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Semester 2 > MoD Session 11 > Flashcards

MoD Session 11 Flashcards

1
Q

Which 6 cancers have the best survival rates?

A 
Testicular
Malignant melanoma
Breast
Hodgkin lymphoma
Prostate
Uterine
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2
Q

Which 5 cancers have the worst survival rate?

A 
Stomach
Brain
Oesophagus
Lung
Pancreas
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3
Q

Why does pancreatic cancer have a disproportionate number of deaths considering it is a rare cancer?

A

Presents late so there is deceased survival

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4
Q

What factors affect the mean 5-year survival rates of cancers?

A 
Age of patient
General health status
Tumour site and type
Intrinsic aggressiveness
Treatment available
Stage
Amount of differentiation
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5
Q

Which three cancers are specific to children

A

Leukaemias
CNS
Lymphomas

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6
Q

What does tumour staging indicate?

A

How much tumour is present in the body

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7
Q

What is T1-4 in the TNM classification of tumour staging?

A

Size of primary tumour

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8
Q

What is N0-3 in the TNM classification of tumour staging?

A

Extent of regional node metastasis

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9
Q

What is M0/1 in the TNM classification of tumour staging?

A

Is distant metastasis present?

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10
Q

What is done before classifying a tumour as stage I-IV?

A

TNM tumour staging

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11
Q

What sort of treatments are used generally to treat stage IV tumours?

A

Chemotherapy/radiotherapy

Palliative care

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12
Q

What TNM stages indicate a stage I tumour in a theoretical cancer?

A 
T = 1/2
N = 0
M = 0
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13
Q

What TNM stages indicate a stage II tumour in a theoretical cancer?

A 
T = 3/4
N = 0
M = 0
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14
Q

What TNM stages indicate a stage III tumour in a theoretical cancer?

A 
T = any
N = 1 or more
M = 0
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15
Q

What TNM stages indicate a stage IV tumour in a theoretical cancer?

A 
T = any
N = any
M = 1
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16
Q

What type of cancer is Ann Arbor staging used for?

A

Lymphoma

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17
Q

Describe the four stages of Ann Arbor tumour staging.

A 
I = single node region
II = two or more nodes on the same side of the diaphragm
III = two or more nodes in either side of diaphragm
IV = involvement of one or more extra-lymphatic organs
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18
Q

Which type of staging is used clinically in the UK instead of the worldwide preferred TNM staging for colorectal carcinoma?

A

Duke’s

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19
Q

What type of cancer is Duke’s staging used for?

A

Colorectal carcinoma

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20
Q

Describe stages A-D in Duke’s staging.

A 
A = invasion into muscularis propria
B = invasion through muscularis propria
C = involvement of lymph nodes
D = distant metastases
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21
Q

Which stage of Duke’s do most colorectal carcinomas present as?

A

B-D

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22
Q

How does the 5 year survival rate of colorectal carcinoma compare at Duke’s stage A to stage D?

A 
A = 93%
D = 6%
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23
Q

What does tumour grade measure?

A

Degree of differentiation

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24
Q

Why is tumour grading a more subjective way of classifying tumours than staging?

A

Grading criteria less defined

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25
Q

Describe the four tumour grades used in squamous cell/colorectal carcinoma.

A 
G1 = well differentiated
G2 = moderately differentiated
G3 = poorly differentiated 
G4 = undifferentiated/anaplastic
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26
Q

What grading system is used internationally for breast carcinoma?

A

Bloom Richardson

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27
Q

What does the Bloom Richardson grading system score?

A

Presence of tubules
Mitoses
Nuclear pleomorphism

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28
Q

What is the percentage survival difference between G1 and G3 on the Bloom Richardson scale?

A

~40

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29
Q

Which types of cancer is tumour grading important for both planning treatment and estimating prognosis?

A 
Soft tissue sarcoma
Primary brain tumours
Lymphomas
Breast cancer
Prostate cancer
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30
Q

What two things are usually more important for planning treatment and estimating prognosis in cancers where tumour grading is less important?

