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BPT Sadness 😔 > Medical Oncology (+ anti-neoplastics) > Flashcards

Medical Oncology (+ anti-neoplastics) Flashcards

1
Q

What are examples of alkylating agents and what is their MOA?

A

Chlorambucil, cyclophosphamide, melphalan, ifosfomide, bendamustine, carmustine, busulfan, temozolomide, thiotepa

MOA: abnormal crosslinking of DNA via alkyl group

Toxicities: BM suppression, alopecia, nausea, secondary malignancy

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2
Q

What is a bladder complication of cyclophosphamide and what is it’s treatment?

A

Haemorrhagic cystitis, treated by Mesna

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3
Q

Which cytotoxic agent is associated with hypomagnesaemia?

A

Cisplatin - possibly by a direct injury to mechanisms of magnesium reabsorption in the ascending limb of the loop of Henle +/- as the distal tubule

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4
Q

What does trastuzumab/Herceptin target, and what conditions does it treat?

A

HER2 receptor
- HER2 receptor positive Breast Ca, also stomach cancer

Toxicity - mostly cardiotoxicity
- Reversible with discontinuation (vs. anthracycline toxicity - irreversible)
- TTE every 12 weeks on treatment

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5
Q

What does bevacizumab target, and what conditions does it treat?

A

Multiple cancers - GBM, colorectal, ovarian, liver
- MOA: blocks angiogenesis by inhibiting vascular endothelial growth factor A (VEGF-A)

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6
Q

What does ipilimumab target, and what condition does it treat?

A

CTLA-4; which downregulates the immune system
- Metastatic melanoma

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7
Q

What does nivolumab target, and what conditions does it treat?

A

MOA: anti- PD-1
- Metastatic melanoma
- Metastatic NSCLC

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8
Q

Which phases in the cell cycle is a cell most vulnerable to damage?

A

G2 to M

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9
Q

What is the reduction in risk of prophylactic bilateral mastectomy for BRCA1 or BRCA 2 mutation carriers?

A

Greater than 90%

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10
Q

Tamoxifen and raloxifene are examples of what types of chemoprophylaxis?

A

Selective oestogen receptor modifiers; block oestrogen uptake in breast tissue
- Decrease risk of breast Ca by 28-65% and given for 5 years

Raloxifene is better at reducing risk of INVASIVE cancer

BUT tamoxifen increases risk endometrial cancer

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11
Q

Anastrazole and exemestane are examples of what type of chemoprophylaxis?

A

Aromatase inhibitors; prevent conversion of androgens into oestrogen
- Decrease risk of breast Ca by 28-65% and given for 5 years

Needs screening for BMD

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12
Q

In BRCA1/BRCA2 carriers, by how much does prophylactic BSO decrease the risk of ovarian, fallopian tube and primary peritoneal cancers by?

A

Greater than 80%

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13
Q

HER2 positive breast cancer good or bad

A

HER2 positive tend to grow and spread faster than breast cancers that are HER2-negative, but are much more likely to respond to treatment with drugs that target the HER2 protein

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14
Q

What part of the cell cycle do you normally perform karyotyping?

A

Metaphase (mitosis) - when cell is most condensed and visible

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15
Q

What secondary malignancies can cyclophosphamide predispose to?

A

Non-melanoma skin cancer (e.g. SCC), AML, bladder Ca

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16
Q

What are some platinum-based chemotherapies and what is MOA?

A

Cisplatin, carboplatin

MOA: abnormal crosslinking of DNA bases
- NB: similar to akylating agents without alkyl group

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17
Q

What chemoprophylaxis agent for breast cancer is indicated in pre-menopausal women?

A

Tamoxifen (selective oestrogen receptor modulator)
- Use gosrelin
- BUT do not use if FHx endometrial cancer - increases risk

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18
Q

Hormone therapy in post-menopausal women?

A

Preferred are aromatase inhibitors
- Anastrazole, letrozole
- Prevents ADRENAL conversion into oestrogen, but not OVARIAN

Can also use tamoxifen

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19
Q

Treatment of early stage invasive breast Ca?

A

Initial excision > RTx > adjutant chemo

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20
Q

Is chemotherapy used to treat DCIS?

A

NO YOU FOOL

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21
Q

Paget disease of the breast Ix?

A

Skin biopsy/scrape cytology > breast MRI

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22
Q

What percentage of breast cancers are hormone receptor positive?

A

75-80% positive
- Treat with hromone therapy for minimum 5 years

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23
Q

In inflammatory breast cancer, is staging PET/CT indicated?

