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FRACP > Oncology > Flashcards

Oncology Flashcards

1
Q

What stage of melanoma does a patient have if biochemistry suggests elevated LDH?

A

Stage IV (patient has M1c) with the elevation of LDH alone.

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2
Q

What are 3 prognostics factors of stage III melanoma?

A

3 prognostic factors of stage III melanoma:

  1. Number of met LNs
  2. Size of LNs – micro vs. macro
  3. Ulcerations – upstages the disease
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3
Q

What are the ABCDE clinical features of melanoma?

A

Clinical features of melanoma (ABCDE):

A. asymmetry
B. border is irregular
C. colour: blue, black, brown, pink
D. diameter >6mm with change
E. evolution/enlargement
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4
Q

Describe the 4 stages of melanoma?

A

Stages of melanoma:

I Less than 1mm +/- ulceration (upstages)

II More than 1mm +/- ulcerations (upstages)

III LN mets

IV Distal mets / elevated LDH levels (automatically stage IV)

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5
Q

For stages II-IV, what 3 imaging modalities are employed? What is their purpose?

A

Imaging modalities for stage II-IV melanoma:

  1. Brain-MRI: for brain mets
  2. CT-CAP: for distal mets
  3. PET-scan: for resectable distal mets and monitor effect of biologics
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6
Q

Describe the differences in treatment of Stage I and II melanoma.

A

Rx of melanoma according to stages:

I – full thickness resection with wide margins (both Dx/Rx)

II – LN resection +/- radiotherapy (if >4cm or 4#) +/- clinical trial

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7
Q

What are the 2 most common chemotherapy options in melanoma? What are the indications? What are the MOA of these drugs?

A

2 most common chemotherapy option in melanoma:

  • Darcarbazine (if NO brain mets) – alkylating agent
  • Fotemustine (monoRx if brain mets) – alkylating agent
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8
Q

What are 3 common mutations in melanoma? What types of populations do they occur in?

A

3 common mutations in melanoma:

  1. BRAF (45%) - intermittent sun exposure
    e. g. doctors
  2. KIT/NRAS (15%) - Acral (unrelated to sun exposure)
    e. g. mole
  3. KIT (<5%) - chronic sun exposure / Acral
    e. g. surfer
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9
Q

What cancers are BRAF mutations implicated in?

A

BRAF mutation implicated in:

  1. Common: Melanoma (sporadic) / Prostate
  2. CRC with no KRAS mutation
  3. Others (COT): cholangiocarcinoma, ovary, thyroid
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10
Q

What are the biologics used in RCC (renal cell carcinoma) treatment?

A

RCC Rx (VMP):

VEGF-A inhibition only = bevacizumab

mTOR inhibition = temsitolimus

VEGF and PDGFR inihibition = sunitinib and sorafenib

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11
Q

What is PD-L1 and how is it implicated in cancers?

A

PD-L1 is found on many tumours, it bind to PD-1 receptors on T-cells and prevent cytokine release and tumour cell destruction via CD4 + and CD8+ cells.

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12
Q

What is Nivolumab?

A

Nivolumab is a PD-1 inhibitor that is used in advanced melanoma

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13
Q

What are the AEs of ipulimumab?

A

AEs of ipulimumab include ‘autoimmune reaction’ of a variety of organs:

Skin – rash
Colon – colitis
Pituitary – hypopituitarism
Thyroid – hyper or hypo
CNS – GBS, MG, neuropathy
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14
Q

What is the most common SE of vemurafenib (BRAF inhibitor)?

A

Rash.

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15
Q

What is the MOA of alkylating agents in chemotherapy?

A

Alkylating agent insert alkyl group into DNA of tumour cells.

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16
Q

What is the clinical significance of EGFR expression in tumour cells?

A

High EGFR expression in tumour cells suggests:

  1. End-stage disease / poor outcome
  2. Poor response to chemotherapy/hormone therapy
  3. Likely invasive and metastatic disease
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17
Q

Which 2 types of cancer is EGFR found highly expressed?

A

NSCLC and prostate cancer (>40%)

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18
Q

What is the semantic difference between prognostic and predictive markers?

