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DEN203 > G&D- Cancer > Flashcards

G&D- Cancer Flashcards

1
Q

NAME 4 Types of (tissue) disorders: (can be developmental or due to a response from a certain stimulus)

A
  • Too much (e.g. tissue)?
  • Too little
  • Wrong type
  • Wrong place
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2
Q

How might cell stress lead to cell death?

A

Cell stress (with high dose intensity and cell vulnerability) -> Injury-> Irreversible injury -> DEATH

Dividing cells are more vulnerable to radiation! Cells can metabolically or structurally adapt in response to chronic stress. But cell may not be able to cope… resulting in injury and eventually death.

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3
Q

How might a cell adapt to stress in normal conditions (3)

A

Atrophy
Hypertrophy
Hyperplasia

Not normal: metaplasia…

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4
Q

What is atrophy?

A
  • Decrease in cell size

- Decrease in cell number

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5
Q

What is hypertrophy?

A

Increase in cell size

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6
Q

What is hyperplasia?

A

Increase in cell number

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7
Q

Name 3 types of cells (relating to their diving qualities)

A

1- Labile
2- Permanent
3- Stable

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8
Q

What are labile cells?

  • Examples?
  • What happens with cell stress?
A

continually dividing

Epidermal/ endothelial, GI tract lining, bone marrow, Immune

 Stress in these cells results in INCREASED rate of cell division as they have the capacity to divide -> Hyperplasia

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9
Q

What are permanent cells?

  • Examples?
  • What happens with cell stress?
A

(In an adult) No longer have capacity to divide:

Cardiac, Neurones

 Stress may be high BP, Heart has to pump harder-> Hypertrophy occurs)
 Heart attack-> Death of Myocytes-> No real way of regenerating

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10
Q

What are stable cells?

A

Ceased cell division but retained the capacity to divide:

Liver (Hepatocytes)

 If half of liver removed, can regrow!

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11
Q

What is the cell cycle?

A

controlled way in which cells copy the nucleic acid and divide

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12
Q

Name a developmental condition where there is Too much tissue

A

Hamartoma

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13
Q

What is a Hamartoma?

A

Tumour-like overgrowth
Grows in patient’s growth period (child) but stops growing when they reach adulthood.
Tissues are normal for site but excessive.

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14
Q

Give 3 examples of hamartomas

A
  • Pigmented naevi (moles)- patch of naevi melanocytes (lots of melanin pigment)
  • Haemangioma- blood vessels, can be big or small, knots of BVs (too much) – can cause problems with bleeding (common in older px as their mucosa thins and it becomes more apparent)
  • Odontomes- teeth abnormalities, extra tooth or disorganised dental hard tissue
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15
Q

Name a reactive/adaptive condition where there is Too much tissue

A

Hyperplasia.

Hypertrophy.

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16
Q

What is hyperplasia?

A

increase in cell numbers

Response to stimulus, Regression once stimulus removed!

Increase in size and function of a tissue.

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17
Q

Give some examples when hyperplasia occurs-

A

Endocrine (Physiological)- normal growth and devleopment, puberty, pregnancy

Endocorine, Pathological: parathyroids and thyroid

  • Chronic irritation/ inflammation
  • Bone marrow, lymphoid tissue
  • Thyroid hyperplasia with iron deficiencies- Fe+ needed to make thyroid hormone! Will feed back to thyroid gland and cause cells to divide!
  • Gingival hyperplasia- long term chronic inflammation stimulates division of epithelial and fibroblast cells; improve with OHI? Can be caused by medication
  • Hyperplasia of the tonsils- immune response
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18
Q

What is hypertrophy?

A

increase in cell size

Often occurs with hyperplasia.

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19
Q

Name some Pure hypertrophy examples:

A
  • Muscle- mechanical stimulus
  • Skeletal- exercise
  • Smooth- pregnancy
  • Cardiac- LVH in hypertension- High BP, resistance to which heart is pumping has increased, increase power of pump!
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20
Q

What is neoplasia?

A

growth which is uncontrolled and does not stop. Persists after the stimulus is removed!

