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4th Year Drugs > Oncology > Flashcards

Oncology Flashcards

1
Q

What is chemotherapy in general?

A

Group of cytotoxic agents used to SYSTEMATICALLY manage cancer

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2
Q

Why is it necessarily for chemo to systemically Tx patients, rather than being just localised?

A

Metastasis kills patients, not local recurrence in primary organ

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3
Q

What is the % of people with cancer who will require chemotherapy?

A

60-70%

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4
Q

What is the mechanism by which chemo exerts its anti-cancer action?

A

Most target DNA directly/indirectly

Preferentially toxic to actively proliferating cells ∴ work best on rapidly dividing tumours

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5
Q

What are the uses for chemo?

A
  • NEOADJUVANT - Tx of operable tumour pre-op to reduce its size ∴ allow for less radical Tx. Also Tx micro mets.
  • PRIMARY - initial Tx for inoperable tumour - reduce tumour bulk to allow surgical resection (↑ cure rates)
  • ADJUVANT - post op Tx for micro mets after complete resection (↑ cure rates)
  • PALLIATIVE - relieve Sx and prolong life when incurable. Balance so not to ↓ QoL
  • CURATIVE - mostly germ cell, (non)Hodgkin’s lymphoma, childhood cancer WITHOUT surgery, even with mets! ∴ justifies intensive Tx with ↑ toxicity
  • PROPHYLACTIC - hormonal Tx before overt malignancy appears e.g. tamoxifen for in-situ breast cancer before invasive carcinoma
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6
Q

Cytotoxic chemo is most commonly given in combo of different drugs. Why is this?

A
  1. Different mechs of action give highest chance of result (several sub-lethal cell injuries can kill cell in combination- synergism)
  2. ↓ chance of drug resistance
  3. Different drugs = different toxicity effects ∴ dose can be maintained
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7
Q

How are most schedules of chemotherapy treatments given?

A

Cyclically - every 3-4 weeks

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8
Q

Why are chemotherapy treatments scheduled cyclically (i.e. every 3-4 weeks)?

A

Allows normal cells to recover from toxicity - low blood counts (myelosuppression) and mucositis

Repeated cycles required for full clearance as only a proportion of tumour cells killed each time

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9
Q

Why are many chemotherapy treatments only maximally effective after a 6 month course?

A

Due to resistance emergence (chemo sensitive die and resistant remain ► replicate) and increased toxicity

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10
Q

Why do most people with cancer take conventional doses of chemotherapy?

A

Known to be effective against the particular malignancy in majority of PTs

Side effects are tolerable

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11
Q

Why is it bad to take high doses of chemo?

A

Higher toxicity, and potentially lethal SEs (1-2% mortality) (bone marrow suppression) → specialised supportive care required (GFs, rescue stem cells/bone marrow, ABx)

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12
Q

What cancers are ones where high doses of chemo are justified?

A

High doses justified only when long term survival or cure possible (HELL-MUG):

Hodgkins

Ewing’s sarcoma

Leukaemia

Lymphoma

MUltiple myeloma

Germ cell tumours of testis

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13
Q

Why is prolonged chemotherapy to maintain remission not advised/advantageous?

A

Increased resistance and toxicitiy

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14
Q

What condition/group of patients is maintenance chemotherapy advised?

A

Childhood Leukaemia - 18 months maintenance Tx post remission

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15
Q

What is the advantage of giving chemo orally?

A

Freeing the patient from lenghty hospital visits and invasive procedures

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16
Q

What is the disadvantages of taking chemo orally?

A
  1. Doesnt reduce toxicity - requires regular review
  2. Only few chemo drugs avaliable orally (cyclophosphamide, etoposide, capecitabine, tamoxifen)
  3. Absorption issues can effect levels in circulation
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17
Q

How is most chemotherapy given?

A

IV mostly as bolus injection or short infusion.

Can be continuous infusion via central line

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18
Q

Chemotherapy Tx can be administered regionally. What are the methods?

A

Intravesical - high doses given at site, ↓ systemic absorption and toxicity e.g. superficial bladder cancer

Intraperitoneal - for trans-coelomically spread tumour e.g. ovarian cancer

Intra-arterial - for tumours with well-defined blood supply (e.g. hepatic artery infusion for liver mets). ↑ doses to involved site ↓ systemic absorption

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19
Q

How are chemotherapy doses calculated?