A

Prognostic markers give information about outcome independent of treatment

Predictive markers give information about outcome dependant upon a specific treatment

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19
Q

What are 2 biologic therapies used in advanced melanoma?

A

Treatment for advanced melanoma:

Ipulimumab (CTLA-4 inhibition)

Nivolumab (PD-1 inhibition)

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20
Q

How does one treat the AEs of ipulimumab? What is a consideration of one of these treatments? Are these AEs reversible?

A

Ipulimumab AEs are essentially autoimmune reactions that generally respond well to steroids, mycophenolate mofetil and TNF-inhibition.

Upon response to treatment, steroid should be weaned slowly as rebound is possible.

With treatment these autoimmune reactions are reversible.

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21
Q

Which interleukin is implicated in T-cell proliferation after activation?

A

Upon activation of T-cells IL-2 secretion by T-cells mediates further proliferation.

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22
Q

What are CTLA-4 receptors, what role do they play in the normal immune system?

A

CTLA-4 receptors are co-inhibitory receptors found on T-cell bind preferentially to B7 on APC instead of CD28 and prevent T-cell activation and proliferation. It plays a role in preventing autoimmunity.

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23
Q

In the treatment of advanced melanoma, describe 3 therapeutical options that target specific genetic mutations.

A

Targeted treatment of advanced melanoma depending on genetic mutations:

  1. Vemurafenib – BRAF (V600E mutation) inhibition
  2. Trametinib – MEK inihibition
  3. Imatinib – cKIT inhibition
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24
Q

What is the clinical significance of ‘ulcerations’ in a melanoma?

A

In melanoma the presence of ulcerations ‘upstages’ the prognostic stage i.e. confers worse prognosis.

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25
Q

Describe 2 immunohistochemical tests used in the diagnosis of melanoma.

A

Immuno-histochemical tests that assist with the diagnosis of melanoma:

  1. MART/melan-A – specific for melanoma
  2. S-100 protein – monitor treated melanoma
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26
Q

Are primary melanomas visible? Is it useful to screen for melanomas?

A

> 90% of primary melanomas are grossly visible, therefore non-invasive screening with skin examinations is useful.

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27
Q

What is beta-2 microglobulin? What is the significance of beta-2 microglobulin in haematological tumours? What is the risk of having elevated levels?

A

B2-microglobulin is light chain of MHC Class I molecules. Determines burden in haematological tumours (myelomas and lymphomas). Elevated levels may form amyloid.

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28
Q

What are 3 predictive factors in a melanoma?

A

Predictors of behaviour of melanoma: thickness, bleeding and ulceration.

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29
Q

What are the features of Binet staging of CLL and what is it useful for?

A

Binet staging predicts untreated survival of CLL:
A = < 2 LNs
B = > 3 LNs
C = Anaemia / Thrombocytopenia

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30
Q

Give 4 SEs of VEGF-A inhibition.

A

VEGF-A inhibition SEs (HHRR):

Haemorrhage / tumour lysis

HTN – predictive sign of good response, Rx with ACEi

Renal impairment / proteinuria

Reversible posterior leucoencephalopathy (aka PRES)

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31
Q

What is ipulimumab?

A

Ipulimumab:

  • Biologic therapy used in metastatic melanoma
  • CTLA-4 inhibition: CTLA4 is a co-inhibitor that normally binds preferentially to B7 preventing CD28 binding, causing inhibition of activation of T-cells and proliferation (mediated by IL-2).
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32
Q

What is the response rate of BRAF inhibition with Vemurafenib in melanoma?

A

Vemurafenib (BRAF inhibition) – 50-70% response rate in Rx of melanoma

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33
Q

What is Lynch Syndrome?

A

Lynch syndrome (aka HNPCC) is a familial form of CRC (2-3% of CRCs) that should be considered if a family member with CRC or Lynch-related cancer (ESO: endometrial, SB and ovary) at a young age.

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34
Q

In CRC what is the significance of KRAS and BRAF mutations?

