🩸 Oncology, Haematology and Special Populations

1. Why are cytotoxic regimens given in cycles separated by a rest interval rather than continuously?

1. Because the drugs would lose their chemical stability if administered on consecutive days
2. To allow normal tissues, especially bone marrow and gut mucosa, to recover between doses while the tumour recovers less well
3. Because provincial funding rules limit the number of treatment days per month
4. Because tumour cells only divide during the rest interval

Cycling exploits the faster recovery of normal proliferating tissue relative to tumour, which is why dose intensity and the interval both matter. Regimen design is not driven by chemical stability or funding, and tumour proliferation does not pause between cycles. Source: BC Cancer and Cancer Care Ontario systemic therapy protocols.

2. A patient telephones ten days after chemotherapy with a temperature of 38.5 °C and no other symptom. What is the correct action?

1. Direct the patient to emergency care immediately.
2. Advise acetaminophen and a call tomorrow if the fever has not settled.
3. Advise a cough and cold remedy and rest.
4. Advise waiting for the next clinic visit.

Fever during the neutrophil nadir is febrile neutropenia, a medical emergency requiring blood cultures and empiric antibiotics within an hour, because a neutropenic patient may have no other sign of overwhelming infection. Antipyretics at home mask the only warning available. Source: Cancer Care Ontario febrile neutropenia guidance.

3. When does the neutrophil count usually reach its lowest point after a conventional cytotoxic cycle?

1. About two months after the last cycle of the whole course of treatment.
2. Within two hours of the infusion, before the patient leaves the treatment unit.
3. Only after four complete cycles.
4. Roughly 7 to 14 days after the dose, with recovery by about day 21.

The nadir for most regimens falls between the first and second week, with recovery by about day 21, which is why counts are checked before the next cycle and why fever in that window is treated as an emergency. Source: BC Cancer systemic therapy manual.

4. When is antiemetic prophylaxis given for a highly emetogenic regimen?

1. On the third day after treatment, when delayed nausea is statistically most likely.
2. Only after the patient has vomited once, so that unnecessary medication is avoided.
3. Before the first dose of chemotherapy, and continued into the delayed phase.
4. Mixed into the cytotoxic infusion bag.

Prophylaxis is far more effective than rescue, so a combination such as a 5-HT3 antagonist, dexamethasone, an NK1 antagonist and often olanzapine is given before treatment and continued to cover the delayed phase. Waiting for vomiting establishes anticipatory nausea that is then hard to control. Source: Cancer Care Ontario antiemetic guideline.

5. Which agent is used specifically for anticipatory nausea before a chemotherapy appointment?

1. A short-acting benzodiazepine such as lorazepam.
2. Another dose of the 5-HT3 antagonist given at the appointment.
3. A proton pump inhibitor the evening before.
4. A tapering course of oral prednisone.

Anticipatory nausea is a conditioned response and responds to anxiolysis rather than to more antiemetic; the best treatment is prevention by controlling nausea from the first cycle onward. Acid suppression and steroids do not address the conditioning. Source: Cancer Care Ontario antiemetic guideline.

6. Which route of administration is invariably fatal for a vinca alkaloid?

1. Peripheral intravenous.
2. Intrathecal.
3. Subcutaneous.
4. Oral, swallowed whole.

Intrathecal vincristine causes ascending paralysis and death, which is why it is labelled 'for intravenous use only — fatal if given by other routes', dispensed in a minibag and never sent to the ward at the same time as an intrathecal product. Source: ISMP Canada and national safe handling standards for vinca alkaloids.

7. What is the immediate action if a vesicant extravasates during an infusion?

1. Remove the cannula and massage the area, pressing firmly over the whole swollen area.
2. Increase the rate to flush the drug away so that none of it remains in the tissue.
3. Stop the infusion, leave the cannula in place and aspirate what can be withdrawn.
4. Continue, and apply a warm compress.

Stopping and aspirating limits the volume deposited; the cannula is retained for any antidote, and thermal application depends on the drug — cold for anthracyclines, warm for vinca alkaloids. Massage disperses the drug through more tissue. Source: BC Cancer extravasation management guideline.