A

Most calculated according to patients body surface area (DuBois and DuBois formula):

BSA = (Weight (kg) 0.425 x Height (cm) 0.725) x 0.007184

Others:

  • Carboplatin - renal function
  • Newer drugs e.g.traztuzumab - body weight
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20
Q

What type of ADVANCED cancers is chemo most effective (i.e. cure of advanced disease in >50%)

A

Hodgkins disease

Testicular/germ cell cancers

Acute lymphoblastic leukaemia

Choriocarcinoma

Paediatric cancers e.g. leukaemia, lymphoma, sarcoma

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21
Q

What are the ADVANCED cancers where chemo is less effective (<50% cure)

A

Non-Hodgkins

Ovarian cancer

Paediatric Neuroblastoma

Osteosarcoma, Ewings Sarcoma, Rhabdomyosarcomas

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22
Q

What types of REGIONAL cancers will chemo increase cure rates?

A

Breast

Colorectal

Non-small cell Lung

Oesophageal/gastric

Bladder

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23
Q

What types of cancer will chemo result in remission in most pts?

A

Those in list of curable cancers.

Breast

Small cell lung cancer (very chemo sensitive)

Ovarian cancer

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24
Q

What types of ADVANCED REGIONAL cancer will chemo prolong survival but NOT cure in most?

A

Non-small/small cell lung cancer

Colorectal cancer

Gastric cancer

Breast cancer

Bladder

Prostate

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25
Q

What types of cancer is chemo only really effective for pallitation of Sx?

A

Renal Cancer

Melanoma

Head and neck cancer

Pancreatic

Billiary Tract cancers

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26
Q

What are the IMMEDIATE GI SEs of chemotherapy

A

N&V - direct stimulation of vomiting centre, peripheral stiumlation and anticipatory.

GI - rapidly dividing cells ∴ susceptible.

  • Mucositis (especially oral)
  • Diarrhoea (colitis/inflammation)
  • Constipation (dehydration, other drugs e.g. opioids)
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27
Q

What are the IMMEDIATE bone marrow related SEs of chemotherapy?

A

Myelosuppression - kills haematopoietic progenitor cells.

  • ↓WCC (< 1 x 109), ↓platelets (rare if standard doses used) - after 10-14 days.
    • Higher doses - cause worse/longer leucocyte fall (but drug dependent)
    • Lowest point of drop = nadir.
    • Recovery after 3-4 weeks.
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28
Q

What are the immediate hair related SEs of Chemo?

A

Alopecia - hair follicles rapidly dividing (reversed with discontinuation) - ↓ with cold cap

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29
Q

What are the immediate neurological SEs of chemotherapy?

A
  • Peripheral/Autonomic neuropathies (mainly sensory) (e.g. cisplatin, taxanes, vinca alkaloids)
  • Central toxicity - ifosfamide induced encephalopathy, 5-FU induced cerebellar toxicity
  • Ototoxicity (e.g. pernament cochlear damage with cisplatin)
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30
Q

What are the immediate genitourinary SEs of chemotherapy?

A
  • Nephrotoxicity - e.g. cisplatin, ifosfamide - renally excreted ∴ adequate renal func required
  • Bladder toxicities e.g. cyclophosphamide, ifosfamide - haemorrhagic cystitis
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31
Q

What are the immediate cardiac SEs of chemotherapy?

A
  • Arrythmias e.g. doxorubicin, paclitaxel
  • Cardiac ischamia (coronary art spasm) - 5-FU
32
Q

What are the immediate hepatic SEs of chemotherapy?

A
  • ↑LFTs (transient)
  • Failure (rare)
33
Q

What are the immediate skin and soft tissue SEs of chemotherapy?

A
  • Extraversion (leakage of IV drugs) - some chemo = highly vesicant and can cause dmg ∴adminsiter through fast running drips, use dilutants and withdraw if EV occurs
  • Palmar plantar erythema (Hand foot syndrome) - temporary
    • ​ 5FU, caecitabine, some targetted agents.
    • Cause unknown.
    • Tx with emollients.
  • Photosensitivity - 5FU, use high factor sunscreen
  • Skin/nail Pigmentation - beau lines - bleomycin (+ pilmonary fibrosis)
34
Q

What are the ‘other’ immediate SEs of chemotherapy?

A
  • Myalgia and arthralgia - paclitaxel (Tx with NSAIDs)
  • Allergic reactions - paclitaxel and docetaxel ass with hypersensitivity
  • **Lethargy** - general malaise = common and debilitating. Unknown aetiology
35
Q

What are the long term complications with chemotherapy?

