2.2 MoD Tumours & Cancer Flashcards

(116 cards)

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
Failure of cells to to differentiate into organ-specific tissues. Aplasia Agenesis Dysgenesis Hypoplasia
Aplasia
26
Embryonic cell mass formation failure. Aplasia Agenesis Dysgenesis Hypoplasia
Agenesis
27
Reversible change where one differentiated cell transforms into another type of cell.
Metaplasia
28
In metaplasia, the differentiation of cells is due to stem cells differentiation. True or False?
TRUE
29
What effect does cigarette smoke have on bronchial epithelium structure?
Pseudostratified ciliated epithelium > Squamous epithelium
30
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?
Transitional epithelium > Squamous epithelium
31
What effect does chronic trauma have on fibrocollagenous tissue?
Fibrocollagenous tissue > Bone
32
What effect does acid reflux have on oesophageal epithelium?
Squamous epithelium > Columnar epithelium
33
Metaplasia of epithelia to adapt to changes in stimuli serves to protect the tissue, however this is not the case. Why?
Predisposes neoplasia development (carcinomas, tumours etc.) e.g. CIN development in cervix
34
Abnormal tissue growth that is reversible.
Dysplasia | this precedes neoplasia which is irreversible
35
Define carcinoma.
Cancer that arises in the epithelial tissue of the skin or lining of organs.
36
Define carcinoma in situ.
Cancer that has stayed in the place where it began and not spread to neighbouring tissue (non-invasive).
37
Why is recognition of dysplasia important?
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)
38
Extreme form of systemic atrophy that may be associated with a pathological loss of appetite.
Cachexia
39
Condition that arises due to a defect in the synthesis of haem.
Porphyria
40
Term used to describe the change associated with the growth of breast tissue during pregnancy and lactation.
Hyperplasia
41
Connective tissue framework that usually supports solid tumours.
Stroma
42
The term used to describe a complete lack of differentiation in a tumour.
Anaplasia
43
The commonest type of cancer in men.
Prostate
44
The type of cellular adaptation where cells respond to disease-related stimuli.
Pathological
45
Clinical description of poorly differentiated neoplastic tissue.
High grade
46
Which cell in the body can survive severe metabolic stress without harm?
Fibroblasts
47
Tumour of epithelial cells.
Carcinoma
48
Tumour of connective tissue.
Sarcoma
49
Tumour of lymphoid / haematopoietic cells.
Lymphomas / Leukaemias
50
The most common cancer affecting men in the UK.
Prostate
51
The most common cancer affecting women in the UK.
Breast
52
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?
Incidence: 1. Breast 2. Prostate 3. Lung 4. Bowel Mortality: 1. Lung 2. Bowel 3. Breast 4. Prostate
53
What 4 factors are used to differentiate between a benign and malignant tumour?
1. Rate of growth 2. Differentiation 3. Local invasion 4. Metastasis
54
# Define differentiation. How is it graded?
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
Define anaplasia.
Neoplasms composed of such poorly differentiated cells that they show no resemblance to the normal tissue.
56
What is pleomorphism?
Variation in size and shape of cells. | type of differentiation
57
What abnormal nuclear morphology (features of nuclei) would be suggestive of a tumour?
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
What morphological changes are seen in differentiation?
1. Abnormal nuclear morphology 2. Mitoses (weird mitotic spindle figures) 3. Loss of polarity (orientation of cells disturbed) 4. Pleomorphism
59
Little resemblance to tissue of origin, highly anaplastic appearance. 1. Well differentiated 2. Moderately differentiated 3. Poorly differentiated 4. Undifferentiated
3. Poorly differentiated undifferentiated/anaplastic tissue cannot be identified by morphology alone, it requires molecular techniques.
60
Type of tumour with no capacity to infiltrate, invade or metastasise.
Benign
61
Malignant neoplasm spreads by penetrating into a natural body cavity, most commonly the peritoneal cavity.
Direct seeding very common in ovarian cancer
62
Most common pathway for carcinoma spread.
Lymphatic spread
63
What is haematogenous spread?
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
Benign vs Malignant tumours. Rate of growth? differentiation? Local invasion? Metastasis?
Benign = Slow (variable), well differentiated, No, No Malignant = Rapid (variable), variable differentiation, Yes, Yes
65
What is stroma?
Connective tissue framework which supports cells. provides mechanical support, intracellular signalling, nutrition. Essential in supporting neoplastic tissue.
66
What is a desmoplastic reaction?
Stroma becomes fibrous due to the release of various factors from tumour cells.
67
What does the stroma contain?
