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BPT > Oncology > Flashcards

Oncology Flashcards

1
Q

What sort of chemo drug is Doxorubicin?
Side effects?
Risk factors?

A

Anthraxycline
Cardiomyopathy
RF = female, high dose, heart failure, trastuzumab

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2
Q

What sort of drug is cyclofosfamide?
What is a CNS side effect?
Treatment?

A

Alkylating agent
Encephalopathy
Cessation, electrolyte correction and methylene blue

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3
Q

How does fluorouracil cause chest pain?
How can this be prevented?

A

Vasospasm, some metabolites are cardiotoxic
Angiogram and stenting prior to chemo

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4
Q

What sort of chemo is Cisplatin/carboplatin/Oxaliplatin?
Side effect?
How does this occur?
Which one is most likely to have side effects?

A

Platinum based chemo
Peripheral neuropathy - acute and chronic
Oxaliplatin
Effects on voltage gated sodium channels

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5
Q

Intrathecal methotrexate causes what CNS side effect?
What is the timeframe for this to occur?
Prevention?

A

Aseptic meningitis
2-4hrs post injection
Corticosteroids

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6
Q

What does the MEN2A gene cause?
What is the percentage risk?

A

Predisposition to medullary thyroid cancer (MTC), pheochromocytoma, and primary parathyroid hyperplasia.
90 percent for MTC, approximately 40 to 50 percent for pheochromocytoma, and 10 to 20 percent for multigland parathyroid hyperplasia.

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7
Q

What is the difference between MEN2A and MEN2B?
What gene is implicated in both?

A

MEN2A - Medullary, phaeo and parathyroid tumours
MEN2B - Medullary + Phaeo tumours, NOT parathyroid, instead Neuromas + marfanoid
Gene = RET

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8
Q

Treatment for medullary thyroid cancer?
What mutation do you need to confirm this?
What other tumours should you look for?
How do you monitor recurrence?

A

Thyroidectomy before age 20
RET mutation
Phaeo + parathyroid
Calcitonin level

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9
Q

What type of HPV infection is highly oncogenic?
What cancers is it associated with?

A

HPV infection type 18: Along with type 16
associated with cervical and other anogenital cancers, as well as some head and neck cancers.

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10
Q

What type of tumour most commonly causes SIADH?

A

Small cell lung cancer

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11
Q

What type of cancer can cause gynaecomastia?
How does this occur?

A

Testicular cancer
B-HCG produced by tumour activates LH receptors on testes, this increases testosterone release and excess testosterone is converted into oestrogen by aromatase in peripheral tissues

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12
Q

An adolescent 16 year old female has been treated successfully with radiotherapy for Hodgkin’s disease.
Which of the following tumour is most likely to occur when she reaches adulthood (After more than 10 years following treatment)?
Non-hodgkins
Thyroid
Breast
Acute Leukaemia
Ovarian

A

Breast cancer

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13
Q

Which biomarker is the most independently predictive of immune check point inhibitor induced myocarditis?
BNP
CK
Troponin
CK-MB

A

CK-MB

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14
Q

What tumours are linked to the below markers?
Which one predicts overall prognosis with normalisation?
Beta-HCG
CEA
Ca19.9
CA-125
CA15.3

A

Beta-HCG - Testicular
CEA - Colorectal
Ca19.9 - Pancreatic
CA-125 - Ovarian
Ca15.3 - Breast

Beta-HCG levels are linked to prognosis i.e. decreased levels post treatment = good survival

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15
Q

What are the 1st, 2nd and 3rd line therapies for early clear cell RCC disease?
What about advanced disease?
What is more common: clear cell or spindle cell?

A

1st - Sunitinib
2nd - Bevacizumab
3rd - Nivolumab
Advanced = Ipi/Nivo
Most common = clear cell

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16
Q

What is first line treatment for immune-mediated colitis?
Second line?

A

High dose glucocorticoids
Second line is Anti-TNF alpha therapy

17
Q

Which of the following is a good prognostic marker of Sunitinib therapy?
Why?
Pyrexia
Diarrhoea
Flu-like symtpoms
Myalgia
Hypertension

A

Hypertension
Sunitinib is a VEGF TKI, so when its working it acts on vasoendothelial cells causing vasoconstriction and hence hypertension

18
Q

When is Pembrolizumab used in high risk Renal cell carcinomas;
Pre or post op?

A

Post resection

19
Q

What is the most common side effect of Bleomycin?
What are the risk factors?
What DLC0 change prompts immediate cessation?
Is there blood eosinophilia?

A

Pulmonary toxicity
Higher dose, renal failure, exposure to high dose oxygen, smoking
DLCO decrease >25%
Eosinophil = no

20
Q

What is the leading cause of death for survivors of testicular tumors following successful chemotherapy?
Second primary cancers
Lung fibrosis
Renal failure
Myocardial ischaemia
Thromboembolic event

A

Second primary cancers

21
Q

What is the difference in side effects between Ifosfamide and Cyclophosphamide ?

A

Ifos = Acute Nephritic syndrome
Cyclo = hemorrhagic cystitis

22
Q

Which of the following medication has been associated with cases of male breast cancer?
Finasteride
Metoprolol
Spironolactone
Acetazolamide
Doxazosin

A

Finasteride

23
Q

Which of the following cancers have the best chance of long term survival even with the presence of metastasis?
Treatment?
- prostate cancer with bone metastases
- ovarian cancer with malignant ascites.
- lung cancer with brain metastases.
- breast cancer with bone metastases
- germ cell cancer with lung metastases.

