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3b specialties > Oncology > Flashcards

Oncology Flashcards

1
Q

What is the defining characteristic of a malignant tumour?

A

It’s ability to invade and metastasise to other tissues

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2
Q

Give a definition of cancer cells

A

Cells which undergo uncontrolled and unregulated cell proliferation with the ability to metastasise to other places in the body.

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3
Q

Name 4 of the 10 hallmark characteristics of cancer cells according to Hanahan and Weinberg.

A 
Sustaining proliferative signalling
Evading growth suppressors
Avoiding immune destruction
Enabling replicative immortality
Tumour-promoting inflammation
Activating invasion and metastasis
Inducing angiogenesis
Genome instability and mutation
Resisting cell death
Deregulating cellular energetics
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4
Q

Name the 5 stages of the cell cycle and what happens at each

A 
G0= resting phase
G1= pre-DNA synthesis
S1= DNA synthesis
G2= post-DNA synthesis
M= Mitosis
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5
Q

What are the 3 different sub-populations of cells present in a tissue at one time?

A

1) Cells in resting phase that can be recruited into cell cycle
2) Cells that are terminally differentiated and can’t be recruited
3) Cells that are actively proliferating

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6
Q

What is the tumour marker in ovarian cancer?

A

Ca-125

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7
Q

What is the UK National Screening Committee definition of screening?

A

A process of identifying apparently healthy people who may be at increased risk of a disease or condition

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8
Q

List 4 of Wilson’s criteria for screening.

A

1- Important health problem
2- Accepted treatment
3- Facilities for diagnosis and treatment
4- Recognisable latent or early symptomatic stage
5- Suitable test or examination
6- Test acceptable to the population
7- Natural history of condition adequately understood
8- Agreed policy on whom to treat
9- Cost-effectiveness
10- Case-finding should be a continuous process

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9
Q

What is the grade of a tumour?

A

The extent to which the neoplasm resembles its cells or tissue of origin

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10
Q

Which type of tumours more resemble their parent tissue: well differentiated or poorly differentiated?

A

Well differentiated
Poorly differentiated tumours do not resemble their parent tissue, tend to grow more rapidly and behave more aggressively compared to well differentiated.

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11
Q

What does the stage of a cancer describe?

A

Its size and how far it has spread

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12
Q

What are the components of the TNM staging classification?

A

Tumour, Nodes, Metastasis

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13
Q

Metastasis to distant organs generally correlates with what stage of cancer?

A

Stage 4

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14
Q

Symptoms with a risk of cancer warrant what type of referral?
What does this mean?

A

Suspected Cancer Pathway Referral. Means a patient will have the appropriate investigations and specialist review within 2 weeks

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15
Q

What is it imperative to identify before deciding on cancer treatment?

A

The aims of the treatment e.g. curative or palliative.

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16
Q

What is the primary treatment for most early/non-metastatic solid tumours?

A

Surgical resection of primary areas and areas at risk of microscopic spread (e.g. sentinel LNs in breast cancer)

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17
Q

What might cause recurrence of disease following resection of a primary tumour?

A

The presence of microscopic disease/micrometastases

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18
Q

What is the difference between neo-adjuvant and adjuvant chemotherapy?

A 
Neo-adjuvant= prior to surgery/radiotherapy
Adjuvant= post-surgery
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19
Q

Briefly outline the mechanism of action of radiotherapy.

A
  • Makes free radicals and ROS are formed
  • They react with covalent bonds in DNA
  • Causes apoptosis
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20
Q

What are the three main ways of delivery radiotherapy?

A

External beam therapy, brachytherapy (internal to the body) and systemically

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21
Q

What produces the external beam radiation therapy?

A

A linear accelerator (LINAC)

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22
Q

What does the radiation dose entail and what is it measured in?

A

The amount of irradiation absorbed by each kilogram of tissue, measured in Grays (Gy)

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23
Q

When treating a patient with curative intent with radiation, what treatment regime (total dose, dose pe fraction) would be used and why?

A

High total dose but spread over many fractions to reduce the risk of long term adverse effects

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24
Q

When treating a patient with palliative intent with radiation, what treatment regime (total dose, dose per fraction) would be used and why?

