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Pathological Processes > PP 8+9+10 Neoplasia > Flashcards

PP 8+9+10 Neoplasia Flashcards

1
Q

Tumour meaning

A

Swelling
Palpable bump

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2
Q

Neoplasm meaning

A

Abnormal growth of cells that persist after initial stimulus is removed

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3
Q

Oncology

A

Study or tumours + neoplasms

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4
Q

Neoplasia meaning

A

New, abnormal tissue growth

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5
Q

Is neoplasia reversible or irreversible?

A

Ireversible

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6
Q

Benign neoplasm meaning

A

Growth which remains localised + won’t spread

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7
Q

Cancer meaning

A

Malignant neoplasm

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8
Q

Malignant neoplasm meaning

A

Abnormal growth of cells that persists after initial stimulus is removed which can spread

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9
Q

Metastasis meaning

A

Malignant neoplasm which has spread from primary site

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10
Q

Dysplasia meaning

A

Pre-neoplastic alteration where cells show disordered tissue organisation

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11
Q

Examples of non neoplastic tumours

A

Abscess
Haematoma

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12
Q

Is dysplasia reversible or irreversible?

A

Reversible

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13
Q

How is a benign tumour differentiated?

A

Well differentiated

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14
Q

What does a benign tumour look like in histology?

A

Well differentiated
Closely resembles parent tissue
Normal nuclear:cytoplasmic ratio
Uniform cells
Few mitoses

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15
Q

What is a primary malignant tumour?

A

Tumour at original site
Has not spread yet but has potential to

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16
Q

What is a secondary malignant tumour?

A

Tumour has spread from original site

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17
Q

How is a malignant tumour differentiated?

A

Well to poorly differentiated
More often poorly

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18
Q

What does a malignant tumour look like in histology?

A

High nuclear:cytoplasmic ratio
Necrosis?
Irregular outer margin + shape
Pleomorphism
Many mitoses

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19
Q

Anaplastic meaning

A

Cells with no resemblance to any tissue

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20
Q

Poor differentiation presentation on histology

A

Increase in nuclear size
Increase in nuclear:cytoplasmic size
Increase in nuclear staining - hyperchromasia
Increase in mitotic figures
Abnormal mitotic fibres - Mercedes logo
Pleomorphism

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21
Q

Pleomorphism meaning

A

Variation in size + shape of cells + nuclei

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22
Q

What is a description of an abnormal mitotic fibre in poor differentiation histology?

A

Mercedes logo

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23
Q

Low grade vs high grade tumour

A

Low grade - well differentiated
High grade - poorly differentiated

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24
Q

Reasons for neoplasia

A

Carcinogensis
Non-lethal genetic damage

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25
Q

Describe the process of neoplasia

A

1- accumulated mutations in somatic cells
2- mutations caused by initiators (mutagenic agents)
3- promoters cause cell proliferation
4- clonal expansion of single precursor cells > tumour
5- neoplasm formed by progression

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26
Q

What is a monoclonal growth?

A

Growth which has originated from a single cell

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27
Q

List some mutagenic agents/initiators

A

Chemicals - smoking, diet + obesity, alcohol
Infectious agents - HPV
**Radiation **
Inherited mutations

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28
Q

List classes of normal regulatory genes

A

Growth promoting proto-oncogenes
Growth inhibiting tumour suppressor genes
Genes that regulate apoptosis
Genes involved in DNA repair

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29
Q

What genes are targets of cancer-causing mutations?

A

Growth promoting proto-oncogenes
Growth inhibiting tumour suppressor genes
Genes that regulate apoptosis
Genes involved in DNA repair

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30
Q

Function of proto-oncogenes

A

Part of signally pathway which drive proliferation

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31
Q

What does a mutation in proto-oncogenes do?

A

Proto-oncogene > oncogene > oncoprotein

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32
Q

What type of mutation effect proto-oncogene?

A

Dominant mutation
Only 1 allele need to be impacted

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33
Q

What happens when proto-oncogenes become mutated?

A

Favour neoplasm formation

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34
Q

Function of tumour suppressor genes

A

Stop cell proliferation

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35
Q

What type of mutation effects tumour suppressor genes?

