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Y2 EMS > 2.2 MoD Tumours & Cancer > Flashcards

2.2 MoD Tumours & Cancer Flashcards

1
Q

Reversible cellular changes in response to changes in the environment or demand.

A

Adaptation

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2
Q

Give 4 ways a cell can adapt.

A
  1. Size
  2. Number
  3. Phenotype
  4. Metabolic activity
  5. Function
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3
Q

How susceptible to adaptation are fibroblasts?

A

Do NOT need to adapt.

They can withstand a lot of metabolic stress
e.g. hypoxia

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4
Q

How susceptible to adaptation are epithelial cells?

A

Adapt very easily.

Labile cell population which are constantly under different types of stress so need to be able to adapt.

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5
Q

How susceptible to adaptation are cerebral neurons?

A

Cannot adapt.

Terminally differentiated permanent cell population.
Highly specialised and sensitive cells which cannot adapt to change.

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6
Q

What is the difference between physiological and pathological cellular adaptation?

Are they mutually exclusive?

A

Physiological = responding to normal changes in physiology or demand (slight fluctuations to what we’re used to).

Pathological = responding to disease causing change.

No, if a physiological change is excessive or prolonged, it can become pathological and harm the cell.

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7
Q

How would a cell respond to increased cellular activity?

A

Increase in size + number.

opposite if there is decreased cellular activity

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8
Q

Define hypertrophy.

A

Increase in size of cell.

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9
Q

Define hyperplasia.

A

Increase in the number of cells.

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10
Q

Which cell population is hypertrophy very common in? Give an example.

A

Permanent cell populations.

e.g. cardiac muscle + skeletal muscle.

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11
Q

How does the myocardium respond/adapt to an aortic stenosis?

A

Hypertrophy of the heart muscle.

has to work harder due to the narrowing/stiffening of the valve

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12
Q

What problems (symptoms) are associated with LVH (left ventricular hypertrophy)?

How would you diagnose?

A 
Shortness of breath
fatigue
chest pain
worse after exercise
heart fluttering/palpitations
dizziness

displaced apex beat
irregular heart rhythm
x-ray = prominent heart outline
ECG = bigger peaks, S waves which shouldn’t be there, echocardiogram = thickened heart muscle. Due to exercise?

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13
Q

Barbiturates (sleeping pills/psychiatric drugs) can cause hypertrophy in what?

A

Endoplasmic reticulum of hepatocytes (subcellular hypertrophy).

Increased demand of P450 enzymes to metabolise the drug leads to hypertrophy of the SER to produce more.

(alcohol consumption also increases demand for P450 enzymes)

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14
Q

Is hyperplasia of the liver after donation of a liver segment physiological or pathological?

A

Physiological - compensatory

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15
Q

Is Grave’s disease a result of hypertrophy or hyperplasia?

A

Hyperplasia of thyroid

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16
Q

Define atrophy.

A

Reduction in size of an organ/tissue by a decrease in the size and number of cells.

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17
Q

Reduction in size of tissue during embryogenesis, uterus after pregnancy or menopause are examples of what?

A

Involution - physiological atrophy

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18
Q

Give 4 examples of what can cause atrophy.

A
  1. Decreased workload (disuse atrophy)
  2. Loss of innervation (denervation atrophy)
  3. Diminished blood supply
  4. Inadequate nutrition
  5. Loss of endocrine stimulation
  6. Pressure
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19
Q

What can renal artery stenosis cause?

A

Atrophy of the kidney due to a decreased blood supply.

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20
Q

The thymus undergoes physiological hypertrophy as you get older.
True or False?

A

FALSE

thymus gets smaller (physiological ATROPHY) because you don’t need it as much when your older

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21
Q

Why is it important in a patient chronically taking steroids, that you ease them off the medication rather than just stopping it all together?

A

Your adrenal glands undergo atrophy due to chronic steroid therapy which reduces ACTH drive (stimulates adrenals to secrete glucocorticoids).
If you suddenly stop steroid medication, your adrenals cannot cope and produce enough steroids which is very dangerous.

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22
Q

What is the most common cause of LVH?

A

Hypertension

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23
Q

A horseshoe kidney is an example of?

Aplasia
Agenesis
Dysgenesis
Hypoplasia

A

Dysgenesis - failure of the tissues to organise themselves into the correct organ structure.

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24
Q

Failure of an organ to grow to full size

A

Hypoplasia

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25
Q

Failure of cells to to differentiate into organ-specific tissues.

Aplasia
Agenesis
Dysgenesis
Hypoplasia

A

Aplasia

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26
Q

Embryonic cell mass formation failure.

