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Hematology Pharm > Hemetaological Malignancy Drugs > Flashcards

Hemetaological Malignancy Drugs Flashcards

1
Q

What is the goal of treatment for hematologic malignancies?

A

Myelosuppresion

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2
Q

What is the most life-threatening aspect of hematologic malignancy treatment?

A

The fact that myelosuppression leads to immunosuppresion

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3
Q

Define Induction

A

High dose combination chemotherapy

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4
Q

Define Consolidation

A

Repetition of induction treatment during remission

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5
Q

Define maintenance treatment

A

Long term, lower dose therapy during remission

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6
Q

Neo-adjuvant?

A

Treatment given before or during surgery

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7
Q

Adjuvant?

A

Treatment given after surgery

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8
Q

What are the advantages of combination vs. single agent therapy?

A

Increased Maximum cell kill, heterogeneous cell populations killed, resistance to drug treatment reduced

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9
Q

What is metronomic dosing?

A

Daily administration of lower drug doses

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10
Q

Describe Hormesis and how metronomic therapy attempts to solve this problem.

A

In medicine, hormesis refers to the adaptive response of cells and organisms to a moderate stress. In treatment of malignancies, its been shown that at low drug levels, some drugs may produce a pro-proliferative eddect that may enhance tumor growth,
Metronomic therapy voids this by keeping constant pressure on the tumor.

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11
Q

Define adaptive therapy

A

Treatment aimed at preserving the ratio of resistant to non-resistant cells so as to keep the cell population sensitive and promote lifelong treatment instead of a one time cure.

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12
Q

Define adaptive resistance

A

the ability of a tumor to adapt so as t evade the therapeutic blockade by inducing or accentuating mechanisms that enable neovascularization

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13
Q

Define Intrinsic non-responsiveness

A

A pre-existing condition defined by the absence of any beneficial effect of an anti-angiogenic therapy. Tumors grow even when faced with anti-angiogenic therapy.

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14
Q

How does metronomic chemotherapy work>

A

Induces anti-angiogenic effects, decreases number of tReg cells, promotes dendritic cell maturation, reactivates anticancer immune response

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15
Q

How does cyclophosphamide work>

A

Its an alkylating agent therefore it crosslinks DNA preventing RNA synthesis. Inhibits T reg cell production

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16
Q

What about Vinblastine

A

Promotes dendritic cell maturation

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17
Q

What are the possible toxic effects or metronomic therapy?

A

Must be careful with extended use in children, angiogenesis is important to growth. Most common effects are nausea and vomitting along with anemia, neutropenia, leucopenia, lymphopenia

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18
Q

Most common drug combo to Acute Myeloid Lymphoma?

A

ARA-C, Tioguanine, Daunorubicin

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19
Q

Toxicity risk of Daunorubicin?

A

Cardiotoxic as well asthe usual immunosuppression

20
Q

What is unique about Gemtuzumab?

A

Its an antibody against CD33, thus it works by carrying a toxin to cells expressing CD 33 instread of inducing complement or ab-mediated cytotoxicity.

21
Q

What is Acute Promyelocytic Leukemia treated with?

A

ATRA and Arsenic Trioxide

22
Q

How do ATRA and Arsenic trioxide?

A

Both induce differentiationof APL cells and then arsenic trioxide induces apoptosis

23
Q

What are some of the toxicities of Arsenic Trioxide?

A

AV block, QT prolongation, electrolyte imbalance, CV PROBLEMS (differentiaion syndrome involves pulmonary infiltrates, fever, dyspnea, leukocytosis

24
Q

Acute Lymphoblastic leukemia most common treatment

A

Prednisone + vincristine + anthracycline

25
Q

What about treatment for ALL patients with teh Philadelphia Chromosome>

A

Imatinib

26
Q

How does Imatinib work

A

Oral inhibitor of BCR-ABL tyrosine kinase.

27
Q

What are some common toxicites of Imatinib

A

Nausea, rise in liver enzymes

28
Q

Resistance Mechanism to Imatinib?

A

ATP binding site mutation

29
Q

What is the most common treatment for Chronic Lymphocytic Leukemia

A

Fludarabine, Cyclophosphamide, Rituximab

30
Q

How does Rituximab work?

A

It is a CD 20 ab. CD 20 is found on the B cell precursors and mature B cells. Marks these for complement dependent and antibody dependent cell mediated cytotoxicity.

31
Q

Alemtuzumab can be substituted for which of the drugs used to treat CLL?

A

Rituximab.

32
Q

How does Alemtuzumab work?

A

Bnds CD52 and induces complement dependent and antibody dependent lysis.

33
Q

What in the hell is Bendamustine and what does it treat?

A

Treats CLL, it is an alkylating agent (DNA crosslink induction) and an anti-metabolite. Activates p53 to induce apoptosis and stops replication at mitotic checkpoints. Less susceptible to resistance than other drugs.

34
Q

Three drugs used to treat hairy cell leukemia

A

Cladribine, Interferon alfa 2A, Pentostatin

35
Q

Toxicity of Hairy cell treatment>

A

Cuses CD4 suppresion, potential risk of second malignancy

36
Q

What is the affect of synthetic interferons>

A

Anti-proliferative effect and activate T cells, NK cells, macrophages resulting in increased phagocytosis and increased toxicity to tumor cell.

37
Q

Which is more common: Leukemia or Lymphoma?

A

Lymphoma

38
Q

Two divisions of Lymphoma

A

Hodgkin and Non-Hodgkin

39
Q

Most Hodgkin Lymphomas are treated with what types of drug combos?

A

Combos containing an anthracycline, doxorubicin, mitotic spindle inhibitor, vincristine, alkylating agent, cyclophosphamide or bleomycin, a corticosteroid. Wide range of mechanisms discourages resistance and lessens toxicities.

40
Q

Low phase Non-Hogkin treatment

A

COMP treatment.

41
Q

High Stage Non-Hodgkin Lymphoma

A

Add rituximab to the COMP treatment

42
Q

Toxicity of NHL treatment.

A

Sterility from pelvic irradiation or high dose cyclophosphamide, secondary malignancy, left ventricular dysfunction, Myelodysplastic syndrome and acute myelogenous leukemia

43
Q

Fetal exposure to chemo

A

Effects still uncertain. Studies show no glaring problems but subtle changes in cardiac and neurocognitive measurements exist.

44
Q

What is the most comon post-remission therapy in AML?

A

Cytarabine (dose intensive)

45
Q

How does Arsenic trioxide work?

A

Degrades PML-RARA fusion gene

46
Q

What are the potential toxicities of ARsenic trioxide. ARSENIC TRIOXIDE IS VERY TOXIC.

A

AV block, QT prolongationelectrolyte imbalance.

47
Q

How does Interferon work?

A

Prolongs cell cycle phases and induces proliferation (anti0proliferative), also induces T cells and NK cell sagainst the tumor

Hematology Pharm (2 decks)

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