A

Recessive
Both alleles must be damaged

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36
Q

What happens if there’s a mutation in tumour suppressor genes?

A

Inactivate them
Failure of growth invitation
Tumour grows

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37
Q

What happens as a result of a mutation in apoptosis regulating genes?

A

Less cell death
Enhanced survival of cells

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38
Q

What happens as result of a mutation with DNA repair genes?

A

Impaired ability of cells to recognise + repair non-lethal genetic damage
Cell mutations occur at increased rate

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39
Q

What do benign tumours often end in?

A

-oma

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40
Q

What do malignant tumours often end in?

A

-carcioma (epithelial)
-sarcoma (stromal)

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41
Q

Name of benign neoplasm in strafited squamous epithelium

A

Squamous papilloma

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42
Q

Name of benign neoplasm in transitional epithelium

A

Transitional cell papilloma

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43
Q

Name of benign neoplasm in glands

A

Adenoma
Cystadenoma

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44
Q

Name of malignant neoplasm in stratified squamous epithelium

A

Squamous cell carcinoma

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45
Q

Name of malignant neoplasm in transitional epithelium

A

Transitional cell carcinoma

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46
Q

Name of malignant neoplasm in glands

A

Adenocarcinoma

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47
Q

Name of neoplasms in testis

A

Malignant teratoma
Seminoma

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48
Q

Name of neoplasm in ovary

A

Benign treatoma (dermis cyst)

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49
Q

Invasion meaning

A

Breach of basement membrane with progressive infiltration and destruction of surrounding tissues

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50
Q

Describe the process of metastasis

A

1- neoplasm grows + invades at primary site
2- enters transport system + lodges at secondary site
3- growth at secondary site to form a a new tumour (colonisation)

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51
Q

Haematogenous spread meaning

A

Spread via blood vessels

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52
Q

Transcoelomic spread meaning

A

Spread via fluid in body cavities

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53
Q

Transport systems metastases can travel in

A

Blood vessels
Lympathic vessels
Fluid in body cavities

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54
Q

What does invasion involve?

A

Altered adhesion
Stromal proteolysis
Motility

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55
Q

What is epithelial to mesenchymal transition?

A

Cells take on phenotype for like mesenchymal cells than epithelial

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56
Q

What causes epithelial to mesenchymal transition?

A

Altered adhesion
Stromal proteolysis
Motility

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57
Q

What is the greatest barrier to successful metastasis?

A

Failed colonisation

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58
Q

What is the size of most malignant cells at secondary site?

A

Tiny
Undetectable

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59
Q

What happens to most malignant cells at the secondary site?

A

Die
Failed growth to detectable tumour

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60
Q

What are micrometastases?

A

Surviving microscopic metastatic deposits that fail to grow into tumours

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61
Q

What determine the site of secondary tumours?

A

Regional drainage of blood, lymph or coelomic fluid

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62
Q

Where do lymaphtic metastasis predictability drain to?

A

Lymph nodes

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63
Q

How does breast cancer typically travel to secondary site

A

Via ipsilateral axillary lymph nodes

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64
Q

Where is transcoelomic spread often to?

A

Other areas in coelomic space
Adjacent organs

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65
Q

Where do blood borne metastasis often spread to?

A

Next capillary bed that the malignant cell encounter

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66
Q

How do carcinomas often travel?

A

Via lymph

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67
Q

How do sarcomas often travel?

A

Via blood stream

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68
Q

What is the ‘seed + soil’ phenomenon?

A

When one metastases don’t go to expected location

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69
Q

What is the ‘seed + soil’ phenomenon usually due to ?

A

Due to interactions between malignant cells + local tumour environment at secondary site

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70
Q

Where does metastatic disease in bone often take place?

A

Axial skeleton

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71
Q

How does metastases travel to bone?

A

Haematogenous sread

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72
Q

Symptoms of metastatic disease to bone

A

Mostly asymptomatic
Mainly pain if symptomatic

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73
Q

What are common neoplasms that spread to bone?

A

Great
Bronchus
Kidney
Thyroid
Prostate

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74
Q

What type of metastases does prostate neoplasms cause?

A

Osteosclerotic metastases

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75
Q

What is the most common site of neoplasm spread to bone in women?