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21
Q

Name 3 developmental condition where there is Too little tissue

A
  • Agenesis
  • Aplasia
  • Hypoplasia
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22
Q

What is agenesis?

A

does not develop at all (Missing tooth?)

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23
Q

What is Aplasia?

A

Present but fails to develop normal structure (e.g. major bodily organs, 2 kidneys but changed structure)

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24
Q

What is hypoplasia?

A

: Present, normal structure but Less tissue formed (smaller)

 Achondroplasia- problem with development of the long bones
 Enamel hypoplasia
 Amelogenesis Imperfecta
 Hypoplastic mandible and malocclusion

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25
Q

Name a reactive/response condition where there is Too little tissue

A

Atropy

  • Localised
  • Generalised
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26
Q

What is atrophy?

A

decrease in size/number after growth… Can be physiological (embryology)

Mechanisms: Imbalance of cell loss/production

  • Reduced proliferation
  • Apoptosis rather than necrosis (mostly)
  • Reduction in structural components of the cell, esp proteins
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27
Q

What is generalised atrophy?

A

 Nutritional deficiency(starvation)- shiny tongue= iron deficiency

 Senile (when people age)

 Endocrine (physiological hypoplasia e.g. oestrogen, sexual hormones)

 Bone- osteoporosis, reduction in bone mass/ density as trabecular structure becomes less compact (tendency in older females due to oestrogen levels and menopause)

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28
Q

What is localised atrophy?

A

 Ischaemic (heart)- due to reduction in blood supply!

 Pressure

 Disuse (similar to below) – stop working out= lose muscle mass

 Neuropathic/ denervation- nerve damage by trauma, atrophy of muscle

 Immune mediated (autoimmune)

 Idiopathic- Unknown reason

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29
Q

What is an Atrophic mandible?

A

bone resorption as tooth absent (rate varies between Px)

 Important factor in denture retention

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30
Q

3 Examples of atrophy

A
  • atrophic mandible
  • Alzheimer’s (white/grey matter)
  • Romberg’s disease- hemifacial
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31
Q

Name 2 conditions where tissue is the wrong type

A
  • Metaplasia

- Dysplasia

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32
Q

What is metaplasia?

A

Abnormal differentiation

  • Change from one differentiated tissue to another (within the same germinal layer)
  • Result from changes in environmental demands.
  • Epithelium: mucous, squamous, mesenchymal
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33
Q

Give an example of metaplsia in smokers

A

(may be first step on the route to cancer)

  • Squamous metaplasia in bronchi of smokers ( epithelium undergoes squamous metaplasia changes from respiratory type of epithelium to squamous)
  • Px can get cancer
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34
Q

Give an example of metaplsia in px with acid reflux

A
  • Gastric metaplasia in oesophagus of patients with acid reflux
  • Squamous-> Gastrix type of epithelium
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35
Q

What is dysplasia?

A
  • abnormal growth and differentiation in a tissue, with abnormal cells and tissue architecture.
  • May be premalignant
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36
Q

Name the condition where tissue is in the wrong place

A

Ectopia- Developmental abnormality; Normal tissue but abnormal site!

e.g. Left kidney in wrong place or Max canines angled in the wrong direction!

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37
Q

What causes cancer?

A
  • Cancer (neoplasia) is caused by abnormal cell growth
  • This results from changes in the levels or function of proteins regulating proliferation, differentiation and survival of cells
  • This is caused by mutations in genes
  • These mutations may be genetic, environmental or viral
  • A number of mutations are required to cause cancer
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38
Q

Why might a mutation not lead to cancer?

A
  • Doesn’t necessarily change protein sequence
  • Cells are usually good at noticing changes in bases
  • DNA in a cell is huge and a lot of DNA doesn’t actually code for proteins
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39
Q

What is DNA transcription?

A

involves mRNA, leaves nucleus to cytoplasm, tRNA bring an amino acid which is complementary to the base sequence.

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40
Q

Name 3 Types of mutations:

A

1) Point mutations
a. Change in amino acid
b. Frameshift
c. Introduce STOP codon
d. Change splicing

2) Gene amplifications
3) Chromosomal translocations

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41
Q

What is a chromosome translocation?