1. Cancer-associated fibroblasts 2. Blood vessels 3. Lymphatic infiltrate 4. Myofibroblasts
68
Benign tumour of non-glandular epithelium.
Papilloma e.g. squamous cell papilloma
69
Benign tumour of glandular epithelium.
Adenoma e.g. colonic adenoma
70
The most common skin cancer.
Basal cell carcinoma
71
Malignant tumour of secretory/glandular epithelium.
Adenocarcinoma
72
Benign tumour of bone.
Osteoma
73
Benign tumour of adipose tissue.
Lipoma
74
Malignant tumour of cartilage.
Chondrosarcoma | malignant mesenchymal tissue = sarcoma
75
Metastasis of cancers from the brain to the rest of the body is a common occurrence. True or False?
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
Type of tumour which can contain multiple different types of tissue.
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
What is a dysgerminoma?
Germ cell tumour of ovaries.
78
What is a seminoma?
Germ cell tumour of testes.
79
Malignant tumour of lymphocytes in lymph nodes/solid tissues.
Lymphoma | doesn't follow normal pattern
80
Malignant tumour of lymphocytes in bone marrow/blood.
Leukaemia
81
What causes 'pepper pot skull'?
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
What is a myeloma?
Malignant plasma cells.
83
What is a hamartoma? How does this differ to a choristoma?
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
Benign tumour of blood vessels and fat.
Angiolipoma
85
Malignant tumour of epithelium and stroma.
Carcinosarcoma | ``` epithelium = carcinoma (stroma = mesenchymal = sarcoma) ```
86
Malignant tumour of mesothelium.
Mesothelioma
87
Malignant tumour of melanocytes.
Melanoma | skin cancer
88
LEARN THE TABLES OF TUMOUR CLASSIFICATIONS
Lecture 19 - MoD Tumour classification | at the end
89
Carcinogen that is produced whenever we burn something organic e.g. diesel, bread, steak, coal, tobacco etc.
PAHs
90
Identify 3 mineral carcinogens.
1. Nickel 2. Cadmium 3. Asbestos
91
Asbestos causes cancer in what tissue?
Mesothelium (lung pleura)
92
Aflatoxins are produced by fungi on agricultural crops. | What tissue does it cause cancer in?
Liver
93
What is the most important causative agent associated with breast cancer?
Oestrogen
94
HBV causes what type of cancer?
Liver cancer
95
HPV causes what type of cancer?
Cervical cancer
96
What is an initiator carcinogen?
Genotoxic carcinogens which can chemically modify or damage DNA. (these mutations can then be passed on cell to cell)
97
What is a promoter carcinogen?
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
Give an example of a 'complete' carcinogen.
UV light complete carcinogen = initiator AND promoter
99
How many rounds of DNA replication are required for a mutation to become fixated?
2
100
This type of carcinogen can stimulate clonal expansion of mutated cells, enabling further mutations.
Promoter carcinogen
101
What is the relationship between stem cell divisions and risk of cancer?
Greater number of stem cell divisions = higher risk of cancer
102
What effect can base pair substitutions, amplification, translocations, inversions have on the function of a cell?
Gain of function | activation of proto-oncogenes -> oncogenes
103
What effect can base pair substitutions, frameshifts, deletions, insertions, chromosomal rearrangements, chromosome loss, promoter methylation have on the function of a cell?
Loss of function | inactivation of tumour suppressor genes
104
What is the most common tumour suppressor gene inactivation event?
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
What are procarcinogens?
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
Component of tobacco smoke and burnt food that can be metabolically activated into a potent carcinogen.
Benzopyrene | converted to ultimate carcinogen: BPDE
107
Site of tumours usually associated with the condition XP.
Skin
108
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
DNA replication
109
Give 4 examples of defence mechanisms against carcinogens.
1. Dietary antioxidants 2. DNA repair enzymes 3. Detoxification mechanisms 4. Apoptosis of unrepaired genetic damage 5. Immune response to infection + abnormal cells
110
Usually the first site of metastatic spread by carcinomas.
Lymph nodes
111
Tobacco smoke combined with alcohol leads to a 100-fold increased risk of developing what type of cancer?
Head and neck cancer
112
Give 4 examples of the carcinogenic effects of alcohol.
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
What is the most important causative agent associated with breast cancer?
Oestrogen | complete carcinogen
114
The inflammatory response in chronic inflammation is a complete carcinogen. True or False?
TRUE ``` initiation = DNA damage from free radical release by immune cells promotion = growth factor induced cell division to repair damaged tissue ```
115
What are the 3 stages of carcinogenesis?
Initiation Promotion Progression
116
What environmental/behavioural factor is associated with the highest exposure to carcinogens?
Diet | followed by tobacco and infection