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Principles of Disease > Tumour Pathology > Flashcards

Tumour Pathology Flashcards

1
Q

How are tumours classified?

A

Location and wether or not its benign or malignant.

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2
Q

Why are tumours classified?

A

To aid understanding of tumour behaviour .

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3
Q

What does the name of a tumour convey?

A

It’s behaviour.

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4
Q

What does tumour nomenclature depend on?

A

Tissue type where it is found.

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5
Q

What is tumour nomenclature used for?

A

Identifies what therapy should be considered.

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6
Q

What are the two types of epithelial tissue where tumours are found?

A

Glandular and Squamous.

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7
Q

What is the benign and malignant tumour found in glandular tissue?

A 
Benign= adenoma
Malignant= adeno-carcinoma
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8
Q

What is the benign and malignant tumour found in Squamous tissue?

A 
Benign= squamous papilloma 
Malignant= squamous carcinoma
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9
Q

What are the tumours found in bone?

A 
Benign= osteoma
Malignant= osteo-sarcoma
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10
Q

What are the tumours found in fat?

A 
Benign= Lipoma 
Malignant= Lipo-sarcoma
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11
Q

What are the tumours found in fibrous tissue?

A 
Benign= Fibroma 
Malignant= Fibro-sarcoma
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12
Q

What are the tumours found in WBCs?

A

Malignant= leukaemia

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13
Q

What are the tumours found in lymphoid tissue?

A

Malignant= lymphoma

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14
Q

Where are tumours found in germ cells?

A

Teratomas

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15
Q

What are the tumours found in teratomas?

A 
Benign= ovarian 
Malignant= testicular
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16
Q

What type of tumour has an invasive growth pattern?

A

Malignant

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17
Q

What type of tumour is encapsulated?

A

Benign

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18
Q

What type of tumour has no metastases?

A

Benign

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19
Q

What type of tumour has cells that are normal and well-differentiated?

A

Benign

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20
Q

What tumour is more lethal?

A

Malignant

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21
Q

What type of tumour loses it’s normal function?

A

Malignant

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22
Q

In what type of tissue is there evidence of spread?

A

Malignant

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23
Q

What are the 4 features of cancer cells?

A

Altered genetics, altered cellular function, abnormal structure and independent growth

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24
Q

What are altered genetics?

A

Gain of oncogenes and loss of suppressor genes

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25
Q

How are cellular functions altered?

A

Change in tumour-related proteins.

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26
Q

What does the abnormal structure of cancer cells allow?

A

Diagnosis

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27
Q

What are the affects of independent growth?

A

Failure to respond to cell-cycle regulations and uncontrollable division

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28
Q

What is the process in which cancer spread?

A

Metastasis

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29
Q

What is Metastasis?

A

The formation of secondary tumours

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30
Q

What is local spread?

A

Malignant tumour invasion in surrounding connective tissue into lymph and BVs

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31
Q

What is lymphatic spread?

A

Tumours attach and invade lymph vessels and form secondary tumours in the lymph nodes

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32
Q

What can lymphatic spread be used for?

A

Clinical evidence

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33
Q

What is blood spread?

A

Tumour cells invading blood cells and forming secondary tumours in tissues

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34
Q

What is trans-coelomic spread?

A

Spread of tumours across body cavities

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35
Q

Where are trans-coelomic tumours shown?

A

Stomach, ovaries, colon and lungs

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36
Q

What are the common sites for tumour formation?

A

Liver, lung, brain, bone and adrenal glands

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37
Q

What are the uncommon sites for skeletal muscle?

A

Spleen, kidneys, skeletal muscle and heart

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38
Q

What are the local effects of benign tumours?

A

Pressure and obstruction

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39
Q

What are the local effects of malignant tumours?

A

Pressure, obstruction, pain, tissue destruction and bleeding

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40
Q

How are tissues destroyed?

A

Ulceration and infection

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41
Q

How do tumours cause bleeding?

A

Anaemia and haemorrhage

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42
Q

How do tumours cause pain?

A

Pressure on nerves and bone fractures

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43
Q

What are the 3 systematic effects of tumours?

A

Hormone secretion, weight loss and treatment effects

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44
Q

What are the 2 types of hormones secreted?

A

Normal and Abnormal

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45
Q

How are normal hormones secreted?

A

Tumours produced in the endocrine organ

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46
Q

What is the function of normal hormones?

A

Abnormal control of production and secretion

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47
Q

How are abnormal hormones secreted?

A

Tumour produced in an organ that does not normally produce hormones

48
Q

What type of hormone is most commonly secreted?

A

Abnormal

49
Q

What causes weight loss?

A

Cachexia

50
Q

What is the earliest stage of detecting cancer?

A

Pre-invasive stage

51
Q

What is detected at the pre-invasive stage?

A

Dysplasia

52
Q

What is dysplasia the same as?

A

Intraepithelial neoplasia

53
Q

What is dysplasia 1?

A

Pre-malignant change and the earliest visualised change

54
Q

What is dysplasia 2?

A

No invasion and can progress to cancer

55
Q

Where is dysplasia 2 located?

A

Epithelium

56
Q

What is meant by a high grade of dysplasia?

A

Higher chance of progressing to cancer

57
Q

What can’t occur if there is no invasion?

A

Detection of spred

58
Q

What is a cell cycle?

A

Time interval between mitotic divisions

59
Q

What is the normal cell cycle?

A

Mechanism of cellular replication

60
Q

Cellular replication is also known as?

A

Proliferation

61
Q

Is the normal cell cycle reversible?

A

No

62
Q

What are the 4 steps of the normal cell cycle?

A

G1, S, G2, M

63
Q

What happens in G1?

A

Cells can respond to external signals and components required for DNA synthesis are synthesised

64
Q

What happens in S?

