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Principles Of Disease Year 1 > Tumour > Flashcards

Tumour Flashcards

1
Q

What are the layers of embryonic development?

A

Ectoderm
Mesoderm
Endoderm

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2
Q

What is mucosa?

A

The epithelium and the connective tissue

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3
Q

What are the 2 main types of epithelium concerning cancers?

A

Squamous epithelium
Glandular epithelium

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4
Q

What is hyperplasia ?

A

Increase in the size of organs due to the increase in number of cells
Pathological or physiological

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5
Q

What is hypertrophy?

A

Increase in organ size due to increase in cell size

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6
Q

What is atrophy?

A

Decrease in organ size due to decrease in size of cells

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7
Q

What is metaplasia?

A

Complete transition of 1 differentiated cell to another differentiated cell

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8
Q

What are examples of tumour?

A

Swellings due to masses or inflammation

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9
Q

What is neoplasia?

A

Abnormal growth of tissue due to uncoordinated proliferation
Persists even after cessation of stimuli

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10
Q

Benign neoplasm

A

Neoplasm that doesn’t invade

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11
Q

What’s carcinoma?

A

Malignant neoplasm in epithelium

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12
Q

What is sarcoma?

A

Malignant neoplasm in adipose tissue

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13
Q

What is adenoma?

A

Tumour in glandular of epithelium

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14
Q

What is papilloma?

A

Tumour in the skin

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15
Q

How does papilloma look?

A

Finger like projection

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16
Q

What does the suffix -Oma?

A

Benign tumour

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17
Q

What does carcinoma mean?

A

Malignant epithelium cancer

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18
Q

What are the exceptions to generic cancer naming?

A

Leukaemia is malignant.
Lymphoma is malignant alongside myeloma, glioma and melanoma

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19
Q

What is sarcoma?

A

Malignant cancer in connective and muscle tissue (bones and fat included)

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20
Q

How can you identify carcinoma from histology?

A
  • Looks messy
  • can see intercellular bridges as the cells are pushed out
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21
Q

A benign tumour is part of the neoplasm. True or false

A

True.

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22
Q

How is the growth rate of benign and malignant tumours different?

A

Benign tumors grow much slower

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23
Q

How are the borders of tumours (malignant and benign) different?

A

Benign ones are encapsulated hence are smooth whilst malignant is irregular

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24
Q

How do benign tumours spread compared to malignant ones?

A

Benign ones are confined the by basement membrane whilst malignantones invade locally (adjacent cells) and spreads over a distance (metastasis)

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25
Q

Do malignant and benigntissue resemble the normal tissue?

A

Benign are well differentiated and malignant are poorly differentiated

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26
Q

What are the treatments and recurrence for benign tumours

A

Benign tumours require surgery but has alow chance of recurrence whilst malignant is likely to reoccur and needs chemo or radiotherapy alongside surgery

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27
Q

How to identify benign and malignant tumours?

A

Benign are well defined whilst malignant is messy and depending on the location you can tell if it’s secondary

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28
Q

Osteoma is the most common bone cancer True or false

A

False. Bones tend not to yet cancers its often osteosarcoma and has glandular epithelial looking cancer

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29
Q

How does adenoma look?

A

Glandular epithelium.
Lobes with a lumen in between

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30
Q

How do cancer cells look under a microscope ? (5)

A
  • Pleomorphic
    -Hyperchromatic
  • coarse chromatin
  • highly mitotic and abnormal forms
  • disorganised structure
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31
Q

What does pleomorphic mean?

A

All the cells have a different shape and sizes

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32
Q

What does hyperchromatic mean?

A

The nucleus stains dark in colour

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33
Q

What is coarse chromatin?

A

Lumpy chromatin

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34
Q

What are behaviours of cancer cells?

A
  • Unregulated growth
  • loss of cohesion
  • immaturity
  • immortality
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35
Q

Why do cancer cells have a lack of cohesion?

A

They are able to break off and spread

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36
Q

How do cancer cells hide from the immune system?

A

They temporarily hide their cell/cancer markers

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37
Q

How are cancer cells immortal?

A

Gain the ability to hide from and avoid telomeres

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38
Q

How do cancer cells invade and spread? (4)

A
  • Lack of cohesion between the cells
  • over densely packed (with collagen) so it requires enzymes to breakdown and remodel the connective tissue to grow
  • it uses the new blood cells which the cancer created as an escape route
  • also uses lympathic system to move
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39
Q

How do cancer cells get nutrients?

A

They induce angiogenesis. They make new blood vessels by secreting certain protein

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40
Q

How do cancer cell metabolise?