A

Mr Lynch is KRAS and full of BullShit

Lynch = KRAS 
BRAF = Sporadic cases
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35
Q

What type of receptors are the following ligands for:
VEGF (vascular endothelial growth factor)
bFGF (basic fibroblast growth factor)
PDGF (platelet derived growth factor)

A

Tyrosine kinase receptors

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36
Q

What type of biological intervention might a tumour with high EGFR expression be responsive to?

A

Tyrosine kinase inhibitors

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37
Q

List 3 tyrosine kinase inhibitors and give a common indication for each.

A

PEC:

Panitumumab: CRC with normal wild-type KRAS gene.

Erlotinib: NSCLC (refractory to platinum based chemotherapy) and advanced pancreatic cancer

Cetuximab: advanced CRC and advanced SCC of head/neck

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38
Q

What is the typical patient that will have EGFR+ adenocarcinoma of the lung?

A

Young asian female non-smoker with adenocarcinoma of the lung have 90% chance of being EGFR + → treatment will be effective.

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39
Q

What SE is a predictor of good response with the use of tyrosine kinase inhibitors. What is the treatment of the SE?

A

Rash - higher grade rash suggests higher probability of response rate.

Rx: dose reduction of TKI , cream/steroids, +/- ABx (Keflex)

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40
Q

With NSCLC is an EGFR mutation a good predictive marker or poor predictive marker?

A

o EGFR mutation improved survival with treatment
o EGFR wild type poor survival with treatment
o EGFR status predicts good response to treatment (therefore good predictive marker)

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41
Q

True/False: CRC with KRAS mutation treated with Cetuximab tend to have a good response.

A

False.

CRC treated with Cetuximab:

KRAS mutation = poor survival with treatment

KRAS wild type = improved survival with treatment

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42
Q

Give the type of defect in the DNA repair pathway for the following clinical syndromes:

  1. HNPCC
  2. BRCA 1/2 breast or ovarian cancer
A
  1. Mismatch repair leads to mispaired bases.

2. Homologous recombination repair leads to double strand breaks

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43
Q

With regards to the cell cycle, in what state are most cells in?

A

Majority of cells arrested in quiescent state G0 state

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44
Q

Which of the following is NOT a checkpoint in the cell cycle:

  1. G0
  2. G1/S
  3. Intra-S
  4. G2/M
  5. Spindle
A

G0

Minimize error checkpoints exist at 4 different points in the cell cycle: G1/S, Intra-S, G2/M and Spindle checkpoint (metaphase to anaphase transition)

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45
Q

In the cell cycle what occurs at G0-G1?

A

Movement from quiescent state to first gap phase where cell is preparing itself for cell division.

Near end G1 phase passes through key transition point called restriction point where it becomes fully committed to undergoing division.

Summary: gets ready for cell division!

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46
Q

In the cell cycle what occurs at G1-S?

A

Chromosomes are only replicated ONCE

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47
Q

In the cell cycle what occurs at G2-M

A

Chromosome segregated and 2 daughter cells created

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48
Q

Where is the DNA damage checkpoint?

A

G1/S = DNA-damage checkpoint (p53)

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49
Q

What is p53?

A

Guardian of the genome:

  • Multiple triggers for activation.
  • Activation leads to cell cycle arrest/apoptosis
  • > 50% of cancers have loss of p53 function
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50
Q

What is the MOA of topoisomerases inihibitors in the treatment of tumour? Give examples.

A

Topisomerases are enzymes that regulate the overwinding or underwinding of DNA. Inhibitors cause breaks in DNA leading to apoptosis.

Examples: Etoposide and Ironotecan

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51
Q

Which checkpoint are topoisomerases associated with?

A

G2

52
Q

What is the utility of the spindle checkpoint?

A

Spindle checkpoint acts to ensure there is appropiate partitioning of chromosomes

Previous checkpoints focus on steps the cell takes to prevent propogation of DNA errors to the daughter cells.

53
Q

Which chemotherapies interfere with the spindle checkpoint.

A

Taxanes (Paclitaxel, Docetaxel)

Vinca Alkaloids (Vincristine, Vinblastine, Vinorelbine)

54
Q

How do PARP (poly-ADP-ribose-polymerase) work?

A

PARP repairs DNA damage

55
Q

What is the usual function of BRCA 1 and BRCA 2 in the body?

