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Qs Flashcards

1
Q

Diagnosis of melanoma

A

Over 6mm, assymetric, uneven borders, shades of colour, enlargement, FIRM

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2
Q

Two major types and their Subtypes of melanoma

A

Rapid growth phase which inc superficial spreading which is commonest, lentigo maligna, acral lentiginous

And vertical growth phase inc nodular which has poor prognosis,

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3
Q

Prognostic factors in melanoma

A

Dermal thickness is most critical, ulceration upstages all else, LDH important in metastatic disease

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4
Q

Staging in melanoma

A

Stage 0 is in Situ, 1 is under 2mm without ulceration or under 1mm with ulceration

Stage 2 is more than 2mm without ulceration or more than 1mm with ulceration

Stage 3 is LN

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5
Q

Main site of met in melanoma

A

Lung

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6
Q

Management of stage 1-3 melanoma

A

Wide local surgical excision .
For stage 3 also do lymph node resection (TLND)

If over 1mm or if over 0.75mm but with high risk features- do sentinel node biopsy . And if this is positive only do complete LN dissection

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7
Q

Commonest mutation in melanoma

A

BRAF

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8
Q

Management of metastatic melanoma

A

Surgical resection of Mets

If BRAF mutant, do combo BRAF (dabrafenib>vemurafenib, only dabrafenib has CNS activity and inhibits all V600) with MEK (trametinib) inhibitor. Another targeted therapy is cKIT (imatinib) also can be used (this activates RAS)

Second line is immunotherapy or if wild type BRAF- nivo/ipi combo esp for CNS disease

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9
Q

What happens if BRAF inhibitor used in their own

A

Higher risk of keratoacanthoma and squamous fell cancer

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10
Q

Immunotherapy SEs and management

A

Pseudoprogression with antiCTLA4 (thus don’t scan too early), GI immunotoxicity esp with ipi, whilst nivo causes more hypothyroidism. Mx- symptom relief alone if mild, if moderate steroids . If severe may need additional mycophenolate
Grade 4 colitis May need prolonged steroid weaning and TNF blockage and bowel resection

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11
Q

List mutations causing breadt cancer and which has highest causative link

A

BRCA (esp 1), TP53 (Li Fraumeni has highest!), STKII (Peutz Jegher), MSH/MLH

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12
Q

Role and pathogens is of PARP inhibitor in BRCA breast cancer

A

Like BRCA, PARP is another DNA base excision repair - they result in higher mutations causing genomic instability - tumor selective cell death via synthetic lethality

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13
Q

Commonest breast cancer type

A

Invasive carcinoma not otherwise specified

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14
Q

Describe staging of breast cancer

A

Stage 1 is small and node negative

Stage 2 is large and/or under 4 LNs, stage III is inflammation on chest wall or more than 4 LNs.

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15
Q

Screening in normal risk, moderately high risk and high risk women

A

Normal risk mammogram every 2 from age 50-74
Moderately increased risk is if one FDR under 50 years, 2 SDR with one under 50 in same side of family, annual mammogram from age 40. If two FDR in same side both over 50, annual mammogram from 50

If high risk (2 or more FDR under 50)- MRI annually from age 30

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16
Q

Management of stages 1-3 breast cancer

A

Wide local excision with RTX (sane outcomes as mastectomy) - mastectomy preferred if multi centric tumors, high tumor to breadt ratio, risk reduction, contraindication to RTX (e.g. prev RTX to same field lymphoma)
If high risk mastectomy parients (triple neg or node pos tumor over 5cm) also do RTX

Need to do sentinel biopsy in all at axillary . If pos- LN clearance

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17
Q

Describe the adjuvant systemic breast cancer therapies in non metastatic disease

A 
If ER pos and low risk- endocrine . 
If ER pos and high risk- endocrine AND chemo 
If HER2 pos , trastizumab AND chemo 
If triple neg- chemo 
Bisphosphonate increases survival!