A

Yes; one third have distant metastases at diagnosis

Also needs MASTECTOMY

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24
Q

Between BRCA 1 vs. BRCA 2, which has highest risk of ovarian cancer?

A

BRCA 1; ov4r1an (44% risk of ovarian in BRCA 1, 17% in BRCA 2)
- Overall 70% risk breast Ca
- Bilateral mastectomy age 40
- BSO at 35 in BRCA1 vs. BSO at 45 in BRCA 2

NB: 80% HCG cancers arise from fimbrae/fallopian tubes, rarely actual ovary
- Nil benefit from hysterectomy

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25
Q

Triple negative breast Ca, higher in BRCA 1 vs. 2?

A

Both are ~75% ER positive, however in BRCA 1 - 70% are TNBC
- However HER2 is NOT associated with BRCA 1 or 2

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26
Q

What syndrome is most likely in someone presenting with breast, brain, adrenal cortex, leukaemia/lymphoma and sarcoma? And what gene mutation is implicated?

A

Li-Fraumeni syndrome, TP53
- Li-FrauMANY

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27
Q

Which hereditary syndrome + gene mutation:
colorectal, breast, gastric + pancreatic cancer?

A

Peutz-Jegher, STK11

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28
Q

Which hereditary syndrome is implicated in someone with breast, enDometrial, thyroid Ca with colonic polyps?

A

CowDen syndrome, PTEN

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29
Q

Lynch syndrome predisposes to which cancers, and what is gene mutation?

A

Colorectal, endometrial, ovarian + skin cancer
- Gene mutation = DNA mismatch repair genes

Autosomal dominant

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30
Q

Treatment options in ER positive/HER2 negative breast Ca?

A

Combination of AI + CDK 4/6 inhibitors
- CDK 4/6 inhibitors: palbociclib, ribociclib, and abemaciclib
- CDK 4/6 inhibitors prevent binding of cyclin D1 to form CDK/cyclinD1 complex
- Work on G1-S phase of cell cycle

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31
Q

1st line treatment for metastatic HER2 positive breast Ca?

A

Trastuzumab + pertuzumab + paclitaxel (taxane)
- If ER positive (10% are triple positive), add endocrine therapy

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32
Q

Which types of breast Ca have highest risk of brain metastases?

A

TNBC + HER2 positive

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33
Q

Treatment triple negative breast Ca?
NB: is 10% breast Ca

A
  • If small and LN negative > surgery
  • If >5mm, then adjuvant chemotherapy + paclitaxel > surgery
  • If >1 cm > neoadjuvant chemotherapy

NB: poorer prognosis, but also lower late recurrence risk

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34
Q

What is Meig’s triad?

A

Ovarian fibroma (usually benign), pleural effusion and ascites

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35
Q

The most common route of spread of epithelial ovarian cancer is via?
1. Direct spread to adnexae and other pelvic organs
2. Haematogenous spread to lungs
3. Lymphatic spread to para-aortic LN
4. Transcoelomic spread

A

Transcoelomic spread; via peritoneal cavity

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36
Q

Most ovarian cancers arise from which structure?

A

Fallopian tubal epithelium

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37
Q

What is the most common histology in cervical cancer?

A

Squamous cell carcinoma = 69-75%

2nd most common = adenocarcinoma, 25%

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38
Q

Which HPV subtypes are considered high risk for cervical cancer?

A

HPV 16 and 18
- 16 = 50%
- 18 = 20%

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39
Q

Which has worse prognosis in colorectal Ca?
- Left-sided or right-sided?

A

Right-sided of large intestine
- Caecum, ascending colon, proximal 2/3 transverse colon
- More likely to present with IDA

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40
Q

What are the predominant genetic mutations in colorectal cancer?

A

Deficient mismatch repair (dMMR) CRC > increased microsatellite instability (MSI) in the cancer cell’s DNA
- 20% of dMMR tumours will have Lynch syndrome (autosomal dominant)

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41
Q

Risk factors in CRC?

A

Alter screening:
- FAP, Lynch, syndrome, MAP
- IBD; 15 x increase in CRC
- Pelvic RT
- CF; 10 x esp. post transplant
- Acromegaly

Doesn’t alter screening
- Obesity - 25% increased risk
- Diabetes - 40% increased risk
- Processed meat
- Smoking - 18% increased risk
- EtOH >4/day - 50% increased risk
- ADT - 30% increased risk
- Streptococcus bovis/gallolyticus

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42
Q

Most common germline aberrancies in Lynch syndrome

A

Most common mutation = PMS2 > MSH6 > MLH1 > MSH2

But MLH1 and MSH2 mutations > highest risks of CRC

MLH1 and PSM2 go together

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43
Q

Highest risk of colorectal cancer in the following?
1. FAP1 syndrome
2. HNPCC
3. Cowden’s
4. Li Fraumeni

A

FAP ~100% then Lynch ~70%

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44
Q

Highest potential for malignant transformation in colonic polyps?
1. Hyperplastic
2. Tubular
3. Villous
4. Harmatomous

A

Villous - bad; think villians

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45
Q

Classic histological findings in granulosa cell tumours?