A

Repair DNA damage.

56
Q

BRCA 1 -/- and BRCA 2 -/- patients (i.e. have BRCA mutation and no BRCA function) are sensitive to what type of therapy?

A

PARP inhibition (currently in trials)

57
Q

Which 5 gene mutations are implicated in the risk of developing Lynch syndrome?

A

Variations in the MLH1, MSH2, MSH6, PMS2, or EPCAM gene increase the risk of developing Lynch syndrome.

58
Q

Compare a DNA repair pathways in a normal cell to a cancer cell treated with therapies that target DNA repair pathways. Give an example of a chemotherapy agent that address this

A

2 DNA repair pathways:

Normal cell treated with targeted monotherapy: endogenous DNA damage can not be repaired by repair pathway 1 as it is blocked by treatment, however repair occurs via repair pathway 2 which remains intact, leading to cell survival.

Cancer cell treated with targeted monotherapy: endogenous DNA damage can not be repaired by repair pathway 2 as it is lost due to cancer, neither can it be repaired by pathway 1 as it is blocked by treatment, leading to cancer cell DEATH.

Example: PARP inhibitors (still in clinical trials 2014)

59
Q

What occurs in the following phases of the cell cycle: G0 - G1 - S - G2 - M ( back to G1)

A 
G0 = Rest
G1 = cell enlarges and makes new proteins
S = DNA replication
G2 = preparation for division
M = cell division
60
Q

What is the MOA of Tamoxifen?

A

Competitive oestrogen receptor antagonist with partial oestrogen agonist action on bone.

61
Q

What is the MOA of Anastrozole?

A

Non-steroidal aromatase inhibitor

62
Q

What should be considered if a patient with breast cancer is to be started to an aromatase inhibitor?

A

A baseline BMD is required before starting treatment because aromatase inhibitors cause a rapid and profound decline in serum oestradiol concentration, resulting in rapid bone loss and fractures.

Intervention with a bisphosphonate or denosumab in women with moderate osteopenia (T-score lower than or equal to –2) reduces this bone loss.

63
Q

True/False: Tamoxifen treatment in breast cancer may cause rapid bone loss with risk of fractures.

A

False.

Tamoxifen treatment for breast cancer usually stabilises or increases BMD. In all women, calcium and vitamin D should be optimised.

64
Q

Order the following cancers in terms of best to worse survival rates:

  • prostate
  • bowel
  • lung
  • breast
A

prostate = breast (best) &raquo_space; bowel&raquo_space;> lung (worst)

65
Q

What percentage of breast cancer patients are still alive at 5 years?

A

90%

66
Q

True/False: most breast cancers hereditary (i.e. related to gene mutations).

A

False.

Only 5-10% are gene-related. Most cases are sporadic.

67
Q

What are the genes implicated in breast cancer?

A

BAMP:

BRCA1 / BRCA 2
ATM
MLH1 / MSH2
p54 / PTEN

68
Q

For BRCA1 / BRCA 2 gene mutations, comment upon:

  1. Inheritance pattern
  2. Risk of cancer in males vs. females
A
  1. Autosomal dominant
  2. Cancer risk:

Female: Breast > 50% and Ovarian > 20%

Male (more BRCA 2): Prostate = 40% and Breast = 10%

Both: Pancreatic = 10%

NB: ‘BOPP’ (breast, ovarian, prostate, pancreas)

69
Q

What is Li-Fraumeni syndrome? What abnormality is it due to?

A

Autosomal dominant germline mutation of TP53 gene than encodes for p53 (transcription factor).

AKA: SBLA (sarcoma, breast, leukaemia and adrenal gland) syndrome - early onset of multiple cancers.

70
Q

When does one consider a patient at high-risk of breast cancer (4)?

A
  1. Multiple relative with breast/ovarian cancer (esp. if early onset)
  2. > 1 primary cancer (contralateral breast or concurrent ovarian)
  3. Vertical transmission
  4. FHx of rare malignancies e.g. Li-Fraumeni syndrome.
71
Q

What type of screening is recommended for women at high-risk of breast cancer (3)?