A
  • Secondary malignancies - e.g. alkylating agents/procarbazine
    • Sub -lethal DNA dmg → genetic changes → 2o malignancy
  • ↓Fertility e.g. alkylating agents, high dose
    • consider sperm/ova storage
  • Pulmonary fibrosis/pneumonitis
    • e.g. bleomycin, busulphan, alkylating agents - particularly high dose/prolonged
  • Cardiac fibrosis e.g. docorubicin
  • Psychological and social - ↓QoL
36
Q

What is the Tx of anaemia?

A
  • Hb <10gdl - impair quality of life
    • Transfusion
    • Recombinant EPO - ↓risk of transfusion reaction/viral transmission
37
Q

What are the signs of thrombocytopenia?

A
  • Petechial haemorrhage
  • Nose bleeds
  • Corneal haemorrhage
  • Haematuria
38
Q

What is the Tx for thrombocytopenia?

A
  • Ass with high dose chemotherapy (as opposed to standard doses)

Tx dep on platelet count

  • <10 x 109 - Urgent platelet transfusion
    • sig risk of spontaneous bleeding e.g. intra-cerebral
  • ​10 x 109 - 20 x 109 - supportive platelet tranfusion
  • >20 x 109 - do not need platelet trans routinely
39
Q

What are the potential SEs of repeated administration of blood products?

A
  • Development of specific anti-bodies to blood cells
    • failure to ↑platelet counts immediately after transfusion
    • Reduce development with using single donor donations
40
Q

What are three main types of targetted agent therapies?

A
  1. MONOCLONAL ANTIBODIES (end in -mab) - IV infused
    • Trastuzumab (Herceptin) - HER2 receptor
    • Ipilimumab
  2. TYROSINE KINASE INHIBITORS (end in -ib) - Oral​
    • Erlotinib - anti EGFR for NSCLC
    • sunitinib - anti-VEGFR (palliative for renal cell, pancreatic, GI stromal)
    • Vemurafenib - metastatic melanoma
    • Metabolised by CYP450 - remember drug interactions
  3. mTor INHIBITORS (end in -us) - oral (Everolimus) or IV (temsirolimus)
  • Serine/threonine kinase inhibitor of mTor, part of the apoptosis pathway.
  • Palliative in renal cell and in mets breast cancer ER+HER2+.
41
Q

What are the SEs the targetted chemo therapies?

A
  • Theoretically better than normal chemotherapy
    • More toxic to cancer
    • Less damage to normal cells
    • Better tolerated - long periods with fewer breaks (chronic dosing)
  • However, chronic dosing can lead to:
    • Chronic toxicity - low grade Sx e.g. mild diarrhoea, taste change, rash
      • tolerable for few weeks but can adversely affect QoL long term
    • Emergent toxicity - only apparent after months of Tx e.g. thyroid disturbance with sunitinib
    • Risk of drug interaction
    • Mounting costs
42
Q

What type of cancers are hormonal therapies useful in?

A

Only work in cancers which are ‘hormone dependent’ i.e. cancers arising from tissues under hormonal control

  • Prostate
  • Breast
  • Endometrium
  • Lymphocytic e.g. lymphoma, leukaemia, myeloma
43
Q

At what stages are hormone treatments useful in cancer treatment?

A
  • Shrink 1<span>o</span> tumours before (NEOADJUVANT) OR instead of sugery (1<span>o</span> medical therapy)
  • Prevent/delay growth of micromets following surgery (ADJUVANT)
  • Shrink estalbished mets and improve QoL/prolong survival (PALLIATIVE)
44
Q

Regarding hormone therapies, what techniques are employed to remove SOURCES of hormone production?

A
  • Surgically e.g. oophorectomy, bilateral orchidectomy
  • Radiotherapy induced ablation
  • Reversible Medical castration
45
Q

What are the reversible medical castration methods that are used? Name examples for both

A

LHRH/GnRH blockers e.g. goserelin (zoladex), leuprorelin, degarelix (♂)

  • Block LH/FSH production by pituritary gland (indirectly/directly) (non-menopausal ♀/♂)
  • ∴ ↓ gonadal hormone production
  • Not for post-menopausal ♀ ► oestrogen = extra-gonadal (fat/adrenals)

AROMOTASE INHIBITORs e.g. anastrozole, exemestane, letrozole

  • Post-menopausal ♀
  • Blocks aromatase - converts androstenedione to oestrone
  • ↓ oestrogen synthesis from androgens
46
Q

How do aromotase inhibitors work?