A

High dose per fraction but low overall dose to reduce short-term adverse effects.

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25
Q

Some chemotherapy drugs are radio-sensitising, what does this mean?

A

The chemotherapy makes the cancer cells more sensitive to radiotherapy.

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26
Q

What is the most common acute side effect of radiotherapy. Is this dependent or independent of the area of the body being treated?

A

Fatigue. Independent.

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27
Q

List 4 other possible side effects of radiation.

A

Nausea, vomiting, anorexia, mucositis, oesophagitis, diarrhoea

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28
Q

Side effects are typically worst how long following completion of treatment?
After how long have they typically resolved?

A

2 weeks.

6 weeks.

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29
Q

True or false: early side effects of radiation generally involve local inflammation and late side effects involve local fibrosis.

A

True

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30
Q

Give 2 examples of types of molecular targeted therapies used for cancer treatment.

A

Small molecule inhibitors e.g. Tyrosine kinase inhibitors
Monoclonal antibodies
Immunotherapy

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31
Q

What part of the cell cycle do these anti-cancer drugs affect:
1- corticosteroids
2- vinca alkaloids
3- antimetabolites

A

1- G1
2- Mitosis
3- S1

32
Q

What are the 4 broad categories of cytotoxic chemotherapies?

A

Alkylating agents, antimetabolites, DNA linking agents, and ‘natural products’ (cytotoxic antibiotics, taxanes)

33
Q

How do alkylating agents work?

A

They add an alkyl group to the guanine base of DNA, so crosslinks form between these. This disrupts DNA synthesis by preventing DNA replication and RNA transcription.

34
Q

True or false, alkylating agents only work in phase G1 of the cell cycle?

A

False, they work at all stages of the cell cycle, they aren’t phase specific.

35
Q

Antimetabolites are cell specific. What phase do they particularly effect, and what phase do they have very little effect?

A

Primarily effect the synthetic/S phase. Very little effect on G0

36
Q

Are antimetabolites most effective against slow or rapidly growing cancers?

A

Rapidly growing

37
Q

Generally how do antimetabolites work?

A

Inhibition of enzymes or metabolites involved in DNA or RNA synthesis.

38
Q

How do DNA linking agents work?

A

They contain platinum complexes which produce inter-strand and intra-strand DNA cross links which prevents replication.

39
Q

Are DNA linking agents cell cycle specific or non-specific?

A

Non-specific

40
Q

What is a big reason why many chemotherapy treatment regimens fail?

A

Drug resistance- either natural or developed

41
Q

Give 5 side effects of chemotherapy

A

Nausea, alopecia, heart failure, immune suppression, renal impairment, hepatic impairment, skin rashes, bowel upset, peripheral neuropathy, taste changes

42
Q

What are the three main groups of drugs which make up the molecular targeted therapies?

A

Monoclonal antibodies, small molecule kinase inhibitors, and immunotherapy

43
Q

What two routes are monoclonal antibodies administered?

A

IV or S/C

44
Q

What part of the cell do monoclonal antibodies work on?

A

Recognise specific protein markers on the outside of cells

45
Q

Small molecule inhibitors act intracellularly, typically on what type of pathways?

A

Tyrosine kinase

46
Q

What do small molecule inhibitors names end in? How are they administered?

A

-nib. Usually given orally

47
Q

How does immunotherapy work?

A

Makes cancer cells that have previously managed to hide from the body’s immune system visible again, stimulating the body’s own immune response to kill off the abnormal cancer cells

48
Q

When should patients be treated for neutropenic sepsis?

A

When they have a temperature of >= 38 and an absolute neutrophil count <=1 x 10^9/L

49
Q

You should suspect neutropenic sepsis in any patients presenting with a new clinical deterioration within how many weeks of cytotoxic chemotherapy.

A

Within 6 weeks.

50
Q

Name two associated risk factors with neutropenic sepsis

A

Poor nutrition, mucosal barrier defect, central venous line, abnormal host colonisation

51
Q

What investigations would you perform in suspected neutropenic sepsis?

A

FBC, U&E, LFT, CRP/ESR, coag screen, septic screen (blood cultures, urine output, lactate), clinically relevant swabs/cultures, CXR

52
Q

What is the initial management of neutropenic sepsis?