A

DNA is synthesised and replicated

65
Q

What happens in G2?

A

Mitosis is prepared

66
Q

What happens in M?

A

Mitosis and cell division

67
Q

How does DNA synthesis an mitosis occur?

A

Sequentially

68
Q

What must each daughter cell receive?

A

A full chromosome complement

69
Q

How is the normal cell cycle controlled?

A

By active and inactive enzyme switches in checkpoints

70
Q

What are normal cell cycle checkpoints?

A

System of active and inactive enzymes

71
Q

Where do normal cell cycle checkpoints occur?

A

On several points in the cycle

72
Q

How is an active enzyme complex formed?

A

When CDK is activated by cyclins

73
Q

Are CDK and cyclin always present?

A

No, only CDK is always present. Cyclins are only present when needed

74
Q

What is the function of an enzyme switch?

A

Activates/inactivates and phosphorylates target proteins

75
Q

What is CKI?

A

CDK inhibitor that prevents molecules from binding to the active enzyme complex

76
Q

What is cancer?

A

Abnormal cell cycle function due to uncontrolled cell proliferation via cell cycle dysregulation

77
Q

What is carcinogenesis?

A

Failure of cell cycle control as the balance between proliferation and apoptosis is disrupted

78
Q

What occurs as a result of carcinogenesis?

A

Formation of DNA adducts and a mass of cells with genetic abnormalities. Cell cycle regulators are mutated

79
Q

What are the causes of carcinogenesis?

A

Radiation (UV, X-ray and Gamma), Viruses (Hep. B, HPV and EBV) and a series of mutations

80
Q

What is the process of viral carcinogenesis?

A

Virus genome inserts near a host proto-oncogne which causes port-oncogene over expression. Retroviruses then insert on the oncogenes and causes cell division.

81
Q

What does HPV cause?

A

Cervical cancer

82
Q

What does Hepatitis B cause?

A

Liver cancer

83
Q

What does EBV cause?

A

Lymphomas

84
Q

What is the process of chemical carcinogenesis?

A

Adduct formation at particular chromosome sites that activates oncogenes and suppresses anti-oncogenes

85
Q

What are the 4 cell-regulatory genes?

A

Cyclin D, CDK4, p16 and Rb

86
Q

What happens to cell-cycle regulator genes?

A

They are mutated

87
Q

What pathways of the normal cell cycle does carcinogenesis disrupt?

A

Cyclin pRb and p53 pathway

88
Q

What is the function of p53?

A

It maintains the integrity of the genome and expresses p21 to repair DNA

89
Q

What occurs in the cyclin pRb pathway?

A

pRb acts as a cell cycle brake which controls growth and proliferation

90
Q

What happens when the cyclin pRb pathway is mutated?

A

The pRb brakes are released which causes uncontrolled proliferation

91
Q

What occurs in the p53 pathway?

A

Cell cycle is stopped when the cell sustains damage so it can be repaired

92
Q

What does p53 trigger when cells are badly damaged?

A

Apoptosis

93
Q

What happens when p53 is mutated?

A

Cells do not enter G1 arrest which prevents DNA repair

94
Q

How is the cell cycle prevented from stopping?

A

Mutations, which causes cancer

95
Q

What are DNA adducts?

A

They are covalently bound products that activate oncogenes and causes the loss of anti-oncogenes

96
Q

What are tumour suppressor genes?

A

Recessive anti-oncogenes that are normal regulatory and genes.

97
Q

What is an example of a tumour suppressor gene?

A

pRb (anti-oncogene)

98
Q

What are the functions of tumour suppresser genes?

A

Regulates DNA and mitosis (negatively)

99
Q

What happens when pRb is released from the cell cycle?

A

Cell cycle brakes are released

100
Q

What is the function of pRb?

A

It prevents cells from entering the cell cycle by inactivating E2F

101
Q

What is the difference between somatic and inherited mutations?

A

In somatic, both hits occur in a single cell whereas for inherited there is one defective inherited copy of pRb so both cells are affected

102
Q

What is oncogenesis?

A

Formation of cancer cells, same as carcinogenesis. It is autosomal recessive and takes longer to develop

103
Q

What chemical activates oncogenes?

A

Benzopyrene

104
Q

What is an oncogene?

A

A cell that can transform a cell into a cancer cell. They are derived from photo-oncogenes

105
Q

How are oncogenes activated?

A

Dysregulation of proto-oncogene expression and translocations

106
Q

What do oncogenes form when expressed?

A

Oncoprotein

107
Q

What is a proto-oncogene?

A

Normal cells that promote cell growth and mitosis

108
Q

How do photo-oncogenes promote cel growth?

A

They code for growth promoting proteins

109
Q

What is the connection between oncogenes and proto-oncogenes?

A

Oncogenes are produced when the DNA sequence of photo-oncogens is changed

110
Q

What are the products of oncoproteins?

A

Growth factors and cell cycle regulators

111
Q

What colour signals are used to detect abnormalities in cell cycle regulators?

A

Yellow

112
Q

What type of process in tumour formation?

A

Multi-step

113
Q

What is the process of tumour formation?

A

Normal cells are exposed to carcinogenic factors that causes DNA damage and mutations. This inactivates tumour suppressor genes and activates growth-promoting oncogenes which causes cell cycle dysregulation and the formation of tumours

114
Q

What is formed at the end of the process of tumour formation?

A

A malignant neoplasm

115
Q

What are the major aetiological agents?

A

Predisposition, viruses, radiation and chemicals

116
Q

What type of inheritance is a cancer predisposition?

A

Autosomal dominant

117
Q

What are exmaples of inherited predispositions?

A

Familial retinoblastoma that has an early age of onset

Principles of Disease (8 decks)

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