A

a chromosome abnormality caused by rearrangement of parts between non-homologous chromosomes. A gene fusion may be created when the translocation joins two otherwise-separated genes. It is detected on cytogenetics or a karyotype of affected cells (may be able to see this by staining the chromosomes.

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42
Q

What is amplification?

A

increases the number of copies of a gene without a proportional increase in other genes.

This can result from duplication of a region of DNA that contains a gene through errors in DNA replication and repair machinery as well as through fortuitous capture by selfish genetic elements.

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43
Q

What is a somatic mutation?

A

Somatic- occur in a single body cell and cannot be inherited (only tissues derived from mutated cell are affected)

  • Somatic mutation occurs in non-germline tissues
  • Non-heritable
    e. g. breast cancer
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44
Q

What is a germ-line mutation?

A

occur in gametes and can be passed onto offspring (every cell in the entire organism will be affected)

  • Mutation present in egg/sperm
  • ARE heritable
  • Cause cancer family syndrome
  • All cells affected in offspring
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45
Q

NAme some Characteristics of cancer cells (7)

mutations of genes that regulate the below processes are seen in all cancers!

A
  • Excess proliferation without external stimuli
  • loss of control mechanisms
  • Loss of apoptosis
  • Defects in DNA
  • Irreversible, limitless change
  • Acquisition of a blood supply - angiogenesis
  • Invasion of surrounding structures
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46
Q

Name 4 genes involved in cancer

A

1) Oncogenes (accelerate cancer!)
2) Tumour suppressor genes (Prevent cancer!)
3) Apoptosis genes
4) Mismatch repair genes

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47
Q

What are oncogenes?

A
  • Apply the accelerator to autonomous cell growth and proliferation (normal function…)
  • Code for growth factors and their receptors, signal transducers and cell cycle components
  • Increased expression (activation) in malignancy
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48
Q

What is a proto-oncogene

A

A normal gene which, when altered by mutation, becomes an oncogene that can contribute to cancer.

Proto-oncogenes may have many different functions in the cell. Some proto-oncogenes provide signals that lead to cell division. Other proto-oncogenes regulate programmed cell death (apoptosis).

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49
Q

What are tumour suppressor genes?

A
  • Apply the brakes to cell proliferation
  • Code for factors which control the cell cycle, regulate apoptosis, transcription or cell interactions
  • Normal function in suppressing cell proliferation and maintaining tissue integrity

• Loss of expression (gene deletion) or function (mutations) in malignancy

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50
Q

What are apoptosis genes?

A
  • Genes that regulate normal cell death
  • May see Increased activity of a gene which inhibits apoptosis, eg. bcl-2, myc
  • May see reduced activity of genes which promote apoptosis, eg. p53
  • BCL-2 is overexpressed in lymphomas
51
Q

What are mis-match repair genes?

A

• Code for enzymes important for the repair of damaged DNA

52
Q

How might mis-match repair genes lead to cancer?

A
  • DNA damage is common due to environmental carcinogens
  • Loss of expression (deletion) or function (mutation) in malignancy

• Loss of repair mechanisms increases risk of mutations and activation or loss of oncogenes and tumour suppressor genes.

53
Q

Name 4 factors that affect carcinogenesis

A

1- Genetic
2- environmental
3- chemical
4- viruses

54
Q

Name 2 genetic factors that affect carcinogenesis

A
  • Inherited mutations/deletions: p53, Rb, APC

- Somatic mutations: Sporadic

55
Q

Name 2 environmental factors that affect carcinogenesis

A
  • Sunlight: Lip and skin cancer

- Irradiation: Skin cancer

56
Q

Name 2 chemical factors that affect carcinogenesis

A
  • Nitrosamines (tobacco): Oral and lung cancer

- Aniline dyes: Bladder cancer

57
Q

Name 4 viruses that may lead to cancer

A
  • EBV: Burkitts
  • HBV: Liver
  • HPV: Cervix, oral
  • HTLV: Leukaemia
58
Q

What is a neoplasm?

A

an abnormal mass of tissue from excessive growth

  • Unco-ordinated with that of normal tissues
  • Persists after the provoking stimulus is removed
59
Q

What is invasion (cancer)?