A

Initial empirical antibiotics (Tazocin) within an hour of arriving at hospital. Do not wait for results from blood tests.

53
Q

After how long, if patient is improving, would you swap to oral antibiotics from IV in neutropenic sepsis? What to do if not improving?

A

24-48 hours.

Start second line antibiotics, then if that doesn’t work consider opportunistic infections

54
Q

Give an example of opportunistic infections that may infect patients on chemotherapy.

A

PCP, fungal infections

55
Q

Patients with high risk of developing significant neutropenia should be offered prophylaxis with what three possible agents?

A

Fluoroquinolone antibiotics, anti-fungals, Granulocyte colony-stimulating factor

56
Q

Approximately 40% of circulating calcium is bound to what?

A

Albumin

57
Q

Why should corrected calcium be used for diagnosing hypercalcaemia?

A

Because it’s only unbound, ionised calcium that is physiologically important

58
Q

Give 2 causes of hypercalcaemia

A

Osteolysis (lytic bone mets), humoral (PTHrP in SCLC), dehydration, other tumour specific mechanisms

59
Q

What is the presentation of hypercalcaemia?

A

Bones, stones, groans, and psychic moans

60
Q

Give further investigations for hypercalcaemia.

A

Repeat sample, PTH, ECG, imaging for bone mets

61
Q

What ECG change may be caused by hypercalcaemia?

A

Shortened QT interval

62
Q

What are the two main steps in the management of hypercalcaemia?

A 
1= correct dehydration. (0.9% NaCl 4-6L)
2= IV bisphosphonates (zolendronate or pamidronate commonly used)
63
Q

Give 2 side effects of bisphosphonates

A

Flu-like symptoms, bone pain, myalgia, reduced phosphate levels, nausea and vomiting, headache, osteonecrosis of the jaw

64
Q

What drug is used in persistent or relapsed hypercalcaemia of malignancy and how does it work?

A

Denosumab: monoclonal antibody that inhibits RANK ligand, so inhibiting the maturation of osteoclasts

65
Q

What are the two mechanisms of malignant spinal cord compression?

A

Crush fracture, or soft tissue tumour extension

66
Q

Give 3 possible presenting features of spinal cord compression.

A

Worsening back pain, weakness in limbs below compression, sensory level, bowel or bladder dysfunction (LATE SIGN), radicular pain, UMN signs below that lesion

67
Q

What is the gold standard investigation for malignant spinal cord compression?

A

MRI whole spine

68
Q

What are the 4 components of management of malignant spinal cord compression?

A 
1= high dose corticosteroids
2= definitive treatment depending on tumour and patient (surgery, radiotherapy, chemotherapy, hormone deprivation)
3= Analgesia
4= VTE prophylaxis and pressure sore prevention
69
Q

Recovery from spinal cord compression is uncommon if what two features are present?

A

Paraplegia and sphincter involvement

70
Q

What structure provides the venous drainage of the head, neck, upper limb and upper thorax?

A

Superior vena cava

71
Q

Give 4 causes of superior vena cava obstruction

A

Thrombus, intravascular device, direct tumour invasion, tumour pressing onto the vessel, lung cancer, lymphoma, germ cell tumours, fibrosing mediastinitis

72
Q

Give 3 symptoms of SVC obstruction

A

Chest pain, dyspnoea, cough, neck and face swelling, arm swelling, dizziness, headache, visual disturbance, syncope

73
Q

Give 2 signs of SVC obstruction.

A

Dilated veins (arms, neck, anterior chest), oedema (of upper torso, arms, neck and face), severe respiratory distress, cyanosis, engorged conjunctiva, convulsions and coma

74
Q

SVC obstruction may be a clinical diagnosis but what are two possible investigations you may do?

A

CXR, CT scan

75
Q

What two actions may provide symptomatic relief of SVC obstruction?

A

Elevation of head and oxygen therapy

76
Q

What is the management of SVC obstruction?

A

High dose steroids (acutely), endovascular stenting. May consider chemotherapy, radiotherapy, anticoagulation (if central vein thrombosis present)

3b specialties (15 decks)

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