A

The main aim of a cancercellisto grow but they live in low nutrient environments due to lack of blood vessels. So cancer cells change their normal metabolism

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41
Q

How do mutations affect cancer cells?

A

Cancer cells divide quickly hence are likely to get mutations..
If its a bad mutation, the cell dies.
If it’s a good mutation, the cell benefits and becomes dominant. The cancer cell begins to clone itself

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42
Q

Why do cancer cells cause inflammation?

A

Cancer cells produces molecules for inflammation to prevent damage to the cancer cell itself.

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43
Q

What is apoptosis?

A

Programmed cell death
Active process where the cell breaks down into vesicles to prevent toxic intercellular things from entering connective tissue.

44
Q

What is necrosis?

A

Premature cell death - passive process and messy

45
Q

What are proto-oncogenes?

A

They are normal cells but have the potential to become cancer cells if there is overexpression or mutations

46
Q

What are oncogenes?

A

Normal cells which mutated and causes cancer

47
Q

What are tumour suppressors?

A

Protective molecules that detect DNA damage and inhibit cell growth/division eg. P53

48
Q

How do cancers spread?

A
  • Local spreads-spreads to adjacent cells
  • lymphatic spread- spreads through the lymphatic system
  • haematogenous spread-spreads through the blood (through the newly formed vessels)
  • trans-coelomic spread
49
Q

What is trans-coelomic spread?

A
  • spreads within the body cavity
    Eg. Lung cancer spreads the to pleural cavity
    Or it is peritonealcabdomen)
50
Q

What are common places for metastasis?

A

Liver (due to clearing out toxins from blood)
Brain
Bone ( rich blood supply)
Adrenal gland (melanoma and lung and kidney)

51
Q

What are part of the peritoneal system?

A

Ovaries and abdominal organs

52
Q

What are the local effects of a tumour the brain ?

A

Coma
Seizure
Confusion
Regardless of metastatic, malignant or benign

53
Q

What are the local effects of tumours in the colon ?

A

Constipation tumour is in the way
Haemorrhage- inducing new blood vessels which are more likely to get damaged
Diarrhoea- tumour leaks fluid

54
Q

What are the local effects of tumours in the bone?

A

Anaemia- specialised tissue that produce RBC are damagaed
Pain- tumour presses on nerves
Fractures- cancer affects work of osteoclasts and osteoblasts

55
Q

What are the local effects of a tumour in a liver?

A

Coagulopathy - protein which are involved in clotting are affected since the liver synthesis them.
Jaundice-
Cancer blocks the bile duct

56
Q

What is cachexia?

A

You lose muscle mass more than fat due to alterations in the normal metabolism
It can’t be fixed by changing your diet

57
Q

How is DVT potential sign of cancer?

A

Cancer increases coagulation leading to more blood clots

58
Q

What is paraneoplastic syndrome?

A

Abnormal production of hormones from tumours - like ADH and ACTH.
This causes an autoimmune response and results to nerve damage or moon face

59
Q

How can we detect cancer in the early stages?

A

Some cancers have pre-cancers which are like precursors to cancers

60
Q

What is dysplasia?

A

Disorderred cell growth due to genetic reasons which doesn’t invade

61
Q

What is carcinoma in situ?

A

It’s a pre cancer which looks abnormal and hasn’t spread to nearby tissue

62
Q

How is cervical cancer prevented?

A

HPV vaccines
Cervical screening by taking swabs to find cancer dysplasia

63
Q

What are signal transduction molecules?

A

Messenger molecules which are captivated by receptors at the cell membrane and cause further reactions the cytoplasm and nucleus

64
Q

What is BRAF?

A

Signal transduction molecule is part of a long chain reaction

65
Q

How are molecules activated and inhibited?

A
  1. Phosphorylation
  2. Conformational shape
66
Q

What are transcription factors?

A

Proteins involved in regulation of transcription

67
Q

Where do transcription factors bind?

A

Promoters on DNA

68
Q

How do transcription factors regulate transcription?

A

They often activate enzymes which transcribe DNA to RNA

69
Q

What are the regulatory sequences?

A

Part of DNA which regulates transcription of the gene eg the promoter

70
Q

What are the phases of the cell cycle?

A

G1 S G2 M

71
Q

What are the checkpoints in the cell cycle?

A

G1 G2 and the M checkpoint

72
Q

What happens at both checkpoints?

A

G2 check if it’s correct DNA and cell is big enough
M check if the DNA is correct and the chromosomes are lined down the middle

73
Q

What is the effect of growth factors?