A

unconfined growth into connective tissue, the defining feature of malignant tumours

60
Q

What is a metastasis?

A

spread distant from the primary tumour

61
Q

What is cytology?

A

features of individual cells, often very abnormal

62
Q

Name 4 features of a neoplastic microenvironment

A
  • Blood supply
  • Fibroblasts
  • Immune cells
  • Nerves
63
Q

Name the 2 ways of classifying cancers

A

1- By clinical behaviour
(benign, malignant)

2- by histology/ tissue of origin
( epithelial, mesenchymal)

64
Q

Name some features of a benign tumour

A

Growth pattern: expands, encapsulated, localised.

Slow growth rate.

Cells resemble tissue of origin, are uniform shape and size.

Few mitoses (histology).

65
Q

Clinical effects of benign tumours

A

Localised
Local pressure
Excision cures it!

66
Q

Name some features on malignant tumours

A

Growth pattern: invasion, no capsule, metastasis.

Rapid growth- variable!

There is variable resemblance to tissue of origin… can have cellular/nuclear pleomorphism
- Many mitoses

67
Q

Clinical effects of malignant tumours

A

Infiltration and spread.

  • Local pressure
  • Excision may not cure!
68
Q

name 3 Components of a benign tumour

A
  • Tumour cells
  • Stroma (supporting connective tissue)- BVs, immune cells etc.
  • Capsule (most but not all tumour, may be incomplete)
69
Q

name 3 Effects of benign tumours: (varies by site and tumour, effect is not always benign)

A
  • Pressure (on other structures like BVs, ducts??) – benign brain tumours will have an effect!
  • Obstruction
  • Function (esp hormone secretion)- it may do the same things the tissue it arose from did… e.g. parathyroid benign tumour will produce parathyroid hormone
70
Q

name 2 Components of a malignant tumour

No clear boundary between neoplasm and normal tissue

A

• Tumour cells: invade underlying tissues (and destroying)

  • Cytologically abnormal
  • Differentiation varies: well, moderate, poor
  • Anaplasia
    • Stroma: Fibroblasts, BVs, immune response
  • Angiogenesis
  • Immune response
71
Q

What might there be an ulcerated surface in malignant tumours?

A

Some parts of tissue may undergo necrosis if tumour grows so fast and away from blood supply.

72
Q

Name an example for a malignant tumour

A

squamous cell carcinoma of tongue and larynx

73
Q

Name an example for a benign tumour

A

pleomorphic adenoma in parotid gland. Large, well-defined neoplasm.

74
Q

Classification 2- By histology: Tissue of origin

A

 Epithelial-lining or glandular
(GI tract, salivary glands)

 Mesenchymal- various types (depends on exactly which cell)

75
Q

What % of cancers are epithelial

A

90%

76
Q

How to classify/name benign and malignant epithelial cancers:

A

Benign:
Lining= papilloma (e.g. squamous cell papilloma)
Glandular= adenoma

Malignant:
Lining= Carcinoma
Glandular= (Adeno)carcinoma

77
Q

How to classify/name benign and malignant mesenchymal cancers:

A

Benign: depends on tissue

e.g. fibroma, osteoma, lipoma, myoma, chondroma

Malignant:
Sarcoma

e.g. osteosarcoma, leiomyosarcoma

78
Q

Name 4 Oddities to naming cancers

A
  • Melanoma: melanocytes- all malignant, no benign ones
  • Lymphoma- lymphoid cells, lymphocytes
  • Leukaemia: bone marrow precursors
  • Teratoma: germ cell tumours, most in testes, most malignant (ovarian tend to be benign), can mimic any tissue; cells in ovary/testes can differentiate into anything!
79
Q

Name of a benign lining epithelial cancer

A

Papilloma

80
Q

Name of a malignant epithelial cancer

A

Carcinoma

81
Q

Name of a benign mesenchymal cancer

A

Depends on the tissue

Lipoma, fibroma, osteoma, myoma, chondroma

82
Q

Name of a malignant mesenchymal cancer

A

Sarcoma

83
Q

Name of a benign glandular epithelial cancer

A

Adenoma

84
Q

Inherited factors of carcinogenesis

A
  • Single mutant genes, often tumour suppressor genes
  • Retinoblastoma- can lead to many types of tumours
  • Some colon cancers
  • 10% of breast/ ovarian cancers are hereditary
  • BRCA1 or BRCA2 gene for breast cancer
85
Q

What are familial cancers?