Endocrine therapy for premenopausal is OFS (surgery or GNRH agonist with Goserelin) with AI (anastrozole) best, next is tamoxifen
Another endocrine therapy is fulvestrant (selective estrofen receptor degradation)
If postmenopaisal- AI alone, or tamoxifen

HER2 inhibitor last are trastuzumab and pertumab sometimes uses jointly

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18
Q

SEs of AIs, tamoxifen and HER2 blockers

A

AIs- hot fluishes, osteoporosis, vaginal dryness, CVD risk, higher cholesterol, AIMSS

Tamoxifen- hot flushes, VTE risk, uterine cancer (only in post menopausal- as when used in post menopause there’s low estrogen and thus tamoxifen agonist effects predominate , NAFLD
In premenopausal can increase OP risk but protects bone in post menopausal women

Trastuzumab- reversible myosin shunning , reduces LVEF by 10%- can rechallenge once EF improves

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19
Q

Management of metastatic breast cancer

A

ER pos- endocrine first WITH AI and chemo (and OFS if premenopausal- give chemo first if severely symptomatic or high volume of disease) and CDK4/6 inhibitors (prevent G1 to S progression- inc ribociclib, palbociclob)

If HER2 pos- herceptin and chemo

Chemo used is taxanes and anthracyclines inc doxorubicin

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20
Q

Indication for chemo in ovarian cancer and what agent is used

A

Carboplatin, pacitaxel used.

Adjuvant chemo used if high grade or clear cell histology , stage 2 and beyond

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21
Q

Indication for radiotherapy in ovarian cancer

A

Stage iii , palpitation

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22
Q

Management of low risk, intermediate risk and high risk endometrial cancers (and define risks)

A

Low risk is stage 1 under 50% myometrial invasion- surg alone

If intermediate LN clearance- stage 1 but over 50% myometrium, surg +/- brachytherapy

If high risk- pelvic radiotherapy, local brachytherapy, chemo and surg

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23
Q

Management of advanced invasive cervical cancer

A

Chemo radiation with cisplatin (no surg)

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24
Q

Management of metastatic cervical cancer

A

Carbo/pacitaxol +/- Bevacizumab

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25
Q

Is NSAID RF for gastric cancer

A

No is chemoproctive

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26
Q

Management of gastric cancer with and without nodal involvement

A

If T1aN0 under 2cm confined to mucosa - surg resection alone

If above T1N0- surg and chemo (if adeno- commonest) or chemorad if squamous

If medically fit also do LN dissection

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27
Q

Chemo used in gastric cancer

A

FLOT

5FU, docetaxel, leucovirin, oxaplatin

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28
Q

Management of metastatic gastric cancer

A

If advanced gastric cancer - PD1 blocker

If HER2 positive- herceptin- increases survival in metasisis

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29
Q

Chemo for pancreatic cancer

A

FOLFIRINOX (folinic acid, 5-FU, irinotican, oxaplatin) or gemcitabine alone which has less toxicity

Erlotinib also has a role

Neuadjuvant chemorad for borderline resectable cancers

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30
Q

Describe role of PSMA in prostate cancer screening

A

Highly specific and sensitive - it’s a PET scan with prostate specific membrane antigen and able to identify Mets earlier

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31
Q

Management of castrate sensitive prostate cancer

A

ADT (GnRH agonist like Goserelin or antagonist like degarelax) - if using GNRH agonist esp if bone Mets present MUST use testosterone antagonists like flutamide 7 days prior to 7 days after to reduce flare phenomenon

If high volume disease - also use doxetaxel

Abirarerone shown effective not on PBS

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32
Q

Management of castrate resistant prostate cancer

A

ADT, docetaxel and androgen receptor antagonists
Abiraterone blocks 17a hydroxylase
Enzalutamide is androgen receptor antagonist . Ketaconazole is adrenal androgen inhibitor

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33
Q

Wide effects of abiraterone and enzalatumids

A

Abiraterone blocks 17a hydroxylase which leads to
1. Build up for aldosterone and subsequent hyperaldosteronism

  1. Low production of 17 hydroxyprogesterone -> low cortisol -> thus give with pred
  2. Commonly causes transminitis

Enzatumide- HTN, reduced cognition and confusion, fatigue, seizures (contraindicated in epilepsy)

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34
Q

Implication of AR-V7 mutation in blood in prostate cancer

A

Predicts response to abiraterone and enzulatamide

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35
Q

Predicts of relapse in prostate cancer

A

Gleeson score, PSA doubling time under 10 months

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36
Q

Role of VHL mutation in renal cell cancer

A

VHL keeps hypoxia induction factors in check-> HIF normally promotes angiogenesis and when mutated uncontrolled HIF

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37
Q

First line management in advanced renal cell cancer

And second line

A

TKI- sunitinib has longer survival and higher toxicity than sorafenib (both VEGF inhibitor)

No role for surgery
Cytoreductive chemo also done, minimal benefit

In second line- immunotherapy, mTOR, Bevacizumab

38
Q

What’s better treatment in advanced RCC

A

Note if intermediate or poor risk advanced RCCs- combined immuno better than sunitinib!!