A
  • Blocks Aromotase - Enzyme which aromatases androstenedione (from adrenals) to oestrone (oestrogen synthesis)
47
Q

Why did older versions of aromatase inhibitors require co-prescribed corticosteroids?

A
  • Earlier ones (e.g. aminoglutethimide) used to block earlier stages of steroid synthesis ∴ required corticosteroid supplements.
  • Newer inhibitors e.g. anastrozole, exemestane, letrozole = more specific blockage
48
Q

Regarding hormone therapies, what methods are used to inhibit hormones?

A
  • Block hormone binding in tumour cell receptors
    • Anti-oestrogen - blocks oestrogen receptors e.g. Tamoxifen (breast cancer)
    • Anti-androgen - blocks androgen receptor (tumour and hypothalamus) e.g. Flutamide, bicalutamide, cyproterone acetate
49
Q

What are the side effects of using LHRH/GnRH blockers and hormone blockers?

A
  • Rapid increase in gonadotrophins (‘FLARE’) (7-10 days)
    • Can worsen Sx short term e.g. bone pain
  • Non specific Sx
    • Fatigue
    • Impotence
    • Hot flushes/Sweating
    • Menopausal Sx - vaginal dryness, hot flushes, sweating, ↓labido
    • Breast tenderness/gynaecomastia
    • Hair thinning (♀)
    • Mood changes
    • ↓Memory
    • Oesteoperosis (↓testosterone/oestrogen)
    • ↑weight ∴ ↑cardiac risk
    • Thrombosis (♀) - esp tamoxifen
50
Q

How could you increase the response of hormone therapy in different cancers?

A

Combination hormone therapy

  • Some can produce improved response rates (LHRH blockers + hormone blockers)
  • However, can ↑SEs without increasing efficacy
51
Q

Regarding hormone therapies, what methods are used to increase hormones? (i.e. tumour growth reducing)

A
  • Glucocorticoids - induce apoptosis in malignant lymphoid cells
    • e.g. lymphoid leukaemia, lymphoma, myeloma, Hodgkin’s
  • Sex-hormones to induce -ve feedback loops
    • oestrogen - down-regulate LRHR in prostate cancer
  • Progestogens e.g. medroxyprogesterone acetate
    • ​progesterone sensitive tissues (breast, endometrium)
    • ↓tumour growth by inhibiting progesterone receptor and inducing -ve feedback loops
52
Q

What is radiotherapy?

A
  • Use of ionising radiation for managing loco-regional cance
53
Q

What is the mechanism by which RT works?

A
  • X-rays penetrate body tissue whilst sparing overlying skin
  • Produce electrons/free radicals that damage DNA in cancers/normal cells
    • Normal cells - repair DNA damage and ∴ survive (‘skin sparing’)
    • Cancer cells - defective DNA repair ∴ mitotic/apoptotic cell death
54
Q

At what stages in cancer can radiotherapy be used?

A
  • Radical/curative - if no METs, may be delivered as sole Tx modality (e.g. prostate cancer) or in combo with chemo
  • Neo-adjuvant - reduce risk of local recurrence e.g. rectal ca
  • Adjuvant - reduce local-regional recurrence e.g. breast Ca
  • Palliative - ↓Sx/↓growth
55
Q

What ways is radiotherapy delivered?

A

Delivered by LINEAR ACCELERATOR in form of:

  • Photons/X-rays (External beam)**
  • Electrons
  • Radio-isotopes
  • Protons

** most common in UK

56
Q

What units are used to express doses of radiation delivered to body tissues?

57
Q

How is radiotherapy delivered (doses)?

A
  • Series of small doses (fractions) rather than one large dose
  • Number of fractions and dose (Gy) depends on Tx intent
58
Q

If the intent of RT is curative, what dose/number of fractions would you expect?

A
  • Large dose overall over multiple small fractions
    • e.g. head/neck - 70Gy in 35 fractions over 7 weeks
59
Q

If the intent of RT is palliative, what dose/number of fractions would you expect?

A
  • Alleviate Sx - small number of fractions and lower doses
  • e.g. 8Gy in 1 fraction, 20Gy in 5 fractions, 30Gy in 10 fractions
60
Q

Regarding tumour kill and toxicity of RT, what factors can influence the degree of these?