A

Breast

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76
Q

What is the most common site of neoplasm spread to bone in men?

A

Prostate

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77
Q

What does it mean if a neoplasm is more aggressive?

A

It will metastasise very early on

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78
Q

What are tumour cells recognised by?

A

Immune system recognised them as non-self and destroy them

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79
Q

How are immunosuppressive people more at risk of cancer?

A

Tumours can avoid the immune system via:
- loss or decreased expression of histocompatibility antigens
- expression of certain factors that suppress IS
- failure to produced tumour antigen

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80
Q

What is tumour cell recognition mediated by?

A

Cell mediated mechanisms

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81
Q

Where do tumour antigens present?

A

On cell surface of major histocompatibility complex molecules

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82
Q

What are tumour antigens recognised by?

A

CD8+ cytotoxic T cells

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83
Q

What are local effects of neoplasms?

A

Direct invasion + destruction of normal tissue
Ulceration > bleeding
Compression of adjacent structures
Blocking tubes + orifices
Increased pressure due to tumour growth

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84
Q

Systemic effects of neoplasia

A
  • ^ tumour burden > parasitic effect on host
  • secreted cytokines - decreased appetite
    - weight loss
    - malaise
    - immuosuppresion
    - thrombosis
  • hormone secretion
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85
Q

What is paraneoplastic syndrome?

A

When some cancers exert signs + symptoms are hard to explain based in anatomical distribution or hormone production

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86
Q

What can paranoplastic syndrome mimic?
What is the effect of this?

A

Metastatic disease
Wrong treatment gvien

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87
Q

What are the processes of hypercalcaemia?

A

1- osteolysis : due to cancer from primary bone lesions or secondary metastases
2- production of calcaemic humoral substances by extraosseous neoplasms

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88
Q

What does syndrome of inappropriate ADH secretion normally occur with?

A

Small cell lung cancer
Hyponatraemia

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89
Q

Hyponatraemia meaning

A

Decreased sodium conc

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90
Q

Myositis meaning

A

Inflammation of muscle

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91
Q

List some miscellaneous effects of neoplasm

A

Neuropathies
Skin problems
Fever
Clubbing of rings
Myositis
Hyperglycaemia

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92
Q

Carcinogenesis meaning

A

Causes of cancer

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93
Q

Intrinsic carcinogens

A

Hereditary e.g. breast cancer
Age
Sex- horomones
Chronic inflammatory disease

94
Q

Extrinsic carcinogen

A

External

Behaviour
Environment - chemical
- radiation
- infection
- viruses

95
Q

Prevention of cancer

A

Stop smoking - tobacco
Healthy weight - BMI
Healthy balanced diet - ^ fruit + veg
Sun safety
Less alcohol
Exercise

96
Q

How does obesity increase the chance of cancer?

A

1- fat cells increase inflammation + make extra hormones and growth factors
2- hormones, GFs + inflammation cause cells to divide more
3- increased chance of cancer cells being made
4- if made, will divide + cause a tumour

97
Q

How does smoking increase the chance of cancer?

A

1- cigarettes smoke releases harmful chemicals
2- chemicals enter lungs + effect body
3- chemicals damage DNA
4- other chemicals make it harder for cells to repair damaged DNA
5- DNA damage an cause cancer cells > tumour

98
Q

What are the main modifiable risk factors for cancer?

A

Smoking
Obesity
Alcohol
Unhealthy diet
Lack of exercise

99
Q

What is 2-napthylamine?

A
  • An industrial carcinogen
  • Used in dye manufacturing industry
  • In cigaretters
100
Q

What can 2-napthylamine cause?

A

Malignant neoplasms
Bladder cancer

101
Q

What did the study of 2-napthylamine show?

A
  • risk of cancer depends on total carcinogen dose
  • sometimes there’s organ specificity for carcinogens
  • long delay between carcinogen exposure + malignant onset neoplasm
102
Q

What does chemical carcinogenesis involve?

A

Initiation + promotion
1- initiator must be given first
2- then second class of carcinogen - promoter

103
Q

What is a complete carcinogen?

A

Acts as initiator and promoter

104
Q

Example of a complete carcinogen

A

Tobacco

105
Q

What is the precursor for a carcinogen?