A

Age of patient

Stage of cancer

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31
Q

What is mainstay treatment for cancer?

A

Surgery

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32
Q

How does the intent of surgery performed for stage I tumours differ to that for stage III tumours?

A

Stage I is curative but III is palliative e.g. removal of an ulcer

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33
Q

What is adjuvant treatment of cancer?

A

Given after surgical removal of primary tumour to reduce the chance of recurrence (assumed metastasis is present)

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34
Q

What is neoadjuvant treatment of cancer?

A

Given before surgery to reduce primary tumour size so surgical excision is possible

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35
Q

How does radiation therapy treat cancer?

A

Triggers apoptosis

Interferes w/mitosis

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36
Q

What type of cells does radiation therapy target?

A

Rapidly proliferating

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37
Q

Why is a fractionated dose of radiation therapy used to treat cancer?

A

Allows damaged healthy cells to recover between doses

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38
Q

What type of radiation is used in radiation therapy?

A

X-Rays

Ionising

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39
Q

What DNA damage can be caused by radiation therapy?

A

Direct

Free-radical induced

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40
Q

Which stage of there’ll cycle is particularly affected in radiation therapy?

A

G2

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41
Q

What implications does a double strand DNA break have on cell proliferation?

A

Damaged chromosomes cannot complete M phase correctly

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42
Q

Why does chemotherapy cause hair loss, bone marrow suppression and nausea?

A

Non-specific targeting of rapidly proliferating areas

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43
Q

How do anti metabolites work in chemotherapy treatment?

A

Mimic normal DNA replication substrates

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44
Q

How do alkylating/plantinum-based agents work in chemotherapy?

A

Cross link DNA double helix

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45
Q

How does Doxorubicin carry out its chemotherapy action?

A

Inhibits DNA to poisoners thus inhibiting DNA synthesis

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46
Q

Other than inhibiting DNA synthesis, how else can antibiotics be used for chemotherapy?

A

Cause double strand breaks

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47
Q

How do plant-derived drugs such as vincristine act as chemotherapy agents?

A

Block microtubule and mitotic spindle formation

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48
Q

What are SERMs?

A

Selective oestrogen receptor modulators e.g. Tamoxifen

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49
Q

When is tamoxifen used in breast carcinoma?

A

If the tumour has oestrogen receptors

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50
Q

What hormone therapy is used to treat prostate cancer?

A

Androgen blockade

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51
Q

Which oncogenes are identified in melanoma?

A

BRAF

52
Q

When is herceptin used to treat breast cancers?

A

To inhibit HER-2 signalling in tumours which have HER-2 receptor over expression

53
Q

How does gleevec treat chronic myeloid leukaemia?

A

Inhibits the fusion protein BCR-ABL coded for by the Philadelphia chromosome formed by (t9:22)

54
Q

Why are tumour markers more useful for monitoring tumour burden and follow up after treatment than diagnosis?

A

Most do not have a clear boundary between healthy and cancerous levels

55
Q

Which hormone can be used as a biomarker for testicular tumours?

A

hCG

56
Q

Which oncofetal antigen can be used as a biomarker for hepatocellular and testicular tumours?

A

Alpha-fetoprotein

57
Q

Which specific protein can be used as a biomarker for prostate carcinoma?

A

Prostate specific antigen

58
Q

What is CA-125 used as a biomarker for?

A

Ovarian cancer

59
Q

Which class of biomarkers does CA-125 belong to?

A

Mucins/glycoproteins

60
Q

What is lead time bias?

A

Screening leads to earlier detection and treatment but the point of death is not changed from if the cancer was detected later and treated

61
Q

What is length time bias?

A

More likely to detect slow-growing tumours and miss fast growing, potentially lethal tumours

62
Q

How can length-time bias be used to dispute the effectiveness of prostate cancer screening?

A

Can be argued it doesn’t detect the tumours it is screening for

63
Q

Why is over-diagnosis a problem with cancer screening?