A
  1. 6m breast examinations
  2. Annual mammograms from 40yrs or 5yrs younger than age that relative was diagnosed.
  3. MRI breast if pre-menopausal
72
Q

What type of screening is recommended for women at high-risk of breast cancer to check for ‘ovarian’ cancer (2)?

A
  1. TVUS

2. 6m Ca-125 from 35yrs

73
Q

What prophylactic surgery might be considered in women at high-risk of breast cancer?

A

Bilateral mastectomy - reduces breast cancer risk by 90% (not 100%)

Bilateral salpingoophrectomy - reduces ovarian cancer risk by 90% and breast cancer risk by 50%

74
Q

What type of chemoprevention may be considered in women at high-risk of breast cancer?

A

Oestrogen receptor antagonists:

Tamoxifen: pre- and post-menopause

Raloxifene: post-menopause only

NB: no data for aromatase inhibitors.

75
Q

In the diagnosis of breast cancer, comment on investigations used for:

  1. Screening
  2. Formal diagnosis
A
  1. Screening: mammogram +/- US
  2. Formal diagnosis:

Palpable mass requires ‘triple-testing’

a. Clinical examination
b. Mammogram +/- US
c. FNA / Core Bx

76
Q

What are the 3 stages of breast cancer?

A

Early stage

Locally advanced disease

Metastatic disease

77
Q

For breast cancer, comment on the features of poor prognosis in terms of:

  1. Age of onset
  2. Biopsy findings
  3. Molecular findings
A

Poor prognostic features:

  1. young onset
  2. local invasion (lymphovascular/LNs)
  3. Molecular:

NEGATIVE hormone receptors (ER and PR)
POSITIVE HER2/neu

78
Q

What is the surgical approach to early stage breast cancer?

A

Wide local excision +/- partial/total mastectomy

Sentinel node bx +/- axillary dissection if node positive

79
Q

What adjuvant chemotherapies are used in early stage breast cancer?

A

antracycline +/or taxane

80
Q

What 2 types of hormone therapy is employed in early stage breast cancer?

A

SERM (selective estrogen receptor modulator) e.g. tamoxifen, toremifene

Aromatase inhibitors e.g. anastrazole, letrozole, exemestane

81
Q

What is the MOA of SERMs in the treatment of breast cancer? Benefits vs. adverse effects?

A

Dual MOA:

  1. Antagonist for breast oestrogen receptors
  2. Agonist for bone/uterus/liver

Benefits: improved BMD in women.

Adverse effects: risk of VTE and uterine cancer

82
Q

What is the MOA of aromatase inhibitors in the treatment of breast cancer? Why are they only used in postmenopausal women?
Adverse effects?

A

MOA: blocks DHEA and reduces oestrogen levels to near zero - therefore only used in post-menopausal women.

AEs:

  • Reduces BMD - need to give Ca / vit D supplements
  • Arthralgia common
  • No risk of VTE and uterine cancer.
83
Q

Why is Raloxifene only used in post-menopausal women with breast cancer?

A

Teratogenic.

84
Q

What is the duration of treatment for hormonal therapies in early breast cancer?

A

5-10 yrs

85
Q

What is the approach for adjuvant treatment in HER2-negative breast cancer?

A

Chemotherapy +/- hormone therapy if HR positive (SERM or AI)

86
Q

What is the approach for adjuvant treatment in HER2-positive breast cancer?

A

Chemotherapy + Herceptin (Trastuzumab)

Herceptin is a monoclonal Ab against HER2/neu receptor. HER proteins stimulate cell proliferation.

87
Q

What is an AE of Herceptin?

A

cardiomyopathy that is reversible (unlike antracycline cardiomyopathy)

88
Q

How is HER2+ determined in breast cancer?

A

In-situ hydribisation (FISH/CISH/SISH) - gold standard

89
Q

What is the treatment approach to locally invasive breast cancer?

A

Options:

  1. Chemotherapy +/- surgery
  2. Radiotherapy
  3. Hormonal therapy
90
Q

What is the treatment approach to metastatic breast cancer? 3 aims and 6 options.

A

Aims: symptom control, QoL and improved survival.

