumour location (primary tumour)

35
Q

How can tumours cause malabsorption?

A

If in gut wall, cause thickening which reduces absorption

36
Q

Tumours can cause haemorrhages. They can be chronic or acute. What are the results of these?

A

Acute - possibly fatal, hypovolaemic shock

Chronic - anaemia

37
Q

Why are secondary infections common with tumours?

A

Epithelial ulceration

Immunosuppression

38
Q

What are some indirect effects of tumours?

A

Paraneoplastic syndromes
Hormonal effects
Hypertrophic pulmonary oesteoarthropathy

39
Q

What is paraneoplastic syndrome?

A

Systemic complications caused by tumour cell products, not the tumour itself

40
Q

Do benign or malignant tumours alter hormones more as part of their indirect effect?

A

Benign - keep cell architecture (requires some differentiation)

41
Q

What is tumour cachexia (wasting syndrome)?

A

Loss of fat and muscle due to tumour

Causes anorexia or polyphagia

42
Q

How can tumour cells cause polyphagia/anorexia in tumour cachexia? (Wasting syndrome)

A

Tumour cells produce cytokines

Act on brain to cause change in appetite

Pathology (22 decks)

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