A
  • Family clusters
  • Gene(s) and pattern of inheritance not clear
  • Breast, ovary, colon
86
Q

What is Chemical carcinogenesis – DNA damage!?

What are the 2 stages

A

1) Initiation- permanent DNA damage, primes a cell
2) Promotion- may be reversible, promotes proliferation- might not be DNA damaging but may pushed primed cell to become cancerous

87
Q

What is the latent period

A

time from promotion to clinical tumour

88
Q

What is a pre-carcinogen?

A
  • Pre-carcinogen often metabolised to ultimate -> carcinogen
89
Q

What is a co-carcinogen?

A
  • Co-carcinogens are not carcinogenic but when combined with carcinogen can help/aid it/potency!
90
Q

What’s the difference between direct chemical carcinogenesis and indirect chemical carcinogenesis?

A

Direct= Tumour arises at site of carcinogen application. E.g. smoking and lung cancer

Indirect= Tumour arises at different site from carcinogen application. E.g. aromatic amines- industrial exposure, Initial contact with lungs but cancer occurs someowhere else.

91
Q

Name 4 chemical carcinogens

A
  • Smoking: polycyclic, hydrocarbons, including tars
  • Diet: burnt hydrocarbons
  • Asbestos (from construction work): fibrous silicates, inhaled fibrosis, mesothelioma
  • Synergy in smokers
92
Q

Name some physical carcinogens

A

Ionising radiation/ X-rays

Radioactive metals and gases:
 Radium- bone and bone marrow tumours
 Radon- lung cancer

Atomic bomb

93
Q

Most to least sensitive list of tissues (cells are rapidly dividing/renewed= more sensitive)

A
  1. Embryonic tissues
  2. Haematopoietic organs (spleen, bone marrow)
  3. The gonads
  4. The epidermis
  5. The Intestinal mucous membranes (variable)
  6. Connective tissue
  7. Muscle tissue and nerve tissue
94
Q

How might ultraviolet light cause cancer?

A
  • Damages DNA (causes DNA crosslinks- we have a way of dealing with these)
  • Skin: Squamous cell carcinoma, basal cell carcinoma (most common cancer), malignant melanoma
  • Xeroderma pigmentosum- this condition, px inherits abnormality in ability to repair lesions caused by UV light
95
Q

Name some viruses and the cancers they cause

A

Epstein- Barr virus (EBV) -> Burkitt’s lymphoma/ nasopharyngeal carcinoma

Hep B/C -> Hepatocellular carcinoma

Human papillomavirus -> Cervical carcinoma

96
Q

What does HPV do?

A
  • Sexually transmitted
  • Some genotypes cause cervical cancer and oro-pharyngeal cancer.
  • Viral protein binds to and inactivates the tumour-suppressor p53 gene.
97
Q

Name some influencers (promoters) of cancer

A

Hormones
Drugs
Inflammation

98
Q

2 Examples of how hormones can affect cancer

A

o Breast cancer: hormonal dependence e.g. oestrogen (ovary, adrenal)
o Prostate cancer: testosterone

99
Q

How can inflammation affect cancer?

A

cancers can arise more easily where chronic inflammation is present e.g. leukoplasias

100
Q

% of deaths that are cancer?

A

20%
2nd most frequent cause
- Higher in elderly

90% carcinoma, 10% lymphoma or sarcoma

101
Q

3 ways a cancer develops-

A

1- de novo (nothing preceding it)
2- Via a benign tumour - polyps?
3- via a premalignant lesion

102
Q

What is premalignancy?