Options:

  1. Chemotherapy (multiple) - consider toxicities
  2. Hormone therapy (if ER+ +/or PR+)
  3. HER2 inhibitors
  4. PARP / mTOR inhibition
  5. Radiotherapy
  6. Skeletal protection:
    a. bisphosphonates
    b. denosumab
91
Q

Describe 4 fancy new biologics that involve HER2 inhibition used in metastatic breast cancer.

A
  1. Trastuzumab (Herceptin) if HER2+ but no CNS penetration.
  2. Lapatinib (Tykerb) if HER2+ and EGFR+ with good CNS penetration (trastuzumab refractory disease)
  3. Pertuzumab (Perjeta) is a HER dimerisation inhibitor (1st in it’s class!) - used with trastuzumab + taxane
  4. Trastuzumab emtansine (T-DM1/Kadcyla) - conjugated with antimicrotubule agent, less toxic.
92
Q

What are new agents that are under clinical trial for metastatic breast cancer?

A

PARP inhibitors (Olaparib and Veliparib)

mTOR inhibitors (Everolimus)

93
Q

What is the most important risk factor in lung cancer?

A

Cigarette smoking (90% of lung cancers occur in smokers)

94
Q

Which is the best way to screen for lung cancers?

A

None.

Lung cancers metastasise early - screening has limited utility (CXR/CT-chest - no evidence)

95
Q

Give the 5 main histological groups of lung cancer and what proportion of lung cancers they constitute.

A
  1. Adenocarcinoma 40%
  2. Squamous cell 20%
  3. Other 20% - bronchoalveolar/carcinoid
  4. Small cell (SCLC) 10% - aggressive!
  5. Large cell 5%

Therefore NSCLC = adenocarcinoma/squamous cell/other/large cell

96
Q

Where does lung cancer metastasise to?

A

Often presents with advanced disease.

Mets to liver/bone/brain.

97
Q

What is a Pancoast tumour? How does it present?

A
  1. Usually NSLCL
  2. Pain in should/arm (neuropathic)
  3. Wasting in hand (T1 distribution)
  4. Horner’s syndrome (MAP - miosis/anhydrosis/ptosis)
98
Q

Which of the lung cancers is most likely to cause SIADH?

A

SCLC

99
Q

True/False: SCLC tend to cause clubbing.

A

False: too rapid.

100
Q

For SCLC, give 2 clinical features and 3 biochemical features.

A

Clinical:

  1. Bulky lymphadenopathy
  2. Paraneoplastic syndrome

Biochemistry:

  1. Hyponatraemia/SIADH (CNS mets)
  2. ALP raised (bone mets)
  3. LDH raised (high tumour burden)
101
Q

Describe the 2 stages of SCLC, comment on curability and treatment options.

A

Limited stage:

  • Disease within one radiation field (ipsilateral)
  • Curable (20-30%) with chemoradiotherapy

Extensive stage:

  • Incurable but responds to chemoradiotherapy
  • 12m survival with chemotherapy

Chemotherapy (old regimen) = platinum and etoposide

102
Q

What type of lung cancer does mesothelioma due to asbestos develop?

A

NSCLC

103
Q

Treatment options for mesothelioma?

A
  1. Radical extrapleural pneumonectomy

2. Palliative chemotherapy (cisplatin + pemetrexed)

104
Q

Describe stage I-IV of NSCLC.

A 
I = no LNs
II = ipsilateral LNs 
III = LN but no mets
IV = mets
105
Q

Which stages of NSCLC can be resected?

A

Stages I-III with increasing difficulty - therefore curable.

Not Stage IV (incurable)

106
Q

Treatment options for Stages I-III NSCLC (2)?

A
  1. Chemotherapy (cisplatin + vinorelbine)

2. Radiotherapy

107
Q

What is the median survival of stage IV NSCLC with and without chemotherapy?

A

Without = 6m

With = 12m

108
Q

In addition to chemotherapy, what targeted therapies are available for stage IV NSCLC (3)?

What are the typical phenotypes for these targeted therapies?

SEs?

A
  1. EGFR inihibition: Gefitinib, Erlotinib, Cetuximab.