A

Identify and treat tumours which would never have progressed and led to pathology/death

64
Q

Who is screened for breast cancer?

A

47-73 y.o. females

65
Q

How often is an individual screened for breast cancer assuming there are no other indications?

A

Every 3 years

66
Q

Under what circumstances are women more frequently screened for breast cancer?

A

First degree relative w/ +ve Hx

Presence of BRCA1/BRCA2/Tp53

67
Q

How is a breast cancer screen conducted?

A

X-Ray from above and X-ray into axilla

68
Q

Who is screened for cervical cancer?

A

25-64 y.o. females

69
Q

How frequently are women screened for cervical cancer?

A

25-49 y.o. every 3 years

50-64 y.o. every 5 years

70
Q

How is cervical cancer screening carried out?

A

Pap smear test using liquid based cytology for analysis

71
Q

Who is screened for colorectal cancer?

A

60-74 y.o. females and males

72
Q

How often are people screened for colorectal cancer?

A

Every 2 years

73
Q

How is colorectal cancer screening conducted?

A

FOB test - test still sample for presence of blood which is not normally seen

74
Q

When is measurement of biomarkers in the blood more useful than biomarkers from tissue biopsy?

A

Inaccessible primary tumour e.g. brain

Metastases that do not resemble primary tumour

75
Q

Which four cancer make up ~54% of all new diagnoses?

A

Breast
Lung
Prostate
Bowel

76
Q

Why does the risk of cancer increase with age?

A

Co-morbidities
Lag time
More time for genetic mutation

77
Q

What are the three groups of anti tumour defences?

A

Genes that correct genetic errors or eliminate cells that have them
Immune system
Non-specific responses, primarily inflammation

78
Q

What is the normal action of p53 on G1?

A

Prolong it to allow extra time for correcting defects in DNA

79
Q

What is the normal activity of p53 on genes in differentiation?

A

Stimulates transcription so the cell is set on a path opposite to carcinogenesis

80
Q

Why does p53 have so many effects?

A

Binds to multiple sites in the DNA chain so controls a variety of genes

81
Q

In normal conditions, how much p53 can be detected in the cell?

A

Very little

82
Q

What is p53 turned on by which is prevalent in malignant tumours?

A

Hypoxia

83
Q

How antigenic are tumours in general?

A

Poorly

84
Q

Which types of tumours are the most antigenic?

A

Those induced by viruses

85
Q

How can tumours evade the immune system?

A

Produce cells that are less antigenic

86
Q

What is a malignant effusion?

A

Essentially inflammatory exudates that contain tumour cells and many leucocytes formed when a malignant tumour spreads over a serosal surface

87
Q

What are the 5 reasons why leucocytes can congregate in a tumour?

A

Chemotaxins secreted by tumour cells
Chemotaxins secreted by inflammatory cells
Chemotaxins released by necrotic tumour cells
Bacterial chemotaxins in ulcerated and infected tumours
Adhesion molecules expressed by the endothelium of the tumour’s vessels

88
Q

Does the presence of inflammation in a tumour indicate better prognosis?

A

No but they appear to be performing some defensive functions

89
Q

What are intravesical injections of BCG (attenuated strain of mycobacterium tuberculosis) used in the treatment of?

A

Superficial bladder cancer

90
Q

Describe the timeline of haemangioma in infants.

A

Grows very fast appearing within 2-4 weeks after birth
Begins to regress
Gone by age of 10 usually leaving a scar

91
Q

What is the mechanism of regression of a haemangioma in infants?

A

Not understood - not thrombosis or infarction, endothelial channels fade away

92
Q

Can the primary tumour in melanoma regress?

A

Yes, partially or even completely

93
Q

What explains the occasional finding of metastatic melanoma in the absence of primary melanoma?

A

Regression - primary tumour went unnoticed and the disappeared

94
Q

How does regression of melanoma probably occur?

A

Immunologic mechanism

95
Q

Why can the epidemiology of cancer be described as a ‘spotty’ problem?

A

Genes, parasites, chemicals, lifestyle and age affect incidence

96
Q

What factors does cancer of the colon tend to parallel?