A

Pro-carcinogen

106
Q

What converts pro-carcinogen to carcinogen?

A

Cytochrome P450

107
Q

How does asbestos cause cancer?
What cancer does it increase the chance of?

A

1- causes chronic irritation in lungs
2-chronic inflammation
3- more regeneration
4- increased chance of cancer cells

Mesothelioma - cancer of pleura

108
Q

What type of cancer does Aflatoxin B1 increase the chance of?

A

Liver cancer

109
Q

Radiation definition

A

Any type of energy travelling through space

110
Q

How can radiation damage DNA?

A
  • directly
  • indirectly via free radicals
111
Q

What causes ionising radiation?

A

Radon gas
Medical tests e.g. x-rays

112
Q

How do infections cause cancer?

A
  • directly affect gene that control cell growth
  • indirectly by causing cynic issue injury > regeneration- acts as promoter or causes new mutation from DNA replication errors
113
Q

Example of infection which has a direct effect on causing cancer

A

Human papilloma virus

114
Q

Example of infection which has an indirect effect on causing cancer

A

Hepatitis B + C
Bacteria + parasites

115
Q

Example of infection which causes reduced immunity

A

Human immunodeficiency virus

116
Q

What cancer is HPV associated with?

A

Cervical carcinoma

117
Q

How does HPV cause cancer?

A

Direct carcinogen
Expresses proteins E6+E7 - inhibit p53 - prevents cells from apoptosing

1- virus infects cell + ensures it doesn’t die
2- hijacks DNA replication machinery (interferes with Retinoblastoma protein
3- more viruses made

118
Q

What type of gene is the retinoblastoma gene?

A

Tumour suppressor gene

119
Q

Function of retinoblastoma gene

A
  • negative regulator or G1/S cell cycle checkpoint
  • controls cellular differentiation
120
Q

What does inactivation/mutation of the retinoblastoma gene cause?

A

Uncontrolled cell division

121
Q

What does retinoblastoma gene germ line mutation cause?

A

Familial retinoblastoma

122
Q

What is the two hit hypothesis?

A

1- person with a germ line mutation of TSG on 1 chromosome is more likely to develop a neoplasms
- 1st hit is inherited mutation, only 2nd hit needed

2- person with no germ line mutation - less of a chance of tumour growth - need both hits

123
Q

Function of P35 gene

A
  • repairs damage in S phase
  • causes apoptosis if damage is to extensive
124
Q

What do inherited mutation in p35 gene cause?

A

Li-Fraumeni Syndrome

125
Q

How does Helicobacter pylori cause cancer?

A
  • Causes chronic gastric inflammation + parasitic flukes
  • Which causes inflammation in bile duct + bladder mucosa
  • Increases risk for gastric + bladder carcinomas
126
Q

Why do tumour suppressor genes need two hits?

A

Both alleles must be inactivated

127
Q

Why do proto-oncogenes need one hit to be activated?

A

Only be allele needs to be inactivated

128
Q

What genes inhibit neoplastic growth?

A

Tumour suppressor genes

129
Q

What was the first human oncogene to be discovered?

A

RAS gene

130
Q

What type of gene is the RAS gene?

A

Oncogene

131
Q

Function of RAS gene

A

Codes for G protein which signals for cells to pass restriction point in cell cycle

132
Q

What does a mutation in RAS gene cause?

A

Constant activation of gene
Constant divisions as cells pass restriction point

133
Q

What type of condition is Xeroderma Pigmentosa?

A

Autosomal recessive

134
Q

What is Xeroderma pigmentosa due to?

A

Mutation in genes which affect DNA nucleotide excision repair

135
Q

Why are people with Xeroderma pigmentosa more likely to develop skin cancer at a young age?

A

Sensitive to UV damage
Reduced ability to repair UV damage

136
Q

What type of disease is Hereditary Non-Polyposis Colon Cancer Syndrome?

A

Autosomal dominant

137
Q

What causes Hereditary Non-Polyposis Colon Cancer Syndrome?

A

Germ line mutation affects DNA mismatch repair genes

138
Q

What causes familial breast carcinomas?