Phenotype: young asian non-smoker with adenocarcinoma

SEs:

  • Rash - predictor of good response
  • Pulmonary fibrosis - rare
  • Does NOT cause cytopenias
  1. ALK inhibition: Crizotinib

Phenotype: young non-smoker with adenocarcinoma

  1. VEGF inhibition: Bevacizumab

SE: risk for haemoptysis

109
Q

Here is a letter/number soup, give the relevant cancer(s) for each:

AFP
bHCG
CEA
PSA
CA125
CA15.3
CA19.9

Which of the above are useful for monitoring for treatment response?

A

Tumour markers:

AFP: germ cell/HCC
bHCG: germ cell
CEA: CRC
PSA: prostate
CA125: ovarian
CA15.3: breast
CA19.9: biliary/pancreas

Useful for monitoring:
CEA
PSA
CA125

110
Q

What is the ECOG performance status?

A

ECOG (WHO) Performance status:

0 = asymptomatic
1 = symptomatic but well/active
2 = resting for less than 50% of waking hrs
3 = resting for greater than 50% of waking hrs
4 = bed-bound
5 = dead
111
Q

How do you treat hypercalcaemia of malignancy? At what level is treatment considered?

A

Treat when Ca >3.0 mmol/L (esp. if symptomatic)

FIB:

  • Frusemide when euvolemic
  • IVF
  • Bisphosphonates
112
Q

Which type of lung cancer is prophylactic cranial radiotherapy offered to in stable patients post-chemoradiotherapy for the lung lesion?

A

SCLC - 2/3 have metastases at presentation.

113
Q

What is the most common cause of cancer in 20 - 35 yo?

A

Melanoma.

114
Q

Should a patient with breast cancer be treated with adjuvant tamoxifen for 5 or 10 years?

A

10 years (2014 data)

115
Q

With which 3 cancers is screening recommended?

A

CBC:

Cervical
Breast
Colorectal

116
Q

What is the guideline for breast cancer screening?

Is self-examination an acceptable form of screening?

A

Ages 50-75: 2 yearly mammograms.

> 75 not invited to program.

Self-examination NOT recommended as stand-alone screen.

117
Q

What are the guidelines for colorectal cancer screening for general population?

A

Age 50-75:

  1. Annual FOBT
  2. Colonoscopy every 10 years
  3. Flexisigmoidoscopy every 5 years
118
Q

What are the guidelines for colorectal cancer screening for moderate risk population?

How is moderate risk defined?

A

Moderate risk = 1st degree relative with CRC at < 55yrs.

Screening guideline:
- Colonoscopy every 5 years after 50 yrs OR 10 years younger than relative

119
Q

What is FAP (familial adenomatous polyposis)?

A

Autosomal dominant hereditary cause of CRC with mutations in the APC gene.

Adenoma (polyps) from childhood and get CRC by age 45y.

Preventative colectomy often occurs at age 18.

120
Q

What is the CRC screening process for a patient with FAP?

A
  1. Yearly sigmoidoscopy/colonoscopy from age 12.

2. Endoscopic and duodenal screening from age 25 (or time of colectomy)

121
Q

What is HNPCC (Lynch syndrome)?

A

Autosomal dominant hereditary cause of CRC with mismatch repair gene defect with increased risk of endometrial and genitourinary cancers.

122
Q

Compare the genetic defects in the 2 hereditary forms of CRC.

A

‘Lynch is a collection of mismatched cancers!’

FAP = APC (both have A, Lynch/HNPCC with no A)

HNPCC / Lynch: mismatch repair gene defect

FAP: APC gene mutation

123
Q

What is the CRC screening regimen for HNPCC?

A

Yearly colonoscopy or 5 years younger than relative.

124
Q

Which 3 cancers are most commonly associated with spinal cord compression?

A

PBL:

Prostate
Breast
Lung

125
Q

What is the treatment of cancer-related spinal cord compression?

A

Dexamethasone +/- surgery +/- radiotherapy

126
Q

Cancer patient presents complaining of pressure headache, SOB with cough and a hoarse voice. Noted on examination have facial and arm swelling and epistaxis.

Diagnosis?

What sign might be positive?

A

SVC syndrome (oncological emergency)

Pemberton’s sign

FRACP (20 decks)

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