1. Asparaginase formulations have been proven particularly useful in the treatment of ALL based on their mechanisms of action. Which of the following best describes the mechanism of action of asparaginase-based treatments for ALL?

2. Which of the below formulations is best described as an asparagine-specific enzyme indicated as a component of a multi-agent chemotherapeutic regimen for the treatment of ALL patients who have developed hypersensitivity to E coli-derived asparaginase?

3. Which mode of administration of asparaginase therapy is reported to have an increase risk for hypersensitivity reactions?

4. Which of the following adverse effects is least commonly associated with asparaginase-based treatment?

5. What is the recommended dosing of pegaspargase for patients who are older than 21 years?

6. Which of the following is not appropriate management of infusion or hypersensitivity reaction to pegaspargase?

7. Which of the following best describes pegaspargase-induced thrombosis?

8. Increased risk of toxicity and adverse effects of asparaginase products are associated with which property of the enzyme?

9. Please refer to the following CASE scenario when answering Questions 9 and 10.
KI is a 46-year-old patient with a body mass index (BMI) of 35 who was diagnosed with B-cell ALL, CD19+, CD22+. KI’s PMH includes hypertension and diabetes mellitus, type II. They were initiated on treatment per CALGB 10403 and received pegaspargase 2000 IU/m2 on day 15 of course 1. Their total bilirubin started to increase 1 week post pegaspargase to 2.0 mg/dL; ALT 28 U/L, and AST 144 U/L, and peaked 2 weeks later to a total bilirubin of 22 mg/dL, with ALT 75 U/L and AST 144 U/L.

From which cycle of treatment is KI most at risk for development of grade 3 or 4 liver toxicities?

10. KI's consolidation chemotherapy was delayed for 2 weeks, and their bilirubin gradually declined spontaneously to 0.9 mg/dL. They achieved an MRD-negative CR and subsequently went on to receive consolidation treatment in which they received additional doses of pegaspargase at 2000 units/m2. However, after receiving their third dose of pegaspargase, they developed increased abdominal pain. CT imaging demonstrated diffuse interstitial edematous pancreatitis and homogeneous enhancement and diffuse enlargement of the pancreas with surrounding inflammation consistent with acute pancreatitis. Their amylase was 69 U/L and lipase was 560 U/L. What should be the management of KI's grade 3 pancreatitis regarding continued use of pegaspargase?

Evaluation Questions

11. How confident are you in your treatment choice for KI in the question above?

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