A

Mutation in BRCA1+BRCA2 genes

139
Q

Function of BRCA1+BRCA2 genes

A

Help to repair double strand DNA breaks

140
Q

What is a caretaker gene?

A

Gene that maintains stability
Class of TSG

141
Q

What are the 6 hallmarks of cancer?

A
  • self sufficiency in growth signals - no longer need GFs for cancer to grow
  • resistance to growth stop signals - TSG can’t stop cancer growing
  • cell immortalisation
  • sustained ability to start angiogenesis
  • apoptosis resistance
  • ability to invade + produce metastases
142
Q

What is cell immortalisation?

A

No limitation of the number of times a cell can divide

143
Q

What can proto-oncogenes encode?

A
  • growth factors
  • growth factor receptors e.g. RAS
  • plasma membrane signal trsnducers
  • intracellular kinases e.g. BRAF
  • transcription factor
  • cell cycle regulators
144
Q

What does TNM stand for?

A

Tumour size at primary site 0-3
Node involvement 0-2
Metastatic spread in blood 0-1

145
Q

What are the four most common cancers worldwide?

A

Lung
Female breat
Bowel
Prostate

146
Q

Stages of TNM staging system

A

Stage 1 - early local disease
Stage 2 - advanced local disease N0, M0
Stage 3 - regional metastasis N1, M0
Stage 4 - advanced disease with distant metastasis M1

147
Q

What is TNM stage 1?

A

Early local disease

148
Q

What is TNM stage 2?

A

Advanced local disease
N0, M0

149
Q

What is TNM stage 3?

A

Regional metastasis
N1, M0

150
Q

What is TNM stage 4?

A

Advanced disease with distant metastasis
M1

151
Q

What does grading of neoplasm describe?

A

The degree of differentiation of a neoplasm

152
Q

Explain the stages of grading neoplasms

A

G1 - well differentiated
G2 - moderately differentiated
G3 - poorly differentiated
G4 - undifferentiated or anaplastic

153
Q

What grade is the best differentiated?

A

G1

154
Q

What grade is the worst differentiated?

A

G4

155
Q

Treatments of cancer

A

Surgery
Radiotherapy
Chemotherapy
Horomone therapy
Immunotherapy
Treatments targeted to specific molecular alterations

156
Q

What is adjuvant treatment?

A

Treatment is given after surgical removal of a primary tumour to eliminate sub clinical disease

157
Q

What is neoadjuvant treatment?

A

Treatment is given prior to surgical excision to reduce the size of the primary tumour

158
Q

What are the most common cancers in children younger than 14?

A

Leukaemia
Central nervous system tumour
Lymphomas

159
Q

The majority of cancers are diagnosed in what age group?

A

Over 65 years old

160
Q

Explain radiation therapy

A
  • Kills proliferating cells by triggers apoptosis or interfering with mitosis
  • This kills rapidly dividing cells in G2 of cell cycle
  • Causes direct or free-radical induced DNA damage - detected at checkpoints of cell cycle
  • Double stranded DNA breakages causes damaged chromosomes that prevent M phase from completing correctly
161
Q

Dose of radiation therapy
Why?

A

Fractionated doses
To minimise normal tissue damage

162
Q

Types of radiation therapy

A

External bean radiotherapy
Internal radiation therapy

163
Q

Explain external bean radiotherapy

A

External machine aims radiation of cancer

164
Q

Explain internal radiation therapy

A
  • Source of radiation put into body
  • Brachytherapy (local) - seeds, ribbons or a capsules are placed in or near tumour
  • Systemic - radioactive iodine or I-131
165
Q

Explain brachytherapy

A

Type of internal radiation therapy
Seeds, ribbons or capsules are placed in or near the tumour
Local

166
Q

What can be used to treat some thyroid cancers?

A

Radioactive iodine

167
Q

What can radioactive iodeine be used to treat?