39
Q

Side effects of TKIs

A

Mucositis, stomatitis, HTN, diarrhoea, hypothyroidism, Hand foot mouth syndrome, PRES

40
Q

Tumor marker in seminoma and nonseminoma

A

Seminoma= NORMAL AFP, any BCG, any LDH

Non seminoma = AFP high, BCG & LDH also high

41
Q

Describe staging in testicular cancer

A

Stage 1 is limited to testes, 2 is LN, 3 is distant Mets

42
Q

Management of stage 1 seminoma, and stage 2

What if residual disease

A

Stage 1 orchiectomy

Stage 2- orchdectomy and high dose carboplatin

If residual disease under 3cm- just surveillance
If one or more retroperitoneal LN, LN dissection

43
Q

Management of stage 1 and 2 nonsemionas

A

Stage 1= if no RFs, just orchiectomy

If RFs (e.g. lymphovascular invasion)or stage 2= Orchiectomy plus BEP OR RPLND

44
Q

Management of metastatic testicular cancer

A

BEP (bleomycin, etoposide, cisplatin) resect residual mass. If relapsed- represents cisplatin resistance - mx with vinblastine, ifofamide

45
Q

Describe staging in lung cancer

A

T1 is under 3cm, T2 is 3-7cm, T3 is over 7cm

Stage 1B- T2NO

Stage 2B- T3N1

Stage 3A- T4N2

Stage 3Band C- T4N3

Stage 4- Mets

46
Q

Management of stage 1 and 2 lung cancer

A

Surg if FEV1 over 80%

If unfit- RTX

Adjuvant chemo cisplatin (if can’t tolerate carboplatin)

Do LN biopsy for staging

47
Q

Management of stage 3 lung cancer

A

If resectable- resect and chemoradiotherapy . If borderline resectable consider neoadjuvant chemorad first

If unresectable tumor- chemorad wirh etoposine and cisplatin - main is radiation and chemo just

PD1 blocker durvalimab for 12 months post chemorad shown to improve survival

48
Q

Approach to and management of stage 4 non small cell cancer

A

Need to classify as adenocarcinoma vs squamous cell

Adenocarcinoma- if EGFR, use first gen TKI gefitinib although 3rd gen osimertinib better as overcomes T790M mutation . If ALK pos, 3rd gen TKI approved alectanib as has CNS penetration. If ROS1 translocation can use cirzotinib
Note KRAS commonest mutation but no treatment

If no driver mutation- and PD1 levels over 50 use pembrolizumab. If under 50 use chemo alone

If squamous cell- if PDL1 over 50- Pembro, If PDL1 under 50, pembro and chemo

49
Q

SE of ALK TKIs

A

Visual changes, long QT, neutropenia

50
Q

Evidence for early pal care in NSCLC

A

Improved PFS, QOL and mood

51
Q

Management of mesothelioma

A

Radical extrapleral pnemonectomy (but risk in other lung), palliative chemo cisplatin, pemetrexed, Bevacizumab. Some respond to PD1 blocker

52
Q

Management of small cell lung cancer

A

Limited stage disease - chemorad and if responds - cranial irradiation,

Extensive stage- chemo alone and consider palliative RTX. Adding PDL1 improves survival but not on PBS and used as second line

53
Q

Paraneoplastic seen in Squamous , and small cell

A

Squamous - hypercalcemia, HPOA

Small cell- SIADH , Lambert Eaton (ptosis, absent deep tendon reflexes)
Serum neurone specific enolase in 75% (also dopa decarboxylase, calcitonin)

54
Q

Cause of HNPCC, FAP and MUTYH syndromes- location and of the unit

A

HNPCC more likely right sided, 10% have synchronous. These are Lynch syndrome . Due to MMR mutations (most common is MSH2)

FAP- tumor suppressor genes on chromosome 5, controls beta caretin (involved in cell-cell adhesion)- must do sigmoidoscopy from age 12 and duodenal screen from age 25

MUTYH associated polyposis- aut recessive , base repair gene.