A

Call-Exner bodies

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46
Q

Classic histological finding in yolk sac tumours?

A

Schiller-Duval bodies

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47
Q

MOA bleomycin?

A

Degrades pre-formed DNA
- Associated lung fibrosis

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48
Q

MOA anthracycline e.g. doxorubicin?

A

Disrupt DNA by poisoning topoisomerase (which unwinds DNA for replication and synthesis) > growth arrest and cell death
- Associated cardiomyopathy

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49
Q

MOA vincristine/vinblastine?

A

Inhibits formation of microtubules
- Vincristine: peripheral neuropathy, paralytic ileus
- Vinblastine: myelosuppression

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50
Q

MOA irinotecan?

A

Inhibits DNA topoisomerase I > prevents relaxation of supercoiled DNA

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51
Q

MOA methotrexate?

A

Folate antagonist; inhibits dihydrofolate reductase > preventing BH2 to BH4

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52
Q

Which type of melanoma is most common in dark-skinned people?

A

Acral melanoma

53
Q

Most common BRAF mutation in melanoma?

A

V600E in 75%

(50% melanoma is BRAF mutation)

54
Q

2 examples of PD-1 inhibitors?

A

Pembrolizumab
Nivolumab

55
Q

Metastatic melanoma treatment

A

If BRAF positive and want rapid disease control - give BRAF first (immunotherapy takes a while)

56
Q

Most aggressive type of melanoma?

A

Nodular
- 15%
- Most aggressive due to rapid growth

57
Q

Most common type of melanoma?

A

Superficial spreading
- 70%
- Usually arises from pre-existing nevus

58
Q

Most effective anti-emetic for delayed nausea?

A

Dexamethasone

59
Q

Deficiency of what makes someone intolerant of fluoropyrimidines (e.g 5-fluorouracil/(5FU), capecitabine and tegafur?

A

Dihydropyrimidine dehydrogenase deficiency (DPD)
- An autosomal recessive metabolic disorder in which there is absent or significantly decreased activity of dihydropyrimidine dehydrogenase, an enzyme involved in the metabolism of uracil and thymine

60
Q

Which two antimetabolites are the same drug in different forms?

A

5-FU = infusion, capecitabine = tablet

61
Q

Main SE of gemcitabine?

A

LFT derangement

62
Q

5FU and capecitabine main SE?

A

Coronary artery spasm
H&F syndrome - blistering on palms and soles
Mucositis
Diarrhoea

Think DPD deficiency

63
Q

Most commonly mutated tumor suppressor gene?

A

p53
- High number
- “Guardian of the genome”

64
Q

Most common gene associated with chemotherapy drug resistance?

A

P-glycoprotein (MDRP-1)

65
Q

Role of SERM (tamoxifen, raloxifen) in breast Ca?

A

Pre-menopausal ER positive breast Ca
- Osteoprotective (agonises ER on bone)
- Anti-neoplastic (blocks ER breast tissue)

RISKS
- Thrombotic risk (partial AT III inhibitor)
- Agonist to ER in endometrium > increased risk endometrial Ca
- Hot flushes

66
Q

Role of aromatase inhibitors (letrozole, anastrozole, exemestane) in breast Ca?

A

POST-MENOPAUSAL with ER positive breast Ca
- 5 years adjuvant AI is better than 5 years of tamoxifen

RISKS
- Osteoporosis
- Mood changes
- Hot flushes

67
Q

When to give adjuvant chemotherapy in breast Ca?

A
  • LN involvement (esp. >3 LN) i.e. N2
  • Tumour size >2 cm
  • Ki67 >15%
  • Low ER expression/PR negative (luminal B)
  • Young age

Can use UK PREDICT tool

68
Q

Trastuzumab and when to WH chemotherapy?

A

TTE every 12 weeks
- Cease if LVEF drops to < 45% or >15% from baseline or symptomatic HF
- If symptomatic, refer to cardiology and commence ACEI or BB

If baseline good cardiac Fx (LVEF >/= 45%):
- Continue unless >16% drop in LVEF, then hold for >4 week

If baseline LVEF <45%
- Hold for >4 weeks

69
Q

Treatment of triple negative breast Ca?