A

Some types of thyroid cancer

168
Q

Explain chemotherapy

A
  • Systemic treatment
  • Kills cancer cells that have spread to other parts of body
  • Used in isolation or in conjunction with other chemotherapeutic agents
  • Often used together with other cancer treatments
169
Q

Effects of chemotherapy

A

Hair loss
Mouth sores
Pain
Trouble breathing
Immunosuppressed
Nausea + vomiting
Constipation or diarrhoea
Bruising + bleeding
Neuropathy
Rashes

170
Q

Types of chemotherapy

A

Antimetabolites
Antibiotics
Plant derived drugs
Alkylating + platinum based drugs

171
Q

How does antimetabolites work?
What type of treatment is it?
Example

A

Mimic normal substrates involved in DNA replication
Chemotherapy
e.g. fluorouracil

172
Q

How do alkylating + platinum based drugs work?
What type of treatment is it?
Example

A

Prevent the cross link the two strands of DNA helix
Chemotherapy
e.g. crisplatin + cyclophosphamide

173
Q

What is rumour grade determined by?

A

Degree of differentiation
Appearance of nuclei
Presence of mitoses

174
Q

What is remission of cancer?

A

Partial or complete
Partial - all signs + symptoms of cancer have reduced
Complete - all signs + symptoms have disappeared

175
Q

When is cancer most likely to come back after treatment?

A

Within 5 years

176
Q

How do antibiotics work to treat cancer?
What type of treatment is it?
Example

A

doxorubicin inhibits DMA to poison erase needed for DNA synthesis
bleomycin causes double stranded DNA breaks
Chemotherapy

177
Q

How do plant based drugs work to treat cancer?
What type of treatment is it?
Example

A

Block microtubules assemble + interfere with mitotic spindle formation
Chemotherapy
vincristine

178
Q

What does TNM stage 4 cancer normally mean?

A

Metastasis involved

179
Q

Explain biomarker testing

A

Process to look for genes, proteins, bio markers etc.
Therapies selected based on gene profiling

180
Q

Explain hormone therapy of cancer

A

Selective oestrogen receptor modulators
ramioxifen binds to oestrogen receptors and prevents oestrogen from binding - to treat hormone receptor positive breast cancer

181
Q

What is tamoxifen used for?

A

To treat hormone receptor positive breast cancer
Binds to oestrogen receptors and prevents oestrogen from binding

182
Q

What is Dukes staging system used for?

A

Bowel cancer

183
Q

What is Ann Arbor staging system used for?

A

Lymphomas

184
Q

Explain immunotherapy

A
  • Target immune system to help it fight cancer by recognising and attacking cancer cells
  • Detects and destroys abnormal cells
185
Q

What do tumour infiltrating lymphocytes indicate?

A

The immune system is responding to the tumour

186
Q

What is a sign that the immune system is responding to the tumour?

A

Tumour infiltrating lymphocytes

187
Q

Types of immunotherapy

A

Immune checkpoint inhibitors
T-cell transfer therapy
Monoclonal antibodies
Treatment vaccine
Immune stem modulators

188
Q

How do immune checkpoint inhibitors work?
What type of treatment is it?

A

Block immune checkpoints
Allow immune cells to respond more strongly
Immunotherapy

189
Q

How does T cell transfer therapy work?
What type of treatment is it?

A

Boosts the natural ability of T cells to fight cancer
Immunotherapy

190
Q

How do monoclonal antibodies work?
What type of treatment is it?

A

Immune system proteins that bind to specific targets on cancer cells
Immunotherapy

191
Q

How do treatment vaccines work?
What type of treatment is it?

A

Boost the immune response against cancer cells - strengths natural immune system
Immunotherapy

192
Q

Importance of tumour markers

A

Measured for diagnosis
Asses response to therapy
Assess recurrence
Monitoring tumour burden during treatment

193
Q

Who is cancer screening meant for?

A

Healthy people with no symptoms

194
Q

Purpose of cancer screening

A

Attempts to detect cancer as early as possible

195
Q

Benefits of cancer screening

A
  • Can detect problems early
  • Treatment is more effective the earlier it’s done
  • Can reduce the chance of developing complications
  • Reduce deaths
  • Allow patient to make better informed decisions about general health e.g. no smoking
196
Q

Risks of cancer screening

A
  • Not 100% accurate
  • False positives + negatives
  • Even with a negative result person could still develop cancer later on
  • Anxiety associated with knowledge of health issue
197
Q

Results of cancer screening

A

Normal result - negative
High risk result - positive

198
Q

What does a normal result to cancer screening mean?