A

It is to push the cell along the G1 phase towards the checkpoint by binding to cell surface receptors and causing reaction cascades

74
Q

How does the cell cycle progress?

A

At the restriction point
Phosphorylation of a protein therefore forcing out the bound E2F molecules. The E2F molecules binds to DNA regulatory sequences and the cell cycle happens as normal

75
Q

What is the key protein with the E2F on it?

A

Retinoblastoma gene product

76
Q

What does retinoblastoma do in it’s normal state?

A

Act as a tumour suppressor gene as unless it’s phosphorylated it doesn’t allow the cell cycle to happen

77
Q

Growth factors are the only reason for G1 progression
True or False

A

False other factors like glucose and amino acid levels play a crucial role by inhibiting or promoting phosphorylation

78
Q

What is HER 2?

A

It is typically an inactive receptor which binds to a cell surface receptors when a growth factor binds to which activates the pathway

79
Q

What happens when there is DNA damage?

A

P53 increases which indirectly blocks the formation of phosphorylated retinoblast gene products hence prevents G1 which blocks the checkpoints

80
Q

How is DNA damage repaired ?

A

Mismatched repair genes codes for proteins that recognise and replace the DNA base. For example the MLH1 gene
It induces P53 which stops the cell cycle.

81
Q

What is MLH1 gene?

A

The products of the mutated gene induces P53 production to stop the cell cycle

82
Q

Proto oncogenes tend to be growth factors.
True or False

A

True

83
Q

What is a tumour suppressor gene?

A

A gene that regulates cell division by controlling or blocking proto oncogenes

84
Q

How do cancers happen even with the tumour suppressor gene?

A

The thmour suppressor gene can get deactivated by environmental factors or can get mutated

85
Q

How do muatations cause cancer with respect to oncogenes?

A

Mutations increase the amount of oncogene product or growth factors
Signal transduction world all the to e inste@d of only when triggered

86
Q

How do mutations cause cancers with respect to the tumour suppresor gene?

A

Stop proteins like retinoblast from working
A viral protein binds to the protein. to make it stop workimg
MLH1 mismatch repair protein stops working

87
Q

What else apart from mutation causes cancer?

A

Genes
Retinoblastoma malignant eye tumour

88
Q

Give example of mutagens.

A

Infection
Radiation
Chemicals

89
Q

How can HER-2 cause cancer?

A

Overexpression creates lots of growth factors as pushes G1 forwards

90
Q

What is the most common mutations of BRAF in malignant melanoma ?

A

An amino acids changes to valine at number 600
So it’s called BRAF V600
This turns on BRAF all the time

91
Q

How many retinoblast gene copies do we have?

A

2

92
Q

What is MLH1 gene?

A

It’s a mismatch repair gene which protein product is involved in correcting DNA code

93
Q

How does smoking cause cancer?

A

The chemicals in cigarettes are broken down into carcinogenes in the liver
This gets released into circulation and DNA gets damages or mutated

94
Q

How does HPV cause cancer?

A

Infects the cervix and produces E6 which binds and inactivate P53 so there is uncontrolled cell division which causes pre cancer and then cancer

95
Q

What does c-myc do?

A

Increases proteins to push the cell cycle
Increases proteins to stop cell death
TIGHTLY CONTROLLED

96
Q

How can c myc cause cancer?

A

It breaks off it’s normal chromosome and binds to another one

97
Q

What is the normal c myc chromosome?

A

8

98
Q

What new chromosome might c myc bind to to create a BIG problem?

A

14 the immunoglobulin sequence which releases B and T cells

99
Q

Why is it dangerous for c myc to bind to chromosome 14?

A

Chromosome 14 releases a lot of B and T cells for our immune system so it would produce a lot of c myc protein which pushes forward the cell cycle

100
Q

What is translocation?

A

Parts of the chromosome move and join onto other ones

101
Q

What type of cancer does the move of c myc from 8 to 14 cause?

A

Lymphoma

102
Q

How is translocation denoted?

A

t(8;14)

103
Q

How does alcohol cause cancer?

A

Large amounts gets converted to acetaldehyde which gets into the systemic circulation and breaks double stranded DNA

104
Q

What happens in the epstein barr virus?

A

Virus infects B cells
B cells proliferate
C myc is translated onto B cells
To produce cancer

105
Q

What is multistep cancer?

A

Various factors combining together to lead to cancer

106
Q

Why does cancer increase coagulation?

A

Because the damage to the tissue causes the clotting process to start

Principles Of Disease Year 1 (16 decks)

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