A

Doxorubicin + cyclophosphamide (AC) + paclitaxel

Pembrolizumab is helpful (but not PBS funded)

70
Q

When to give bisphophonates in breast Ca?

A

Post-menopausal setting in those with OP (or osteopaenia in AI)
- Alendronate/risendronate
- Pamidronate/zoledronic acid

71
Q

Treatment for metastatic ER positive HER2 negative breast Ca?

A

Cyclin D/CDK 4/6 inhibitors (palbociclib, ribociclib, amaciclib) with AI

72
Q

Treatment of metastatic HER2 positive breast Ca?

A

Trastuzumab + pertuzumab + paclitaxel

73
Q

What to give in metastatic CRC with K-RAS?

A

Bevacizumab
- Because K-RAS poor response to EGFR
- Vascular problems (i.e. no BM suppression)

74
Q

Spindle cells make you think?

A

Sarcoma
- Connective tissue

75
Q

Stiff Person PNP

A

Anti-amphiohysin
- Otherwise GAD is most common

76
Q

Oxaliplatin SE?

A

Peripheral neuropathy, cold-induced neuropathy

77
Q

Spindle cells and C-KIT makes you think?

A

GIST
- Tx imatinib

78
Q

What part of cell cycle does CDK (cyclin D) 4/6 work in?

A

G1-S

79
Q

What is protective against chemotherapy-induced nausea?

A

High EtOH intake

80
Q

Most emetogenic chemo?

A

Cisplatin
Doxorubicin
Cyclophosphomide

81
Q

4Ts of anterior mediastinal mass

A
  1. Thymoma
  2. Thyroid cancer
  3. Terrible lymphoma
  4. Teratoma
82
Q

Which cancer looks like pneumonia on CXR?

A

Adenocarcinoma in situ

83
Q

Amsterdam criteria for Lynch/HNPCC?

A
84
Q

Which ADT causes testosterone/tumor flare and how is it counteracted?

A

GnRH agonist - maintains GnRH peak
- Leuprorelin, gosrelin
- CI: don’t give in IHD or CCF

Counteract by giving androgen receptor antagonists/anti-androgen 1-2 weeks BEFORE and continue for 1 month
- Bicalutamide, nilutamide, flutamide
- DON’T cause osteoporosis; receptor blocker but don’t deplete levels themselves

85
Q

Which ADT does NOT cause a testosterone flare?

A

GnRH antagonist
- Degarelix

Basically the best one?

86
Q

Treatment of metastatic hormone sensitive prostate Ca?

A

Docetaxel x 6 > ADT forever
- ADT: degarelix or bicalutamide + leuprorelin/gosrelin

OR

Abiraterone (CYP17 inhibitor) + ADT
- Always use with steroids
- Can cause pseudo-Conns; hypokalaemia, HTN, fluid overload

OR

Enzalutamide + ADT
- Androgen receptor blocker

87
Q

Everolimus toxicity?

A

Pneumonitis
- Hyperglycaemia, hyperlipidaemia

88
Q

Patterns for MMR loss in Lynch and which is least suspicious for genetic/familial cause?

A

MSH2 and MSH6 and BRAF negative most pathogenic

MSH2 + MSH6
MSH6 alone
MLH1 + PMS2
PMS2 alone

MLH1 + PMS2 > most likely sporadic
- BRAF V600E = Lynch very unlikely
- Negative BRAF V600E/wild type > test for germline cause
- Methylation of MLH1 = sporadic
- MLH1 deficient = familial cause

89
Q

Do tumour cells have PD1 or PDL-1?

A

PDL-1
- High amounts of PDL-1 on tumour cell can turn off T cell killing of the cancer

90
Q

Mabs in chemo

A
91
Q

Which breast cancer profile is most strongly associated with BRCA1?

A

Triple negative breast Ca

92
Q

Which breast Ca profile is associated with BRCA2?

A

ER +ve, PR +ve, HER2 negative
- Associated with male breast Ca
- Lower risk of ovarian Ca than BRCA 1 (17% vs. 44%)

93
Q

MOA heart failure in carcinoid?

A

Shit made in liver goes up to heart > tricuspid regurg

94
Q

Mammograms underestimate what type of breast Ca?

A

Ductal

95
Q

Treatment of irinotecan induced diarrhoea?