A

Germ cell with lung
Treatment = cisplatin, etoposide and bleomycin.

24
Q

Which of the following gene mutation is associated with increased risk of breast cancer in males?

BRCA 2
BRCA 1
RET
CHEK 2
P53

A

Mutations in both BRCA1 and BRCA2 genes are associated with an increased risk of breast cancer in males, but the BRCA2 mutation carries a higher risk for male breast cancer compared to BRCA1.

Men who carry mutations in the BRCA2 gene have a significantly increased risk of developing breast cancer compared to the general population. The lifetime risk of male breast cancer in BRCA2 mutation carriers is estimated to be approximately 68%, which is markedly higher than in men without these mutations.

25
Q

The Human Papilloma Virus (HPV) is associated with which type of malignancy?

Anal carcinoma
Non small cell lung cancer
Cholangiocarcinoma
Esophageal carcinoma
Hepatocellular carcinoma

A

Anal carcinoma

High-risk HPVs cause virtually all cervical cancers. They also cause most anal cancers and some vaginal, vulvar, penile, and oropharyngeal cancers. HPVs infect epithelial cells.

26
Q

A 68-year-old man with de novo, high-volume metastatic castration-sensitive prostate cancer (mCSPC) is being considered for intensification of therapy. He has a performance status of 1 and no significant comorbidities.

In addition to androgen deprivation therapy (ADT), which of the following treatment strategies is most likely to improve his overall survival based on the recent advances in the management of mCSPC?

Triple therapy with docetaxel chemotherapy, apalutamide and goserelin
Addition of abiraterone acetate to goserelin
Six cycles of docetaxel chemotherapy alone
Addition of enzalutamide to goserelin
Doublet treatment with goserelin and apalutamide

A

Triple therapy with docetaxel chemotherapy, apalutamide and goserelin

For men with de novo, high-volume mCSPC, the addition of docetaxel chemotherapy and an androgen receptor signaling inhibitor (ARSI) to ADT (triple therapy) has shown promise in improving overall survival. This approach combines the cytotoxic effects of chemotherapy with the targeted action of ARSIs against androgen receptor signaling, addressing the disease through multiple mechanisms.

27
Q

Prostate-Specific Membrane Antigen (PSMA) plays a significant role in the diagnosis and treatment of prostate cancer.
Which of the following statements best describes the role of PSMA in prostate cancer management?

PSMA is a cell surface protein overexpressed in most prostate cancers, utilized for diagnostic imaging and targeted radionuclide therapy.
PSMA is predominantly expressed in benign prostatic hyperplasia and is therefore not a useful marker in prostate cancer.
PSMA expression is limited to prostate cancer cells, making it an unspecific target for diagnostic imaging or targeted therapy.
PSMA levels are inversely related to prostate cancer aggressiveness, with lower expression indicating more advanced disease.

A

PSMA is a cell surface protein overexpressed in most prostate cancers, utilized for diagnostic imaging and targeted radionuclide therapy.

28
Q

A 72-year-old man with metastatic castration-resistant prostate cancer (mCRPC) presents for consideration of further treatment. He has previously received androgen deprivation therapy (ADT) with progression to mCRPC and has not received chemotherapy or novel androgen receptor targeted therapies during the castration-sensitive stage. He does not have a known BRCA1/BRCA2 mutation.
Which of the following treatment options is most appropriate for this patient?

Prescribe radium-223 as the first-line treatment for mCRPC, considering its radiopharmaceutical properties.
Start chemotherapy with docetaxel, given the patient has not received chemotherapy in the mCSPC stage.
Initiate treatment with a poly-ADP ribose polymerase (PARP) inhibitor such as olaparib, regardless of BRCA mutation status.
Begin novel androgen receptor targeted therapy with abiraterone acetate, as it has not been used in the mCSPC stage.

A

Start chemotherapy with docetaxel, given the patient has not received chemotherapy in the mCSPC stage.

For patients with metastatic castration-resistant prostate cancer (mCRPC) who have not previously received chemotherapy during the castration-sensitive stage, docetaxel represents a standard first-line chemotherapy option. Docetaxel has been shown to improve survival in mCRPC patients and is typically considered before second-line therapies or when novel androgen receptor targeted therapies are not suitable or have already been used.

29
Q

The following intervention is useful in the management of diffuse large B-cell lymphoma except?

Autologous stem cell transplantation
Prophylactic intrathecal chemotherapy
R-CHOP chemotherapy
Rituximab with dexamethasone, high-dose cytarabine, and cisplatin [R-DHAP]
Rituximab combined with doxorubicin, cyclophosphamide, vindesine, bleomycin, and prednisone (R-ACVBP)

A

Propphylactic intrathecal chemotherapy

30
Q

BRAF mutant or wild type more likely in Lynch syndrome?
Is the APC gene associated with left or right sided cancers?

A

Wild type

APC = left

31
Q

EGFR inhibitors need KRAS to be mutant or wild type?
Why?

A

Wild type
KRAS occurs in the tumour growth pathway before EGFR site, so if its mutated it won’t reach the site of action for the EGFR drugs

32
Q

Mutations in EGFR/RAS pathways are not implicated in which type of cancer?
Which cancers do commonly have these mutations?

A

Cervival
Common - colorectal, lung and melanoma

BPT (13 decks)

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