8. Which antidote is used for anthracycline extravasation?

1. Dexrazoxane.
2. Hyaluronidase.
3. Sodium bicarbonate.
4. Calcium gluconate.

Dexrazoxane by intravenous infusion, started within six hours, is the recognised treatment for anthracycline extravasation, with topical dimethyl sulfoxide used in some protocols. Hyaluronidase is used for vinca alkaloids, not anthracyclines. Source: BC Cancer extravasation management guideline.

9. Which measure reduces the severity of chemotherapy-induced oral mucositis?

1. No oral fluids for a week after each cycle.
2. An alcohol-based mouthwash four times daily.
3. A structured oral care routine with a soft brush and bland saline or bicarbonate rinses.
4. A prophylactic oral antibiotic between cycles.

Systematic oral hygiene with saline or sodium bicarbonate rinses, and oral cryotherapy for certain bolus regimens, reduces mucositis; alcohol-containing mouthwashes and dehydration make it worse, and routine antibiotics are not indicated. Source: Cancer Care Ontario supportive care guidance.

10. Which principle governs handling of hazardous drugs from receipt to disposal in a Canadian pharmacy?

1. Protection during compounding only, because sealed dosage forms present no risk at any other stage
2. Ordinary dispensing precautions, since the hazard exists only for the patient who receives the drug
3. Containment at every step, with defined engineering controls and personal protective equipment.
4. Written policies alone, since a documented procedure removes the need for physical containment

National model standards, aligned with USP chapters on hazardous drug handling, require a documented list, containment ventilation, closed-system transfer where appropriate, garbing, spill procedures and segregated waste across the whole chain. Policies without controls do not protect staff. Source: NAPRA model standards for pharmacy compounding of hazardous sterile preparations.

11. What should a household be told about body fluids after a cycle of cytotoxic chemotherapy?

1. Precautions must continue for a full year after the last cycle of treatment has been given
2. No precaution is needed at any time, since the drug is entirely destroyed before it is excreted
3. Handle them as hazardous for about 48 hours, using gloves and flushing with the lid closed.
4. Only the patient's blood is a hazard; urine, stool and vomit carry no residue of the medicine

Most cytotoxics and their metabolites appear in urine, stool, vomit and sweat for roughly 48 hours (longer for a few agents), so gloves, careful laundering and closed-lid flushing are advised for that period. Source: Cancer Care Ontario patient safe handling information.

12. Which organ toxicity is cumulative and dose-limiting with anthracyclines?

1. Renal.
2. Cardiac.
3. Pulmonary.
4. Hepatic.

Doxorubicin and its relatives cause a dose-dependent cardiomyopathy, so lifetime cumulative dose is tracked and left ventricular function assessed before and during therapy. Nephrotoxicity belongs to cisplatin and pulmonary fibrosis to bleomycin. Source: BC Cancer drug monographs, anthracyclines.

13. Which supportive measure is essential with cisplatin?

1. Complete fluid restriction for 24 hours with no intravenous fluid.
2. Vigorous intravenous hydration with attention to magnesium.
3. A prophylactic oral anticoagulant.
4. Continuous oxygen during the infusion.

Cisplatin is nephrotoxic, and pre- and post-hydration with electrolyte replacement, especially magnesium, is what allows it to be given; ototoxicity and peripheral neuropathy are the other characteristic harms. Restricting fluids would worsen the renal injury. Source: BC Cancer drug monograph, cisplatin.

14. Which cumulative toxicity limits the total dose of bleomycin?

1. High-frequency hearing loss.
2. Loss of bone marrow reserve.
3. Irreversible cardiomyopathy.
4. Pulmonary fibrosis.

Bleomycin causes interstitial pneumonitis progressing to fibrosis, which is why cumulative units are tracked, pulmonary function is monitored and high inspired oxygen is used cautiously afterwards. It is notably marrow-sparing. Source: BC Cancer drug monograph, bleomycin.

15. What is the purpose of folinic acid after high-dose methotrexate?

1. To neutralise methotrexate in the blood so that none of it reaches any normal tissue.
2. To prolong methotrexate inside the tumour tissue for longer after each dose is given.
3. To rescue normal cells by supplying reduced folate that bypasses the blocked enzyme.
4. To prevent the nausea of a high dose.