Aplasia
Agenesis
Dysgenesis
Hypoplasia

A

Agenesis

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27
Q

Reversible change where one differentiated cell transforms into another type of cell.

A

Metaplasia

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28
Q

In metaplasia, the differentiation of cells is due to stem cells differentiation.
True or False?

A

TRUE

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29
Q

What effect does cigarette smoke have on bronchial epithelium structure?

A

Pseudostratified ciliated epithelium > Squamous epithelium

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30
Q

What effect does long standing irritation to the bladder e.g. schistosomiasis, long-standing catheter, bladder stones have on the epithelial lining of the bladder?

A

Transitional epithelium > Squamous epithelium

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31
Q

What effect does chronic trauma have on fibrocollagenous tissue?

A

Fibrocollagenous tissue > Bone

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32
Q

What effect does acid reflux have on oesophageal epithelium?

A

Squamous epithelium > Columnar epithelium

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33
Q

Metaplasia of epithelia to adapt to changes in stimuli serves to protect the tissue, however this is not the case. Why?

A

Predisposes neoplasia development (carcinomas, tumours etc.)

e.g. CIN development in cervix

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34
Q

Abnormal tissue growth that is reversible.

A

Dysplasia

this precedes neoplasia which is irreversible

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35
Q

Define carcinoma.

A

Cancer that arises in the epithelial tissue of the skin or lining of organs.

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36
Q

Define carcinoma in situ.

A

Cancer that has stayed in the place where it began and not spread to neighbouring tissue (non-invasive).

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37
Q

Why is recognition of dysplasia important?

A

You can treat a potentially fatal tumour before it arises, the abnormal cells have not yet developed the capacity for invasion therefore they cant spread.

(the whole basis of the cervical screening programme)

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38
Q

Extreme form of systemic atrophy that may be associated with a pathological loss of appetite.

A

Cachexia

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39
Q

Condition that arises due to a defect in the synthesis of haem.

A

Porphyria

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40
Q

Term used to describe the change associated with the growth of breast tissue during pregnancy and lactation.

A

Hyperplasia

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41
Q

Connective tissue framework that usually supports solid tumours.

A

Stroma

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42
Q

The term used to describe a complete lack of differentiation in a tumour.

A

Anaplasia

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43
Q

The commonest type of cancer in men.

A

Prostate

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44
Q

The type of cellular adaptation where cells respond to disease-related stimuli.

A

Pathological

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45
Q

Clinical description of poorly differentiated neoplastic tissue.

A

High grade

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46
Q

Which cell in the body can survive severe metabolic stress without harm?

A

Fibroblasts

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47
Q

Tumour of epithelial cells.

A

Carcinoma

48
Q

Tumour of connective tissue.

A

Sarcoma

49
Q

Tumour of lymphoid / haematopoietic cells.

A

Lymphomas / Leukaemias

50
Q

The most common cancer affecting men in the UK.

A

Prostate

51
Q

The most common cancer affecting women in the UK.

A

Breast

52
Q

What are the top 4 cancers in the UK with the highest incidence?

What are the top 4 cancers in the UK with the highest mortality?

A

Incidence:

  1. Breast
  2. Prostate
  3. Lung
  4. Bowel

Mortality:

  1. Lung
  2. Bowel
  3. Breast
  4. Prostate
53
Q

What 4 factors are used to differentiate between a benign and malignant tumour?

A
  1. Rate of growth
  2. Differentiation
  3. Local invasion
  4. Metastasis
54
Q

Define differentiation.

How is it graded?

A

How much the tumour cells look like the normal cells of that tissue.

  1. Well differentiated / low grade - closely resembles normal tissue.
  2. Moderately differentiated / intermediate
  3. Poorly differentiated / high grade - cells hardly resemble the normal tissue
55
Q

Define anaplasia.

A

Neoplasms composed of such poorly differentiated cells that they show no resemblance to the normal tissue.

56
Q

What is pleomorphism?

A

Variation in size and shape of cells.

type of differentiation

57
Q

What abnormal nuclear morphology (features of nuclei) would be suggestive of a tumour?

A
  1. Nuclei appear too large for the cell that they are in - little cytoplasm.
  2. Irregular nuclear outline
  3. Hyperchromatic - nuclei are darker than normal (extra chromosomes for replication)
  4. Abnormally large nuclei
58
Q

What morphological changes are seen in differentiation?

A
  1. Abnormal nuclear morphology
  2. Mitoses (weird mitotic spindle figures)
  3. Loss of polarity (orientation of cells disturbed)
  4. Pleomorphism
59
Q

Little resemblance to tissue of origin, highly anaplastic appearance.

