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RACP Written > Oncology > Flashcards

Oncology Flashcards

1
Q

What part of the cell cycle do anti-metabolites act on and name 3 examples of these drugs

A

Inhibit S phase = DNA cycle. Examples are methotrexate, 6-mercaptopurine, thioguanine, Ara-C (Cyarabine), 5-flourocil, Hydroxyurea

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2
Q

What are the side effects of anti-metabolites?

A

Myelosuppression, mucositis, dermatitis. Ara-C can cause cerebellar toxicity. ** Think Methotrexate**

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3
Q

Why is it important to measure TPMT levels?

A

TPMT is used to metabolise Azathioprine/6-mercaptopurine. If there is a TPMT inactivating mutation, can cause severe toxicity with standard doses as dose builds up.

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4
Q

Where does Bleomycin act?

A

G2 phase

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5
Q

What is the action of Actinomycin?

A

Inhibits transcription

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6
Q

What do anti-DNA antibiotics do? What is their mechanism of action?

A

Bind to DNA, intercalation, cleave DNA strands, inhibit DNA transcription
End in -cin. Ie Bleomycin, Actinomycin, Doxorubicin

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7
Q

Where do topoisomerase inhibitors act?

A

Cause DNA strand breaks in late S/early G2 phase

TopoisomeraSSe- S phase

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8
Q

What are the two types of topoisomerase inhibitors?

A

Non-intercalating ie Etoposide, Irinotecan
Intercalating: Anthracycline ie Doxorubicin and Daunorubicin

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9
Q

What is the mechanism of action specifically for doxo and daunorubicin?

A

Topoisomerase inhibitor, intercalating agent and reactive oxygen species
(triple threat)

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10
Q

What are the side effects of doxo and daunorubicin

A

RUBY- RED HEART
Red urine, tissue necrosis, arrythmias, DILATED cardiomyopathy

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11
Q

How and where in the cell cycle does Vincristine work?

A

Binds to Tubulin and inhibits M phase
VIMCRISTINE

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12
Q

What are the side effects of Vincristine

A

neurotoxicity (peripheral, cranial, autonomic), SIADH, constipation/ileus, jaw pain

FATAL IF GIVEN INTRATHECAL

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13
Q

What are the side effects of aspariginase?

A

Coagulopathy (stroke, sinus thrombosis), pancreatitis, diabetes mellitis, allergy/anaphylaxis

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14
Q

How do alkylating agents work and what are some examples?

A

Act by bonding alkyl group to DNA which induces apoptosis
Cyclophosphamide

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15
Q

Side effect of Ifosfomide/Cyclophosphamide?

A

Haemorrhagic cystitis, infertility, nephropathy
IFOSPHAMIDE can cause encephalopathy due to metabolites which cross the BBB. Treat with methylene blue.

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16
Q

Side effect of Cis/Carboplatin?

A

Severe delayed emesis, nephro and ototoxicity,

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17
Q

Side effect of busulfan?

A

Lowered seizure threshold, veno-occlusive disease

Busulfan BLOCKS vessels

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18
Q

Side effect of Etoposide?

A

HIGHEST risk for secondary malignancy and second highest for allergy.

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19
Q

Which chemotherapy agents are the worst for fertility?

A

Alkylating agents et ifosfamide, busulfan, cyclophosphamide

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20
Q

What ions/minerals are involved in tumour lysis syndrome?

A

Ca, Phos, K, Uric acid. HIGH uric acid, potassium and phosphate. LOW calcium. (precipitates with phosphate). LDH also monitored for degree of cell lysis.

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21
Q

What is the mechanism of action for allopurinol vs rasburicase for treatment of TLS?

A

Allopurinol blocks xanthine oxidase inhibitor so reduced urate formation. Rasburicase catabolises uric acid into allantoin to make it more easily excretable in kidneys.

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22
Q

What cancers are commonly associated with superior vena cava obstruction?

A

T-cell ALL, lymphoma, germ cell tumours (teratoma)

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23
Q

What cells/organs synthesise AFP?

A

Fetal yolk sac, liver and intestines. So can be elevated in acute liver disease, biliary atresia, ataxic telangectasia, tyrosinaemia, epithelial liver tumours (hepatoblastoma)

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24
Q

What is the proportion of B:T cell in ALL?

A

Pre-B is 70%, T-cell is 30%

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25
Q

What are the high risk factors in ALL?

A
  1. Age <1 or >10
  2. WCC > 50
  3. Congenital mutations ie BCR:ABL, 4:11, hyPOploidy
  4. CNS diseases (blasts on LP)- essentially any extramedullary disease
  5. Response to induction
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26
Q

What do AMLs present with?

A

Chloroomas (leukocytic deposits), hyperleukocytosis

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27
Q

What are the risk factors for AML

A

Cytogenetics and response to treatment

28
Q

What is the mutation (and location) for acute promyelocytic leukemia?

A

PML-RARA mutation on 15;17

29
Q

What is the treatment for APML?

A

Arsenic/Vit A derivative. Commonly will have cytokine storm on starting treatment (like SIRS response)

30
Q

What syndrome is associated with JMML? What is the mutation?

A

Noonan’s commonly associated, mutation is PTPN11
NF1 also associated

31
Q

What is the classic presentation for HODGKIN’s lymphoma?