Folinic acid (leucovorin) supplies reduced folate that normal cells can use despite dihydrofolate reductase blockade, limiting mucosal and marrow toxicity; timing and duration are guided by methotrexate concentrations, alongside hydration and urinary alkalinisation. Source: BC Cancer high-dose methotrexate protocol.

16. Why is the urine alkalinised during high-dose methotrexate?

1. Alkaline urine converts methotrexate into an inactive metabolite that cannot damage the kidney
2. Methotrexate is more soluble at higher pH and is less likely to crystallise in the tubules.
3. Alkalinisation increases tubular reabsorption of the drug, prolonging the therapeutic effect
4. A high urinary pH is required for folinic acid to be filtered and reach the site of action

Methotrexate and its 7-hydroxy metabolite precipitate in acidic urine and cause obstructive nephropathy, so urine pH is kept above about 7 with sodium bicarbonate alongside a high urine output. Alkalinisation increases elimination rather than reabsorption. Source: BC Cancer high-dose methotrexate protocol.

17. Which common antibiotic must be avoided in a patient taking methotrexate?

1. Trimethoprim-sulfamethoxazole.
2. Amoxicillin, which chelates it.
3. Azithromycin, which blocks secretion.
4. Nitrofurantoin, which displaces it.

Trimethoprim is itself an antifolate and, with sulfamethoxazole, adds antifolate effect and reduces methotrexate clearance, producing severe pancytopenia. NSAIDs and probenecid also reduce its renal clearance and require caution. Source: CPhA Therapeutic Choices, methotrexate monitoring.

18. How is haemorrhagic cystitis prevented during high-dose cyclophosphamide or ifosfamide?

1. An oral antispasmodic four times daily.
2. A prophylactic quinolone antibiotic started the day before.
3. Restriction of oral fluid intake.
4. Mesna with generous hydration and frequent voiding.

Acrolein, the toxic metabolite, is bound by mesna in the bladder, and frequent voiding with hydration dilutes it; the complication is chemical, not infective, so antibiotics and antispasmodics do not prevent it. Source: BC Cancer drug monographs, cyclophosphamide and ifosfamide.

19. Which enzyme deficiency causes life-threatening toxicity from fluorouracil or capecitabine?

1. Dihydropyrimidine dehydrogenase deficiency.
2. Glucose-6-phosphate dehydrogenase deficiency.
3. Thiopurine methyltransferase deficiency.
4. Pseudocholinesterase deficiency.

Dihydropyrimidine dehydrogenase catabolises fluoropyrimidines; partial or complete deficiency causes severe mucositis, diarrhoea and myelosuppression, and DPYD genotyping before treatment is now recommended in Canada. Source: Canadian DPYD screening recommendations for fluoropyrimidine therapy.

20. Which characteristic adverse effect should a patient starting capecitabine be taught to recognise?

1. A dry cough with breathlessness appearing on the second day.
2. Redness, tingling and peeling of the palms and soles.
3. Loss of scalp hair in the first week.
4. Bluish discolouration of the sclerae.

Hand-foot syndrome is dose-limiting for capecitabine and is managed with emollients, avoidance of friction and heat, and dose modification, so early reporting matters; severe diarrhoea and stomatitis also require prompt interruption. Alopecia is not typical of this drug. Source: BC Cancer drug monograph, capecitabine.

21. A patient on warfarin is started on capecitabine. What must be arranged?

1. A switch from warfarin to acetylsalicylic acid.
2. Much more frequent INR monitoring.
3. A permanent doubling of the warfarin dose.
4. No change to the anticoagulation at all.

Capecitabine markedly potentiates warfarin, with bleeding and deaths reported, so the INR is checked frequently and the dose adjusted; the effect can persist after the cytotoxic is stopped. Substituting an antiplatelet would leave the original indication untreated. Source: Health Canada advisory on capecitabine and coumarin anticoagulants.

22. Why is premedication given before a taxane infusion?

1. To prevent the neutrophil nadir.
2. To prevent delayed nausea on day three and the vomiting that goes with it.
3. To prevent hypersensitivity to the drug and its solubilising vehicle.
4. To prevent the cumulative neuropathy.