55
Q

How does lynch syndrome associated endometrial cancer different from normal tome

A

Lynch affects lower uterine segment, more type 2 features (higher grade, older age, occur in obesity, early menarche)- if diagnosed should do early colonscopes

56
Q

Screening guidelines in CRC

A

For average risk - FOBT every 2 years from 50-74 (or scope 10 yearly)

For moderately high risk (one FDR under 55, 2 FDR at any age, one FDR and one SDR from same family at any age)- FOBT every 2 years from 40-49 then scope every 5 years from 50

High risk - 3FDR or SDR at any age with one under 55 years , or 3 FDR any age)- FOBT from age 35 till 45 then scope from 45 five yearly

Low dose aspirin in moderate in high risk

57
Q

Management of stage 1, 2, 3 CRC

A

Stage 1- surg

Stage 2- surg and if high risk adjuvant chemo

Stage 3- surg and 6 months FOLFOX (folinic acid, 5-FU, oxaplatin, ironotican also used often, latest chemo approved is lonsurf ) and radiation (which is sensitiser)

58
Q

Management of metastatic CRC

A

If curable - aggro therapy. Resect if oligometsstatic. If borderline resectable- chemo then surg resection.
If unresectable- chemo +/- targeted therapy- inc Bevacizumab (VEGF inhibitor) and EGFR inhibitor cetuximab (only if RAS wild type, LEFT tumors$

59
Q

Surveillance after surgery for CRC

A

After surgery for first two years clinical review every 3 months and 6 monthly CT staging
Years 3-5- CEA, annual CT
Colonscopy at onset and 2nd yearly!

60
Q

List the ECOG categories

A

0= asymptomstic

1= symptomatic but well/active

2= resting <50% in bed of waking hours

3= resting over 50% of waking hours

4= bed bound

61
Q

Where does microtuble production occur

A

G2

62
Q

Describe Li Fraumeni syndrome

A

Inherited familial predisposition to wide range of cancers- due to p53 mutation tumor suppressor mutations- causing soft tissue and bone sarcomas , breadt cancer and brain tumors

63
Q

Describe peutz jegher syndrome

A

Aut dominant develops benign haemarthomastous polyps in GIT and hyperpigmented macules on lips and oral mucosa- higher risk of cancers of liver/lungs/breast/ovarian

64
Q

Cancers of MEN1, 2a, 2b

A

MEN 1 (3Ps)- pituitary, pancreatic, parathyroid

MEN2a= 2Ps, 1Ms= phaochromacytoma, parathyroid, medullary thyroid cancer

MEN2b= 1P,2Ms= phaeochromocytoma, medullary thyroid cancer, Marfanoid/mucosal neuroma

65
Q

What does tumor market Ca125, CEA, Ca15.3, Ca19.9

A

CEA- colon cancer

Ca125= ovarian

Ca15.3= breast

Ca19.9= pancreatic/biliary cancer

66
Q

Mutations in

  1. APML
  2. AML (good and bad)
  3. CML
  4. MDS
  5. MPD
  6. Burkitts
  7. Mantle cell lymphoma
  8. Follicular lymphoma
  9. CLL (good and bad)
A

APML= t(15;17)

AML poor prognosis- monosomy 7, FLT3 mutant, del5q, del17

Good prognosis- t(8,21)Inv(16)

CML- t(9;22)BCR-ABL

MPD- JAK2 V617F mutation

MDS- 5q minus syndrome

Burkitt lymphoma - MYC, chromosome 8 t(8;14)

Mantle cell lymphoma- cyclin D1 (chromosome 11)- t(11,14)

Follicular lymphoma- Bcl2 chromosome 18 t(14;18)

CLL - good is 13q deletion, bad is del17q which correlated with p53

67
Q

Management of AML

A

If fit , induce with 7 days cytarabinr and 3 days anthrocyclines. Consolidate HIDAC . Then observe vs stem cell if at high risk
If FLY3 mutant- add midostaurin
If CD33 pos- add gemtuzumab

If unfit- Aza and low dose cytarabine
If relapse - BSC vs BMAT

68
Q

Management of ALL

A

ALL is commonest in young

If over 45- hyper CVAD (cyclo, vincristine, adaramycin, dex), MTX and cytarabine (for CNS prophylaxis) as induction. If Ph+= add imatinib
Then consolidate with same . Maintenance with MTX, 6-MP, pred

Cont for 2 yrs
If refractory- BLINATUMOMAB for B ALL & CAR T cells for T cells under 25 yrs

69
Q

MAnagemrnt of CML

A

They’re Ph pos- BCR-ABL

Imatinib/dasatinib
2nd line is interferon and cytarabine
If developed T3151 mutation here - use ponatinib here

70
Q

SEs if BCR-ABL TKI

A

Pleural effusion, pancreatitis, vascular risk, DM

71
Q

CML vs leukamoid reaction

A

CML shows WBC with low ALP score, in leukemoid toxic granules (aka dhole bodies) and left shift neutrophils