A

B symptoms and neck/mediastinal disease. BIMODAL

32
Q

What staging is used for Hodgkin’s lymphoma?

A

Ann-Arbour staging

33
Q

Which cancer has Reed Sternberg cells?

A

Hodgkins

34
Q

What is the distribution for NHL? (ignore this questoin, error)

A

Bimodal

35
Q

What are the common NHL?

A

Burkitts and diffuse large B cell lymphoma- DLBCL

36
Q

What is a known trigger for Burkitts

A

EBV

37
Q

What is the treatment for NHL?

A

RItuximab (anti-CD20)- note high tumour lysis syndrome risk

38
Q

What do patients with T-cell lymphoblastime leukemia OR pre-T cell lymphoma present with?

A

Teenagers with SOB, BM failure and mediastinal mass on CXR due to thymus involvement

39
Q

Staging for NHL?

A

St Judes

40
Q

What is the mutation in retinoblastoma? And presentation?

A

RB1, white reflex with reduced VA and strabismus

41
Q

What embryonic tissue is nephroblastoma (Wilms) derived from?

A

MESOnephros (NephroblastoMA = MEsonephros)

42
Q

What the the gene associated with Wilms tumour?

A

WT1

43
Q

What are the syndromes associated with Wilms

A

Overgrowth so
1. Beckwith Weideman.
2. WAGR (DELETION OF WT1) and Denys Drash (Truncation of WT1)
3. Fanconi anaemia
4. Pearlman syndrome

‘WAGR deleted, Denny’s has a trunk’

44
Q

What is WAGR?

A

Wilms
Aniridia- abnormal development of the eye
Genitourinary- no testes
Retardation

45
Q

What are the 3 features of Denny’s Drash?

A

Gonadal dysgenesis, wilms and nephropathy

46
Q

What is the age presentation of Wilms vs neuroblastoma?

A

Neuroblastoma <2, wilms 2-4

47
Q

What are imaging findings of neuroblastoma vs nephroblastoma?

A

Claw hand in kidney and calcification in NB

48
Q

What is the most common extracranial tumour?

A

Neuroblastoma

49
Q

What cells are mutated in neuroblastoma?

A

Neural crest cells

50
Q

What are the 3 syndromes associated with neuroblastoma?

A

Pepper syndrome, horner syndrome (ptosis, myosis, anhydrosis), opsoclonus-myoclonus ataxia syndrome

51
Q

What is the relationship between NMYC gene and NB outomes?

A

HIGH levels of NMYC= NOT good for prognosis.
Think N for NMYC and N for Neuroblastoma = N for not good

MYC involved in EBV associated lymphoma!

52
Q

What two syndromes are Rhabdomyosarcomas associated with?

A

LiFraumeni and NF1.
Tumour derived from skeletal muscle primitive cells

53
Q

What is the name of tumours with blue cell?

A
  1. Neuroblastoma,
  2. Ewing’s sarcoma
  3. Peripheral primitive neuroectodermal tumours
  4. Non-hodgkin’s lymphoma
  5. Soft tissue sarcomas
  6. Megakaryoblastic leukaemia
54
Q

What is the radiological sign of ewings?

A

Periosteal reaction can be peeling onion or starburst sign

55
Q

Where is the location of Ewings vs osteosarcoma?

A

Ewings in diaphysis (shaft) while osteo is at the growth plate

56
Q

What is the definition of langerhan cell histiocytosis?

A

Disorder of one or more osteolytic bone lesions with histiocyte infiltration

57
Q

What is holoproscencephaly

A

failure of prosecephalon or forebrain to develop. Presents with microcephaly, hydrocephalus, facial abnormalities and cleft lip/palate
Associated with Trisomy 13 and sonic hedgehog pathway
;Hollow at the front’

58
Q

What is Miller Diekr syndrome

A

LISSENcephaly, distinctive facial features, hypotonia, seizures/neurological symptoms

59
Q

What is associated with the sonic hedgehog pathway?

A

Holoprosencephaly, basal cell carcinoma and sporadic tumours
Has been past question

60
Q

What is the sonic hedgehog pathway?

A

Sonic Hedgehog (Shh) signalling pathway is one of the major trafficking networks that regulates the key events during developmental processes i.e growth and patterning of multicellular embryos.

61
Q

What is the origin of a cranipharyngioma?

A

Remnant of Rathkes pouch

62
Q

What are the endocrine effects of a craniopharyngioma?

A

precocious ouberty, pituitary deficiencies

62
Q

What are the endocrine effects of a craniopharyngioma?

A

precocious ouberty, pituitary deficiencies

63
Q

What is a common cause/trigger for post-transplant lymphoprolifeartive disorder?

A

EBV

64
Q

Which blue cell tumour presents in pseudorosette formation

A

Neuroblastoma

65
Q

Which two cancer meds does allopurinol interact with?

A

Methotrexate and Cyclophosphamide

66
Q

Which medication used for tumour lysis syndrome is better for kidney - allopurinol or rasburicase and why

A

Rasburicase because helps convert uric acid to soluble allantoin via urate oxidase. Allopurinol just stops further uric acid formation but can lead to deposition of uric acid in kidneys

RACP Written (18 decks)

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