Corticosteroid with H1 and H2 antihistamines is given before paclitaxel and docetaxel because of hypersensitivity reactions largely attributed to the vehicle; premedication does not prevent the cumulative sensory neuropathy, which is managed by dose modification. Source: BC Cancer drug monographs, taxanes.

23. Which symptom should a patient on a platinum or taxane regimen report early?

1. A mild headache the same evening.
2. Numbness or tingling in the fingers and toes.
3. A metallic taste lasting an hour.
4. Fatigue on the day after treatment that settles by itself.

Peripheral sensory neuropathy is cumulative and may become permanent, so early reporting allows dose reduction or discontinuation before function is lost. Transient headache, taste change and fatigue are common and do not alter dosing. Source: Cancer Care Ontario symptom management guides.

24. What is the meaning of a rising creatinine and falling magnesium during a course of cisplatin?

1. Expected nephrotoxicity that requires review of hydration and of the dose.
2. A laboratory artefact from the antiemetics used to control the nausea of the cycle.
3. Evidence that the tumour is responding.
4. An effect of the corticosteroid given.

Cisplatin damages the proximal tubule, causing creatinine rise and renal magnesium and potassium wasting; hydration, magnesium replacement and dose review follow, and switching to carboplatin is sometimes required. Source: BC Cancer drug monograph, cisplatin.

25. Why is a potent CYP2D6 inhibitor a concern in a woman taking tamoxifen?

1. Inhibition causes acute hepatic failure.
2. Tamoxifen is a prodrug requiring CYP2D6 for conversion to endoxifen.
3. The pair cause rapid loss of bone density within the first three months of use.
4. Inhibitors abolish tamoxifen absorption.

Endoxifen is the main active metabolite, so strong inhibitors such as paroxetine and fluoxetine may reduce efficacy; venlafaxine or citalopram are preferred when an antidepressant or a treatment for hot flushes is needed. Source: CPhA Therapeutic Choices, breast cancer endocrine therapy.

26. Which symptom in a woman taking tamoxifen requires prompt investigation?

1. Occasional mild nausea after the tablet.
2. Mild hot flushes several times a day.
3. Abnormal vaginal bleeding.
4. A slight reduction in libido.

Tamoxifen increases the risk of endometrial hyperplasia and carcinoma, so any postmenopausal bleeding or abnormal discharge is investigated; venous thromboembolism is the other serious risk. Hot flushes and mild nausea are expected and managed symptomatically. Source: Canadian product monograph, tamoxifen.

27. Which long-term risk accompanies aromatase inhibitor therapy?

1. A cumulative cardiomyopathy.
2. A rise in endometrial thickness.
3. A dose-dependent nephrotoxicity.
4. Accelerated bone loss.

Profound oestrogen suppression causes bone loss and fractures, so bone density and calcium and vitamin D intake are addressed and an antiresorptive is added when indicated; arthralgia is the commonest reason for discontinuation. Endometrial risk belongs to tamoxifen. Source: Osteoporosis Canada and Canadian breast cancer treatment guidance.

28. Why is a proton pump inhibitor a problem alongside several oral tyrosine kinase inhibitors?

1. The two form an insoluble complex.
2. Acid suppression speeds their metabolism by inducing the liver enzymes involved.
3. Their dissolution depends on gastric acid, so acid suppression lowers exposure.
4. Exposure to the kinase inhibitor rises to a level that causes unpredictable toxicity.

Agents such as erlotinib and several others are weak bases whose solubility falls sharply as pH rises, so co-prescribed acid suppression can reduce efficacy; where acid suppression is unavoidable, an H2 antagonist separated in time is sometimes used. Source: BC Cancer drug monographs, oral tyrosine kinase inhibitors.

29. Why is grapefruit juice avoided with many oral anticancer agents?

1. It binds the drug in the stomach.
2. It inhibits intestinal CYP3A4 and raises drug exposure unpredictably.
3. It induces intestinal CYP3A4.
4. Its acidity destroys the enteric coating that protects the tablet from acid.