A

Degree of economic development

Consumption of red meat and animal fat

97
Q

Which group of the population has more cancer?

A

Males

98
Q

Males have a larger proportion of which kind of cancers?

A

Self-inflicted e.g. Skin, mouth, lungs

99
Q

Which two types of cancer are increasing in prevalence?

A

Cancer of the lung

Melanoma of the skin

100
Q

Which types of cancer are decreasing in prevalence?

A

Stomach (better food processing and refrigeration so less nitrates)
Uterus

101
Q

How has the mortality rate of breast cancer changed?

A

Steadily increased

102
Q

Name a carcinogen found in tobacco smoke.

A

Benzopyrene

103
Q

What dietary actions can be correlated with the development of cancer?

A 
Salted fish and nasopharyngeal carcinoma
Broiling
Smoking
Frying in fats that have been used over and over again
Nitrites 
Over nutrition
104
Q

What types of cancer does obesity in women predispose them to?

A

Endometrium

Gall bladder

105
Q

Why is the level of oestrogens in the blood directly proportional to the degree of adiposity after the menopause?

A

Fat cells synthesise it from adrenal hormones

106
Q

What can cause large exposure to hormonal stimulation which can increase the risk of breast cancer?

A

Early menarche
Delayed first pregnancy
Induced abortion
Late menopause

107
Q

Why is cervical cancer a venerable disease?

A

It correlated with early sex and multiple partners

108
Q

What does an undescended testicle have a greater risk of?

A

Developing cancer

109
Q

Which HPV types are a risk factor for cervical cancer?

A

16 and 18

110
Q

Which type of cancer has a correlation with genital warts?

A

Anal

111
Q

What is the Bence-Jones protein?

A

Found in the urine and indicates the presence of multiple myeloma

112
Q

What is prostate-specific antigen?

A

Glycoprotein specific for prostatic epithelium whose level in the blood doubles if the prostate is massaged - marker for prostatic cancer and its response to therapy

113
Q

Is PSA seen in the normal adult?

A

Yes, increased by hypertrophy of prostate which can be benign or malignant

114
Q

What is CEA?

A

Carcinoembryonic antigen, an oncofoetal protein not significantly expressed in the adult but becomes depressed in some tumours

115
Q

Where is the gene for CEA mainly active?

A

Normal foetus

116
Q

What type of protein is CEA?

A

Glycoprotein

117
Q

Which types of cancer is CEA seen in?

A

Colon
Pancreatic
Lung
Rectal

118
Q

When is alpha-fetoprotein seen in cancer?

A

Liver carcinoma
Germ cell tumours (except seminomas)
Pancreatic
Stomach

119
Q

What naturally synthesises AFP?

A

Liver
Yolk sac
GI epithelium

120
Q

Which histiological features does grading evaluate the aggressiveness of a tumour from?

A 
Cellular atypia
Architectural atypia
Number of mitoses
Degree of differentiation
Degree of invasiveness
121
Q

Which system is used to grade the adenocarcinoma of the prostate gland?

A

Gleason

122
Q

In grading, what is poor prognosis generally correlated with?

A

Aneuploidy

123
Q

Which type of cancer therapy is appropriate for systemic disease?

A

Chemotherapy

124
Q

What hampers chemotherapy?

A

Safety margin b/w toxicity for tumour and patient is narrow
Metastatic cells hide behind endothelial barriers that are impassable to drugs e.g. Blood-brain barrier
Tumour cells, particularly in metastases can become insensitive to drugs

125
Q

How can tumour cells survive cytotoxic drugs?

A

Adapt their metabolism to inactivate a drug or reduce its action

126
Q

What methods of metabolism alteration can tumour cells carry out to become drug resistant?

A

Modify, reduce or overproduce target proteins
Alter transport mechanisms
Improve DNA repair

127
Q

Why does infection remain a major complication of advanced cancer?

A

Bodily defences are depressed by many factors, including chemotherapy

Semester 2 (45 decks)

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