A

Atropine, loperamide > octreotide

96
Q

Treatment of CRC

A

• Right side - always FOLFOX + bevacizumab
• Left side KRAS mutant: FOLFOX + bevacizumab
• Left side WT KRAS (no mutation): FOLFOX + cetuximab

97
Q

Interaction between PPI and capecitabine?

A

PPI reduces absorption of capecitabine

98
Q

What percentage of seminomas produce HCG?

A

Only 30% prpduce HCG

99
Q

Examples of anti-PDL-1

A

Atelolizumab
Durvalumab
Avelumab

100
Q

Ca 19.9 elevated in

A

Pancreatic Ca
Ovarian cyst
HF
Hashimoto’s thyroiditis
RA
Diverticulitis

101
Q

Treatment of newly-Dx large >5cm triple negative inflammatory breast cancer?

A

Preoperative chemotherapy, mastectomy, irradiation
- Treated with neoadjuvant chemo first because high risk of locoregional spread

102
Q

When to repeat CT scan for suspicious nodule post-infection?

A

NSCLC can upstage in 6 weeks
- Follow to resolution

103
Q

Treatment of PDL1 negative and driver negative lung adenocarcinoma?

A

Pembrolizumab with carboplatin and pemetrexed

104
Q

What is most common mutation in eGFR mutation

A

L858R - deletion mutation in exon 19 or 21
- Carboplatin + paclitaxel + atelizumab + bevacizumab

105
Q

Which EGFR mutation is TKI resistant and needs chemo upfront?

A

Exon 20 insertion mutation

106
Q

TKI for ALK mutation in lung?

A

Alectinib and critozinib

107
Q

Treatment for ROS-1 mutation in lung?

A

Crizotinib, entrectinib

108
Q

Treatment of KRAS mutation in lung cancer?

A

Chemotherapy 1st line
Sotorasib is 2nd line

109
Q

Treatment of SCLC

A

If limited stage - cut it out
Stage II/III - chemoradiation; carboplatin + etoposide

110
Q

Which asbestos is more carcinogenic - blue or white

A

Blue asbestos

111
Q

Mesothelioma types - which is more aggressive?

A

Non-epithelioid AKA sarcomatoid
- More aggressive but also more sensitive to immunotherapy

112
Q

Which Px is better - luminal A or luminal B

A

Luminal Bad

113
Q

Which chemo is non cell cycle specific?

A

Anthracyclines
- Daunorubicin, doxorubicin, idarubicin

Alkylating agents
- Bendamustine, carboplatin, cisplatin, chlorambucil, cyclophosphamide, ifosfamide, melphalan, oxaliplatin, temozolamide

Platinum agents

114
Q

Lynch syndrome AKA HNPCC inheritance?

A

Autosomal dominant

115
Q

Nasopharyngeal cancer most common viral association?

A

EBV
- Esian beak cancer

116
Q

Most breast cancers arise from which part of the breast?

A

Terminal duct lobular units

117
Q

HER2/neu are coated by which gene?

A

ErbB2

118
Q

RF for increase oestrogen exposure

A

Increased exposure
- Nulliparity
- Late 1st pregnancy
- Early menarche
- Late menopause
EtOH
No breastfeeding
Obesity in PMP (conversion to anestrodione > estrone (weak oestrogen)

119
Q

Risk for increased breast Ca in men

A

BRCA 2
Klinefelter’s syndrome (XXY)

Most likely invasive ductal carcinoma

120
Q

Cut off for excision in HER2 breast Ca

A

<2 cm

121
Q

Radiation pneumonitis key features vs. immunotherapy-related pneumonitis?

A

Radiation pneumonitis
- Onset 4-12 weeks after completion of radiotherapy
- Crosses horizontal fissures (unlike ICI pneumonitis)

122
Q

5FU mechanism of action?

A

Thymidylate synthetase

123
Q

Key S/E of lenvatinib and sorafenib?

A
  • Lenvatinib (VEGF) - proteinuria; HCC, thyroid Ca and RCC
  • Sorafenib (TKI): HCC and RCC - palmoplantar erythrodysesthesia
124
Q

Which mutation causes drug resistance against TKI e.g. gefitinib and erlotinib

A

T790M mutation

125
Q

BRAF more common in sun exposed skin or less sun exposed?

A

BRAF mutations are more frequent in cutaneous melanoma from sites with little or moderate sun-induced damage than from sites with severe cumulative solar ultraviolet damage

126
Q

Cetuximab causes which electrolyte abnormality

A

Hypomagnesaemia

127
Q

Least myelosuppressive chemotherapy

A

Vincristine
Bleomycin

128
Q

What is chemo

A

Chemist

BPT Sadness 😔 (20 decks)

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