  1. Well differentiated
  2. Moderately differentiated
  3. Poorly differentiated
  4. Undifferentiated
A
  1. Poorly differentiated

undifferentiated/anaplastic tissue cannot be identified by morphology alone, it requires molecular techniques.

60
Q

Type of tumour with no capacity to infiltrate, invade or metastasise.

A

Benign

61
Q

Malignant neoplasm spreads by penetrating into a natural body cavity, most commonly the peritoneal cavity.

A

Direct seeding

very common in ovarian cancer

62
Q

Most common pathway for carcinoma spread.

A

Lymphatic spread

63
Q

What is haematogenous spread?

A

Invasion of tumour into blood vessels.

Often come to rest at the first capillary bed encountered, usually lungs + liver.
Typical of sarcomas (but also seen in carcinomas).

64
Q

Benign vs Malignant tumours.

Rate of growth? differentiation? Local invasion? Metastasis?

A

Benign = Slow (variable), well differentiated, No, No

Malignant = Rapid (variable), variable differentiation, Yes, Yes

65
Q

What is stroma?

A

Connective tissue framework which supports cells.

provides mechanical support, intracellular signalling, nutrition.

Essential in supporting neoplastic tissue.

66
Q

What is a desmoplastic reaction?

A

Stroma becomes fibrous due to the release of various factors from tumour cells.

67
Q

What does the stroma contain?

A
  1. Cancer-associated fibroblasts
  2. Blood vessels
  3. Lymphatic infiltrate
  4. Myofibroblasts
68
Q

Benign tumour of non-glandular epithelium.

A

Papilloma

e.g. squamous cell papilloma

69
Q

Benign tumour of glandular epithelium.

A

Adenoma

e.g. colonic adenoma

70
Q

The most common skin cancer.

A

Basal cell carcinoma

71
Q

Malignant tumour of secretory/glandular epithelium.

A

Adenocarcinoma

72
Q

Benign tumour of bone.

A

Osteoma

73
Q

Benign tumour of adipose tissue.

A

Lipoma

74
Q

Malignant tumour of cartilage.

A

Chondrosarcoma

malignant mesenchymal tissue = sarcoma

75
Q

Metastasis of cancers from the brain to the rest of the body is a common occurrence.
True or False?

A

FALSE
cancers metastasise TO the brain, generally not vice versa.

(you would probably be dead by the time a cancer in your brain develops the ability to invade other tissues)

76
Q

Type of tumour which can contain multiple different types of tissue.

A

Germ cell tumours.

the germ cells differentiate into different types of tissue during embryonic development, you can end up with a lesion containing hair, teeth, neural etc.

77
Q

What is a dysgerminoma?

A

Germ cell tumour of ovaries.

78
Q

What is a seminoma?

A

Germ cell tumour of testes.

79
Q

Malignant tumour of lymphocytes in lymph nodes/solid tissues.

A

Lymphoma

doesn’t follow normal pattern

80
Q

Malignant tumour of lymphocytes in bone marrow/blood.

A

Leukaemia

81
Q

What causes ‘pepper pot skull’?

A

Myeloma (malignant plasma cells) spread to the skull bone and cause lesions which are easily seen in x-rays.

(Can test for myeloma by doing a simple blood test looking for excessive production of one type of monoclonal antibody.)

82
Q

What is a myeloma?

A

Malignant plasma cells.

83
Q

What is a hamartoma?

How does this differ to a choristoma?

A

BENIGN non-neoplastic tissue overgrowth containing different tissue that is appropriate for the organ where it is found.

e.g. lung hamartoma (common) - there is a mass which contains bronchial epithelium and cartilage. NON cancerous.

(these can be mistaken for malignant neoplasms on imaging)

Choristoma = same thing, but it is heterotopic (tissue shouldn’t be there)
e.g. ocular choristoma - overgrowth on the eye containing cartilage.

84
Q

Benign tumour of blood vessels and fat.

A

Angiolipoma

85
Q

Malignant tumour of epithelium and stroma.

A

Carcinosarcoma

```
epithelium = carcinoma
(stroma = mesenchymal = sarcoma)
~~~

86
Q

Malignant tumour of mesothelium.

A

Mesothelioma

87
Q

Malignant tumour of melanocytes.

A

Melanoma

skin cancer

88
Q

LEARN THE TABLES OF TUMOUR CLASSIFICATIONS

A

Lecture 19 - MoD Tumour classification

at the end

89
Q

Carcinogen that is produced whenever we burn something organic e.g. diesel, bread, steak, coal, tobacco etc.