A

There are some changes in cells and tissue architecture that are seen before invasion occurs…
- Dysplasia

Premalignancy is the basis of cancer screening…

103
Q

Non-metastatic effects of cancer

A

25% will die from cancer-related cachexia (whole-body metabolic effects, systemic/immune etc)

104
Q

How does Invasion occur: local spread

A
  • Path of least resistance
  • Tissue destruction
  • Perineural spread
105
Q

How does Metastasis occur: lymphatic spread

A
  • Invasion of vessels; embolism or permeation
  • Spread to draining lymph node(s)
  • Primary tumour-> distant site
  • No 2 people have the same lymphatic drainage
106
Q

How does Metastasis occur: haematogenous spread

A
  • Invasion: mainly veins

- Organs: liver, lung, bone and brain

107
Q

How does Metastasis occur: transcoelomic spread

A
  • Scoelomic- potential spaces in the body, have fluid and spaces for transmission
  • Spread across serous cavities

E.g. abdominal cavity

108
Q

What do tumour cells do that help them spread

A 
	Motility is enhanced
	Alter adhesion molecules
	Make poor basement membrane
	Increase protease production or reduce inhibitors
	Alter ECM
109
Q

Patterns of spread for

  • Carcinomas
  • Sarcomas
A

 Carcinomas

  • Lymphatic
  • Blood (often later)

 Sarcomas
- Blood (lymphatic spread is very rare)

110
Q

Predictable patterns of spread for:

  • Lungs
  • Tongue
A
  • Lung to local nodes, liver, bone and brain

- Tongue to neck nodes, later lung and spine

111
Q

Effects of tumour spread

A
  • Pressure and obstruction
  • Destruction
  • Haemorrhage
  • Infection
  • Pain
  • Anaemia
  • Starvation and cachexia
112
Q

Non-metastatic effects, or ‘paraneoplastic syndrome’

  • caused by biochemical substances released by tumour cells e.g. TNF-alpha
A

 Fever, anorexia and weight loss/cachexia
 Endocrine syndromes- cushings syndrome, metabolic effects e.g. hypocalcaemia
 Neurological problems e.g. neuropathy
 Haematological syndromes e.g. erythrocytosis

113
Q

2 systems used to predict how tumours will behave-

A

1- Grading of tumours

2- Staging of tumours

114
Q

How are tumours graded?

A
  • Histological assessment
  • Often related to differentiation
  • Linked to prognosis
  • Various methods: numerical, Low/intermediate/ high
115
Q

How are tumours staged?

A
  • Clinical extent of tumour
  • TNM system
  • T= tumour
  • N= nodes (regional)
  • M= metastases- distant
  • Specific staging systems for tissue/ tumour
116
Q

How is cancer diagnosed? )4)

A
  • Biopsy
  • Cytology (FNA)- fine needle aspiration
  • Imaging- CT and MR scanning (cannot rely solely on MRI scans)
  • Molecular analysis, genetic tests
117
Q

Treatments for cancer

A 
Surgery
Radiotherapy
Chemotherapy
Immunotherapy
Palliative care- supportive...
118
Q

What is palliative care?

A

some circumstances where aggressive treatments are too hard to withstand- too ill or disease is too extensive to be cured.

119
Q

what is radiotherapy

A

causes DNA damage in dividing cells and kills them. It is not very specific- head and neck has lots of different tissues that should not be irradiated!

120
Q

Side effects of radiotherapy

A
  • Tiredness
  • Feeling sick
  • Difficulty eating and drinking
  • Skin reaction
  • Hair loss
  • Haematological changes- bone marrow affect
121
Q

Clinical relevance to radiotherapy of oral cancer

A

radiotherapy can cause a horribly dry mouth- irradiation applied to (salivary) parotid gland when tongue tumour…

122
Q

Possible side effects of chemotherapy-

A 
Mucositis
Alopecia
Nausea/vomiting
Diarrhoea
Cystisis
Sterility
Neuropathy
Myalgia
Pulmonary fibrosis
Renal failure
123
Q

What are cancer biomarkers?

A
  • diagnostic tool
  • optimal dose for drug therapy
  • what type of cancer
  • optimal drug?
  • recurrence?
124
Q

Oral problems in cancer management

A
  • Oral mucosal disease
  • Dental disease
  • Discomfort
  • Social embarrassment

Dry mouth, immuno-compromised, difficulting maintaining OH

DEN203 (11 decks)

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