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Pharm 2nd Block > HEME - Anti-tumor Rx > Flashcards

HEME - Anti-tumor Rx Flashcards

1
Q

MECHLORETHAMINE

Mechanism of action:
Clinical Use:
Side effects: 
Administration:
PK/PD
Misc info:
A

MoA: alkylating agent

CU: chemotherapy agent for Hodgkins’s Lymphoma (MOPP protocol)

SE: nausea, vomiting, alopecia

Administration: IV, topical

PK/PD: non-enzymatic hydrolysis (therefore no adjustments are necessary for patients with hepatic and renal failure)

Misc: causes HIGH incidence of secondary cancers (leukemia, lymphoma, MDS), and is not used as often anymore

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2
Q

CYCLOPHOSPHAMIDE

Mechanism of action:
Clinical Use:
Side effects: 
Administration:
PK/PD
Misc info:
A

MoA: alkylating agent

CU: chemotherapy agent for solid/hematologic tumors (breast, ovarian, non-Hodgkins)

SE: hemorrhagic cystitis (caused by acrolein accumulation in the bladder; treat with copious fluids + MESNA Rx), also nausea, vomiting, alopecia

Administration: PRO-DRUG, IV

PK/PD: pro-drug activated by the hepatic p450 system, eliminated by the liver and kidneys (adjustments or alternative drug is used for patients with liver and kidney disease)

Misc: Pro-drug chemical derivative of mechlorethamine; widely used

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3
Q

CISPLATIN

Mechanism of action:
Clinical Use:
Side effects:

A

MoA: alkylating agent (-> DNA cross-linking)

CU: chemotherapy agent for solid tumors (LUNG, breast), genitourinary tumors (testicular, ovarian), and lymphomas

SE: nephrotoxicity, ototoxicity, neurotoxicity (dose dependent

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4
Q

ONDANSETRON

Mechanism of action:
Clinical Use:
Side effects:
Administration:

A

MoA: inhibitor of 5HT-3 receptors in the gut (normally activates the brainstem vomiting reflex pathway via vagus n.)

CU: nausea and vomiting associated with chemotherapy or surgery

SE: headache/constipation

Administration: IV/PO 30 minutes before chemotherapy

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5
Q

METHOTREXATE

Mechanism of action:
Clinical Use:
Side effects: 
Administration:
PK/PD:
Misc info:
A

MoA: inhibits dihydrofolate reductase (DHFR); as a result the thymidylate, a necessary precursor of DNA synthesis, is not produced

CU: Autoimmune disorders (RA, Crohns, psoriasis), Chemotherapy for malignancies (lymphoma, breast, head/neck, osteosarcoma, etc)

SE: bone marrow suppression (can lead to macrocytic anemia), teratogen, pulmonary/GI/Renal, liver toxicity, alopecia

Administration: oral (low dose) for autoimmune d/o, IV (high dose) for malignancies, intrathecally for CNS cancers

PK/PD: s-phase specific; tumor cells can become resistance to MTX

Misc: MTX must be followed by Leucovorin (folinic acid) Rescue - converted into a product that is downstream of the DHFR block, thereby bypassing the inhibited enzyme to provide an adequate supply of activated folate so that DNA synthesis continues (compared to 5FU)

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6
Q

5-FLUOROURACIL

Mechanism of action:
Clinical Use:
Side effects: 
Administration:
PK/PD:
Misc info:
A

MoA: inhibits thymidylate synthase

CU: chemotherapy agent used to treat adenocarcinomas (colon, breast)

SE: bone marrow suppression, GI toxicities, photosensitivity, oral ulcerations

Administration: PRODRUG

PK/PD: s-phase specific

Misc: Addition of Leucovorin (folinic aacid) potentiates the actions of 5FU (makes it more effective in blocking thymidylate synthase), thereby blocking DNA synthesis (compared to MTX)

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7
Q

Cytarabine (ara-C)

Mechanism of action:
Clinical Use:
Side effects: 
Administration:
PK/PD:
Misc info:
A

MoA: blocks DNA polymerase

CU: chemotherapy agent for AML, lymphomas

SE: bone marrow suppression (cytopenia), alopecia, GI toxicity, CEREBELLAR toxicity (ataxia), alopecia

Administration: continuous IV infusion for 7d along with Daunarubicin (part of AML induction regimen)

PK/PD: s-phase specific

Misc: think “C” in ara-C is for Cerebellar

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8
Q

DOXORUBICIN, DAUNORUBICIN (anthracyclines)

Mechanism of action:
Clinical Use:
Side effects: 
Administration:
PK/PD:
Misc info:
A