A

PAHs

90
Q

Identify 3 mineral carcinogens.

A
  1. Nickel
  2. Cadmium
  3. Asbestos
91
Q

Asbestos causes cancer in what tissue?

A

Mesothelium (lung pleura)

92
Q

Aflatoxins are produced by fungi on agricultural crops.

What tissue does it cause cancer in?

A

Liver

93
Q

What is the most important causative agent associated with breast cancer?

A

Oestrogen

94
Q

HBV causes what type of cancer?

A

Liver cancer

95
Q

HPV causes what type of cancer?

A

Cervical cancer

96
Q

What is an initiator carcinogen?

A

Genotoxic carcinogens which can chemically modify or damage DNA.

(these mutations can then be passed on cell to cell)

97
Q

What is a promoter carcinogen?

A

Non-genotoxic (don’t damage DNA) carcinogen, but induce proliferation of cells/tissue (and hence DNA replication) which fixes a mutation into place.

e.g. they will kill cells and cause the surrounding cells to proliferate + regenerate.

(oestrogen is a promotor carcinogen)

98
Q

Give an example of a ‘complete’ carcinogen.

A

UV light

complete carcinogen = initiator AND promoter

99
Q

How many rounds of DNA replication are required for a mutation to become fixated?

A

2

100
Q

This type of carcinogen can stimulate clonal expansion of mutated cells, enabling further mutations.

A

Promoter carcinogen

101
Q

What is the relationship between stem cell divisions and risk of cancer?

A

Greater number of stem cell divisions = higher risk of cancer

102
Q

What effect can base pair substitutions, amplification, translocations, inversions have on the function of a cell?

A

Gain of function

activation of proto-oncogenes -> oncogenes

103
Q

What effect can base pair substitutions, frameshifts, deletions, insertions, chromosomal rearrangements, chromosome loss, promoter methylation have on the function of a cell?

A

Loss of function

inactivation of tumour suppressor genes

104
Q

What is the most common tumour suppressor gene inactivation event?

A

Methylation of gene promotor regions

causes histones to accumulate around the gene (closed chromatin), switching off the gene (transcription factors can’t access it).

105
Q

What are procarcinogens?

A

Carcinogens which require enzymatic (metabolic) activation before they can react with DNA.

(this is in contrast to ‘direct acting’ carcinogens which directly react with DNA and don’t need to be activated e.g. UV light, oxygen radicals)

106
Q

Component of tobacco smoke and burnt food that can be metabolically activated into a potent carcinogen.

A

Benzopyrene

converted to ultimate carcinogen: BPDE

107
Q

Site of tumours usually associated with the condition XP.

A

Skin

108
Q

All of these steps, except ONE influences your risk of developing cancer after being exposed to a carcinogen, which differs between individuals due to genetic variation in the effectiveness of these enzymes.

DNA replication
DNA repair
Metabolic activation
Detoxification excretion

A

DNA replication

109
Q

Give 4 examples of defence mechanisms against carcinogens.

A
  1. Dietary antioxidants
  2. DNA repair enzymes
  3. Detoxification mechanisms
  4. Apoptosis of unrepaired genetic damage
  5. Immune response to infection + abnormal cells
110
Q

Usually the first site of metastatic spread by carcinomas.

A

Lymph nodes

111
Q

Tobacco smoke combined with alcohol leads to a 100-fold increased risk of developing what type of cancer?

A

Head and neck cancer

112
Q

Give 4 examples of the carcinogenic effects of alcohol.

A
  1. Converted to acetaldehyde - can cause DNA damage
  2. Increases levels of oestrogen + testosterone
  3. Acts as a solvent and assists the uptake of carcinogenic chemicals into cells
  4. Reduces folate levels - needed for accurate replication
  5. Can kill surface epithelium, causing unwanted proliferation
  6. Linked to oral, oesophageal, liver, bowel cancer
113
Q

What is the most important causative agent associated with breast cancer?

A

Oestrogen

complete carcinogen

114
Q

The inflammatory response in chronic inflammation is a complete carcinogen.
True or False?

A

TRUE

initiation = DNA damage from free radical release by immune cells
promotion = growth factor induced cell division to repair damaged tissue
115
Q

What are the 3 stages of carcinogenesis?

A

Initiation
Promotion
Progression

116
Q

What environmental/behavioural factor is associated with the highest exposure to carcinogens?

A

Diet

followed by tobacco and infection

Y2 EMS (4 decks)

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