A

At low risk of having cancer
Doesn’t mean that you will never develop it in the future

199
Q

What does a high risk result to cancer screening mean?

A

May have cancer
Offered further tests to confirm

200
Q

What does sensitivity of screening mean?

A

The ability of the screening test to identify people with the condition as positive

201
Q

What does specificity of screening mean?

A

The ability of the screening programme to identify health people as negative

202
Q

What makes a good screening programme?

A
  • disease must constitute a significant public health issue
  • readily available treatment must be available
  • detected at stage where treatment is more effective than if developed
  • can detect high proportion of disease in its preclinical state
  • safe
  • reasonable in cost
  • improves health outcomes due to early detection
  • widely available
203
Q

What can blood spot tests on newborn babies be used to screen for?

A

Sickle cell disease
Cystic fibrosis
Congential hypothyroidism
Phenylketonuria
Homocystinuria
Severe combined immunodeficiency

204
Q

Explain cervical screening programme?

A

Smear test
All women 25-64
Cells are taken from cervix
Check for high risk HPV

205
Q

Future developments for screening

A

Self sampling
Extending recall intervals

206
Q

How long after exposure to asbestos does malignant mesothelioma usually occur?

A

20–40 years

207
Q

How does asbestos cause cancer?

A
  • Is a complete carcinogen - promoter + initiators > forms free radicals
  • Fibres cause chronic irritation in lungs > chronic inflammation > increased repair > increased chance of cancer cell
208
Q

Staging system for lymphomas

A

Ann Arbor staging system

209
Q

What can teratomas contain?

A

Hair
Teeth
Bones
Muscle

210
Q

What tumours can contain hair and teeth?

A

Teratomas

211
Q

What type of cancer in most common in young people’s testis + ovaries?

A

Germ cell tumours

212
Q

What is the common germ cell tumour in testis?

A

Seminoma

213
Q

Examples of non-seminoma tumours

A

Teratoma
Yolk sac tumour
Embryonal
Chriocarcinoma

214
Q

Tumour markers in testicular cancer

A

hCG
AFP

215
Q

What is tumour marker alpha fetoprotein raised in?

A

Hepatocellular carcinoma - liver
Yolk sac - testi or ovaries

216
Q

Types of tumours in testis

A

Seminoma
Non Seminoma - malignant teratoma
- yolk sac tumour
- embryonal
- choriocarcinoma

217
Q

Properties of a Seminoma

A

Negative tumour markers
No basement membrane
Many lymphocytes

218
Q

No tumour markers in testis is indicative of what?

A

Seminoma

219
Q

Hodgkin’s lymphoma

A

Fever
Night sweats
Weight loss

220
Q

Histological presentation of Hodgkin’s lymphoma

A

Eosinophil
Reid sternburg cells

221
Q

Grading system name for breast cancer

A

Bloom Richardson Easton system

222
Q

Major side effect of tamoxifen

A

Agonist for oestrogen receptors in endometrium
Increased risk of endometrial carcinoma

Menopausal symptoms
Increased risk of DVT and pulmonary embolism

223
Q

How does tamoxifen work?

A

Antagonist of oestrogen receptors in breast
Agonist of oestrogen receptors in endometrium

224
Q

What drugs can be used against HER2 positive tumours? (Breast cancers)

A

Herceptin

225
Q

What ages are women screen for breast cancer?
How often ?

A

47-73 years old
Every 3 years

226
Q

How are women screened for breast cancer?

A

Mammogram

227
Q

Are BRCA1+2 proto-oncogenes or TSG?

A

Tumour suppressor genes

228
Q

What cancers are associated with BRCA1+2 genes?

A

Breast
Ovaries
Fallopian tube
Prostate

229
Q

What is a triple negative breast cancer?
What does this mean for treatment?

A

HER2 negative
ER negative
GR negative

Limited treatment

230
Q

Who do we screen for bowel cancer?

A

Anybody with a bowel
60-74

231
Q

How do sarcomas commonly metastasise?

A

Via blood stream

232
Q

How do carcinomas tend to metastasise?

A

Via lymphatics

Pathological Processes (14 decks)

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