MoA: inhibits topoisomerase II, thereby leading to DNA fragmentation

CU: chemotherapy agents

  • Doxorubicin - solid tumors (breast, lung, GI, GU) and hematologic malignancies (acute leukemia, lymphoma, multiple myeloma), Kaposi’s Sarcoma
  • Daunorubicin - acute leukemia (AML, ALL, CML)

SE: bone marrow suppression, alopecia, CARDIOTOXICITY

Administration: IV infusion

PK/PD: hepatic metabolism (decrease dose in patients with liver failure)

Misc: cardiotoxicity arises because anthracyclines are metabolized to produce oxygen free radicals within myocardial cells, leading to subsequent damage; effects avoided by keeping doses below 400mg/m2 and by giving dexrazoxane (compound that decreases free radical formation)

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9
Q

EPIDOPHYLLOTOXINS (Etoposide, VP16)

Mechanism of action:
Clinical Use:
Side effects:
PK/PD:

A

MoA: topoisomerase II inhibitor

CU: chemotherapy agent for solid tumors (lung, genitourinary, Glioblastoma Multiforme. SCLC) and hematologic malignancies (lymphoma, leukemia)

SE: bone marrow suppression (specifically, neutropenia), alopecia, GI upset

PK/PD: S-phase specific

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10
Q

TOPOTECAN, IRINOTECAN

Mechanism of action:
Clinical Use:
Side effects:
PK/PD:

A

MoA: topoisomerase I inhibitor

CU: lung, ovarian, colorectal cancers

SE: life-threatening diarrhea

PK/PD: S-phase specific

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11
Q

VINCRISTINE, VINBLASTINE

Mechanism of action:
Clinical Use:
Side effects: 
Administration:
PK/PD:
A

MoA: binds tubulin and prevents microtubule polymerization (compare to taxol)

CU: chemotherapy agents for lymphomas and various cancers

SE:
VC = peripheral neuropathy, GI upset, alopecia
VB = bone marrow suppression “B for Bone”; GI upset, alopecia

PK/PD: M-phase specific

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12
Q

TAXOL

Mechanism of action:
Clinical Use:

A

MoA: binds tubulin and prevents microtubule depolymerization (compare to vincristine, vinblastine)

CU: chemotherapy used for lung, ovarian, and LOB cancers

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13
Q

VELCADE

Mechanism of action:
Clinical Use:

A

MoA: inhibits the proteasome (resulting in massive accumulation of antibodies inside the cell, thereby activating the “unfolded-protein stress response pathway”, ultimately leading to apoptosis

CU: B-cell malignancies: Multiple Myeloma, Mantle Cell Lymphoma

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14
Q

THALIDOMIDE (anything with -lidomide)

Mechanism of action:
Clinical Use:
Side effects:

A

MoA: immunomodulatory drugs (IMID); mechanism is unclear

CU: leprosy, GVHD, multiple myeloma

SE: teratogenic

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15
Q

What is one of the major side effects of cancer chemotherapy?

What growth factors are available to stimulate maturation of the bone marrow cells in clinical situations (ie cancer)?

A

bone marrow suppression, leading to anemia, granulocytopenia, and thrombocytopenia, which increases susceptibility to infections

Growth factors: G-CSF, GM-CSF, EPO

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16
Q

Growth factors are available to stimulate maturation of the bone marrow cells in clinical situations (ie cancer). What situations would you use these particular growth factors:

G-CSF
GM-CSF
EPO

A

G-CSF, GM-CSF is indicated in patients with:

  • Bone marrow transplants
  • high dose chemotherapy regimens
  • myelodysplastic syndrome (MDS)
  • patients with neutropenia + life threatening infections

EPO is indicated in patients with:

  • chronic renal failure
  • anemia
  • chronic diseases (RA, multiple myeloma, MDS, chemotherapy)
17
Q

What is the first IL to be approved for routine treatment for patients with renal cell carcinoma?

How does this particular IL work?

A

IL-2

works by stimulating an anti-tumor immune response and by stimulating the immune system to fight infections

18
Q

RITUXIMAB

Mechanism of action:
Clinical Use:
Side effects:

A

MoA: monoclonal antibody against CD20 on B cells; Rituximab/CD20 complex induces B cell lysis

CU: Non-Hodgkin lymphoma, chronic lymphocytic leukemia, autoimmune disorders (RA)

SE:

  • infusion reaction (hypotension, respiratory failure, cardiac arrest; avoid by treating with anti-histamine+acetominophen prior to infusion)
  • acute renal failure due to tumor lysis syndrome (build-up of uric acid)
19
Q

5’-AZACYTIDINE

Mechanism of action:
Clinical Use:

A

MoA: blocks DNA methylation enzymes, resulting in the demethylation and subsequent expression of tumor suppressor genes (ie p53)

CU: AML, MDS

Pharm 2nd Block (14 decks)

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