Furanocoumarins irreversibly inhibit enterocyte CYP3A4, increasing the bioavailability of CYP3A4 substrates and the risk of toxicity; the effect lasts well beyond the drink itself, so the fruit and juice are avoided rather than separated in time. Source: CPhA Therapeutic Choices, drug interactions with food.

30. How is a severe immune-related adverse event from a checkpoint inhibitor managed?

1. Switch immediately to a cytotoxic regimen for the remainder of the course.
2. Continue at a reduced dose.
3. Premedicate with an antihistamine.
4. Hold the drug and start systemic corticosteroid therapy promptly.

Immune checkpoint inhibitors can inflame any organ — colitis, hepatitis, pneumonitis, thyroiditis, hypophysitis — and the treatment is early recognition, interruption and immunosuppression, not dose reduction. Endocrine effects usually need lifelong hormone replacement. Source: Cancer Care Ontario immune-related adverse event guidance.

31. What should a patient starting an oral anticancer agent at home be told about missed doses and handling?

1. The tablets may be divided or crushed freely so that the dose can be adjusted to how the patient feels
2. Any missed dose should be replaced by a double dose at the next scheduled time without exception
3. Follow the written schedule exactly, do not double up, and keep the tablets in their container away from others.
4. The medicine may be stored loose in a weekly organiser alongside every other household medicine

Oral cytotoxic and targeted therapy carries the same hazard as an infusion but is managed by the patient, so explicit missed-dose instructions, no crushing or splitting of hazardous tablets, hand hygiene and separate storage are part of every dispensing. Source: NAPRA model standards and Cancer Care Ontario oral therapy safety guidance.

32. What is the role of a granulocyte colony-stimulating factor in a chemotherapy regimen?

1. To raise the platelet count after a cycle in which thrombocytopenia is the main toxicity.
2. To shorten neutropenia when the regimen carries a high risk of febrile neutropenia.
3. To treat the anaemia of chemotherapy by stimulating red cell production in the marrow.
4. To reverse platinum-induced neuropathy.

Filgrastim and pegfilgrastim are given as primary prophylaxis with regimens whose febrile neutropenia risk is high, or as secondary prophylaxis after an episode, in order to maintain dose intensity. They act on the neutrophil line only. Source: Cancer Care Ontario growth factor guideline.

33. Which measures prevent tumour lysis syndrome before treatment of a bulky, rapidly proliferating tumour?

1. A single intravenous bisphosphonate dose given on the day before treatment.
2. A prophylactic broad-spectrum antibiotic started five days before the cycle.
3. Fluid and potassium restriction.
4. Hydration with a urate-lowering agent such as allopurinol or rasburicase.

Massive cell lysis releases potassium, phosphate and urate, causing acute kidney injury and arrhythmia; hydration plus allopurinol, or rasburicase in high-risk patients, with electrolyte monitoring is the preventive strategy. Fluid restriction would worsen it. Source: Cancer Care Ontario tumour lysis syndrome guidance.

34. Which patient must never receive rasburicase?

1. A patient whose urate is already high at the time of the assessment.
2. A patient with glucose-6-phosphate dehydrogenase deficiency.
3. A patient who has taken allopurinol.
4. A patient with mild renal impairment.

Rasburicase generates hydrogen peroxide as it degrades urate, causing severe haemolysis and methaemoglobinaemia in G6PD deficiency, so screening precedes use in at-risk populations. A high urate is the indication, not a contraindication. Source: Canadian product monograph, rasburicase.

35. Why is a bone-modifying agent used in a patient with bone metastases?

1. To prevent chemotherapy-induced nausea in the cycles that are given at the same time as the drug.
2. To eradicate the metastatic deposits and thereby produce a radiological cure of the disease.
3. To replace analgesia altogether.
4. To reduce skeletal-related events such as fracture, cord compression and radiotherapy.

Bisphosphonates and denosumab reduce pathological fracture, cord compression, radiation and surgery, and help with hypercalcaemia of malignancy; they are not antitumour therapy and do not replace analgesia. Dental assessment precedes treatment. Source: Cancer Care Ontario bone-modifying agent guideline.