A
  • Treatment issues e.g. Tx dose, total volume Tx, doses per fraction, Tx time
  • Co-morbidities e.g. DM, IBD, smoking
  • Cancer radiosensitivity
    • ​HIGHLY SENSITIVE - Germ cells, Lymphocytes e.g. Hodgkins
    • MODERATE SENSITIVIE - Epithelial cells
    • HIGHLY RESISTANT - CNS cells (e.g. glioblastoma multiform), Connective Tissue cells
  • Tumour hypoxia - hypoxic cells 2-3x less sensitive
  • Additional treatments (concurrent chemo increases radio sensitivity but also increased toxicity)
61
Q

What is the term used to describe the balance between tumour control and SEs of Tx?

A

Therapeutic index

62
Q

What is the most common external beam radiotherpy used? What is the process?

A
  • 3D conformal radiotherapy - individual tumour mapping to target tumour
    • tumour shape and size measured with CT
    • Patient immboilised
64
Q

When measuring CT slices for radiotherapy, what volume do you get?

A

Gross tumour volume (GTV)

65
Q

Regarding RT, what margin is used to account for potential microscopic spread?

A

Clinical target volume (CTV)

66
Q

Regarding RT targetting, what margin is used to account for minor daily variations in patient/tumour position?

A

Planning target volume (PTV)

67
Q

Why is a RT plan created? (i.e. RT accounting for gross tumour, clinical target and planning target volumes)

A

Allow specific targeting and reduce damage to normal tissue.

68
Q

How is the target of RT defined? (GTV, CTV, PTV)

69
Q

What are the instant SEs of RT?

A
  • Teratogenic - CI in pregnancy
  • Painless during delivery
70
Q

What are the acute SEs of Radiotherapy?

A
  • Localised Tx ∴ SEs related to anatomical areas of body receiving Tx. Usually after first 5-10 fractions. SEs ↑ during Tx and peak in first few weeks
    • Due to damage of normal tissue (reversible)

REMEMBER - SHORT TERM = INFLAMMATION (-itis)

  • Fatigue/weakness
  • Skin - Erythema ► desquamation (peeling, moist, pain) ► ulceration
  • Oral - erythema, ulceration
  • Mucositis/Oesphagitis
  • Gastrititis/colitis- N&V/Diarrhoea
  • Rectum - tenesmus, mucous discharge, bleeding
  • Pneumonitis - cough, dyspnoea, X-ray changes
  • Pericarditis
71
Q

What are the long term side effects of RT?

A
  • >3 months after RT (can manifest yrs after) - often irreversible, worsen with time, difficult to manage

REMEMBER - LONG TERM SE = BROADLY FIBROSIS (-osis)

  • Skin - skin colour change, atrophy, fibrosis, telangiectasia,
  • Oral Mucosa - Dry mouth (salivary gland irridation)
  • GI - mucosal ulceration, fibrosis/obstruction, necrosis
  • CNS - demyelination effects
  • Lung - fibrosis
  • Heart - cardiomyopathy/conduction blocks
  • Infertility/↓labido/impotence
  • Carcinogenic - (2o cancer 5-30yrs after exposure) - esp thyroid/breast (e.g. mantle RT) and in childhood/young adulthood
74
Q

What is brachytherapy? What is it used for?

A
  • Radiation Tx where radiation sources = placed within/close to tumour
    • ↑tumour dose and ↓dose to surrounding tissue
  • Prostate, gynaecological, oesphageal, neck cancers
75
Q

What are the two types of brachytherapy?

A
  1. Intracavity - radioactive material placed INSIDE body cavity e.g. uterus, cervix
  2. Interstitial - material put into target e.g. prostate
76
Q

What is the problem of brachytherapy?

A
  • Patient will be RADIOACTIVE
    • advise patient about radiation risk to others
77
Q

What cancer uses radioisotopes in its therapy? What does it entail and what are the associated risks?

A
  • Radioisotopes - unstable chemical element - emits radiation when it decays
    • Thyroid - iodine I-131
      • Specifically taken up and concentrated by thyroid tissue
      • Emits radiation as it undergoes radioactive decay
  • Patient = irradiated and risk to others
    • ∴ must remain in lead room until radiation is low so not to pose a risk to others (~4 days)

4th Year Drugs (7 decks)

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