72
Q

What’s richters transformation

A

transformation of B cell chronic lymphocytic leukemia (CLL) or hairy cell leukemia into a fast-growing diffuse large B cell lymphoma

73
Q

CLL mx

A

Early stage watch

If symptoms- FCR (fludarabine, cyclo, ritux)
If unfit- Ritux, chlorambucil, or ibrutinib (BTK inhibitor- squeezes CLL cells from LN to periphery

74
Q

If delq17 present in CLL, how does this change management

A

Give ibrutinib or venetoclax (BH3 mimetic), obinutuzumab (antiCD20)

75
Q

Lymphomas associated with EBV, HHV8, HTLV1, Hep C

A

EBV - Butkitts, Hodgkin, HIV associated lymphoma, PTLD

HTLV1= Human T cell lymphoma/leukaemia

Hep C= marginal zone lymphoma

HHV 8= primary effusion lymphoma

76
Q

In Hodgkin RS cells seen. What markers are they positive for

A

CD15 and 30

77
Q

Commonest cause of SVC obstruction in young

A

Hodgkin

78
Q

Management of Hodgkin lymphoma

A

Limited stage- ABVD (adriamycin, bleomycin, vinblastine, docurbrazine) and RTX. If advanced - larger course ABVD called eBEACOPD

IF relapsed- brentuximab (antiCD30), PD1 inhibitor and auto SCT

79
Q

Describe Ann Arbor system

A

For HD divided into A where no sx or just prutitis and B into B symptoms

And also as 1 single LN, 2 as 2 or more LN on same side of diaphragm , and 3 as LNs on both sides of diaphragm , and 4 as spread beyond LN

80
Q

NonHodgkin lymphoma inc follicular lymphoma.

Describe their management

A

Follicular - commonest , mx of stage 1 is curative RTX, stage 3 and 4 and asymptomatic is watch
If stage 3 and 4 but symptomatic CHOP (cyclo, hydrodanorubicin, vincristinr, pred) and obinutumab (antiCD20). Maintainance 2 yrs with ritux or obinutumab

If refractory/relapsed- ibrutinib (BTK inhibitor) , BH3 mimetic (venoteclax), idelalisib (phosphodiesterase 3 kinase inhibitor )

81
Q

NonHodgkin lymphoma inc DLBCL, mantle cell, burkitts and splenic marginal zone lymphomas
Describe their management

A

Universally CD20 positive, R-CHOP.
Similar to obinutumab for follicular lymphoma, polatuzomab developed but not approved .

Mantle cell lymphoma - chemo, venetoclex, ibrutinib

Burkitts- heavy chemo CODOXM-IVAC

82
Q

MGUS vs smouldering myeloma vs myeloma

A

MGUS- M protein under 3 and plasma cell under 10% with no CRAB

Smouldering myeloma- M protein over 3, PC over 10%, and no CRAB

Myeloma- any M protein, PC over 10 and CRAB

83
Q

Describe management of myeloma

A

If transplant candidate (only under 70)- cyclo, bortezomib, dex, melphalan, autoSCT as induction

Then maintenance steroids and thalidomide if standard risk vs bortezomib if intermediate risk
If non transplant- lenalidomodr and dex , it bortezomib and melphalan, or pred and cyclo

84
Q

List the ankylating agents

A

Cyclophosphamide, melphalan, tamezolamide, platinum based (cisplatin)

85
Q

List topoisomerase inhibitors and where it acts

A

Acts on G2

Inc topoisomerase 1 - ironotican
2- etoposide, anthracyclines (doxorubicin)

86
Q

List mitotic inhibitors and their mechanism

A

Vinca alkaloids destroy microtubules inc vincristine

Taxanes are microtubule stimulators inc docitaxel

87
Q

List the subclasses of antimetabolites all of which work at S phase

A

Antifolate
is MTX, pyramidine antagonist is 5FU, cytarabine

Purine analogues are aza

Purine antagonist is fludarabine

Ribonucleotide reductase inhibitors are hydroxyurea

88
Q

Most extravascation causing agents and their mx

A

Anthrocyclines mx by ICE, dimethylsulfoide

Vinca alkaloids mx heat and hyalurasinase

89
Q

Unique SE of cytarabine

A

Cerebellar neuronal effects and conjunctivitis

90
Q

Which chemo agent causes radiation recall teaction

A

Donarubicin

Onc revision (1 decks)

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