ITE Flashcards

1
Q

Tixagevimab/cilgavimab indicaiton

A

Not recommended for any cancer patients due to ineffectivness against COVID-19 variants

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2
Q

SE to know with methadone

A
  • QTc prolongation, contraindicated with QTc greater than 500
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3
Q

Medications contraindicated with palbociclib

A

Strong CYP3A4 inhibitors

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4
Q

If a patient is hospitalized for reason unrelated to study drug does it need be reported?

A

Yes, hospitalization is considered a serious adverse event and must be reported during clinical trials regardless of reason for admission

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5
Q

NTRK inhibitors SE to know + when dose modification is recommended

A
  • neurotoxicity – memory/cognitive impairment
  • G3-4 neurological adverse events
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6
Q

Klinefelter associated with increased risk of which tumors?

A

Germ cell tumors, particularly of mediastinum

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7
Q

Clinical benefit of bevacizumab in ovarian cancer

A

OS benefit

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8
Q

Malignancy associated with pure red cell aplasia

A

Thymoma

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9
Q

Cause of anemia in patient with renal failure

A

Secondary hyperparathyroidism

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10
Q

Management of triple positive APLS patient without thrombosis history

A

Aspirin

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11
Q

Cause if idiopathic splanchnic venous thrombosis

A

JAK2 V617F mutation (in 30% of cases)

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12
Q

Prophylaxis for women with inherited thrombophilias and recurrent early spontaneous abortion

A

NO role for anticoagulation

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13
Q

Drug to avoid in active HIT

A

4 factor PCC (contains heparin)

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14
Q

Primary predictor of CNS involvement at diagnosis in ALL

A

Extramedullary disease

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15
Q

Prophylaxis for mucositis for patients on high-dose melphalan

A

Oral cryotherapy

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16
Q

Motixafortide 1) use 2) mechanism

A

1) Stem cell mobilizer used in combination with GCSF
2) CXCR4 antagonist

17
Q

Clinical benefit of myeloablative conditioning for pts with MDS and AML undergoing transplant

A

Improved relapse-free survival

18
Q

Medication that needs to be held prior to plasma exchange and why

A
  • ACE inhibitors
  • Need to be stopped 24 hours before to avoid risk of anaphylaxis
19
Q

Impact of factor XIII deficiency on PT and aPTT

A

No effect

20
Q

How to reduce CMV transmission with PRBC transfusions

A

Leukoreduction

21
Q

Contraindication to high-dose methotrexate transfusion

A

Effusions

22
Q

Rasburicase mechanism

A

Recombinant urate oxidase

23
Q

Asciminib mechanism of action

A

Asciminib is described as a “STAMP inhibitor,” which means “specifically targeting the ABL myristoyl pocket.” The wild-type ABL has a myristoylated N-terminus, which binds to an allosteric site, but the ABL fusion protein does not have the myristoylated domain. In the wild-type protein, when myristoylated N-terminus binds to the allosteric site, the kinase has reduced activity. Since the mutant fusion protein does not have the myristoylated N-terminus domain, it is not subject to this form of regulation, and thus the fusion protein is constitutively active. Asciminib binds to the allosteric site, resulting in an inhibition of bcr-abl activity.[12]