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FPP-MSS > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

Multi-modal treatments

A

surgery, radiation, chemotherapy

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2
Q

Rationale for anti-neoplastic drugs

A
  1. kill all tumor cells
  2. suppress the growth of tumor but not normal cells
  3. increase host capacity to fight cancer
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3
Q

Ideal Ant-Neoplastic Drug

A
  1. non-toxic to normal cells
  2. kill all tumor cells
  3. broad spectrum of activity
  4. good distribution in body (adequate half-life)
  5. non-immunogenic
  6. low incidence of side effects
  7. low cost, oral dosing
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4
Q

Currently available chemotherapy

A
  1. Poor selective toxicity
  2. Most drugs only affect actively growing cells
  3. Have limited anti-tumor spectrum
  4. high incidence of side effects
  5. Cause secondary malignancy (after treatment of cancer time then develop second cancer)
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5
Q

Risk of Anti-Neoplastic drugs causing secondary malignancy

A

high risk: mechlorethamine, carmustine, topside
low risk: doxorubicin, cyclophosphamide,procarbazine, cisplatin
low risk: vincristine, vinblastine, methotrexate, cyarabine, 5-FC
unknown: paclitaxel, bleomycin

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6
Q

General ways to stop tumor growth

A

Cell death- cell killing compound

  1. direct kill (necrosis)
  2. trigger apoptosis

Stop Growth-cytostatic compound

  1. induce terminal differentiation
  2. interfere with growth signals
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7
Q

Mechlorethamine, Carmustine

A

Cell-cycle nonspecific

Alyklyating agent

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8
Q

Cyclophosphamide

A

Cell-cycle specific/ Phase non-specific

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9
Q

Alkylating Agent

A

Mechanism: introduce alkyl groups into DNA and cross links and cause strand break by forming aziridine ring (unstable)
Side effects: hematopoiesis suppression, GI effects through intestinal mcusoa, nausea and vomiting, alopecia

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10
Q

Alkylating agent

A

Mechlorethamine, Carmustine, Cyclophosphamide

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11
Q

Mechlorethamine

A

Alkylating Agent
MOA: bi functional alkylating agent that produces DNA cross-link

Combination therapy for Hodgkin’s and nOn-hodgkin’

Highly reactive so disappear in blood in seconds to minutes

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12
Q

Cyclophosphamide

A

Alkylating Agent
Prodrug activated by liver cytochrome P450s
Mechanism: The phosphoramide mustard acts as an alkylating agent

Bladder toxicity: sterile hemorrhagic cystitis (prevent with mesna)

Broad spectrum activity against wide variety of cancers (most widely used agent in this class)
Hodgkin’s and non-Hodgkin’s, multiple myeloma, neuroblastoma, leukemia
carcinoma of endometrium, breast, lung

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13
Q

Carmustine (BCNU)

A

Alkylating Agent
Cross the blood-brain barrier–> lipophilic
Uses: brain tumors, multiple myeloma, melanoma
Toxicity: similar to other alkylating agents
cycle-nonspecific

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14
Q

Methotrexate

A

Anti Metabolite Class (Folate Analog)
Mechanism: bind to dihydrogolate reductase (DHFR) and prevent formation of tetrahydrofolate (block FH2–>FH4) needed for thymidine synthesis
Side effects; intestinal epithelium damage, bone marrow suppression, renal tubular necrosis, displace other drugs from serum albumin, hepatotoxicity

Indications: acute lymphocytic leukemia, Choriocarcinoma (can cure)

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15
Q

Leucovorin Rescue

A

High doses methotrexate bind all dihydrofolate reductase (DHFR) and inhibits all activity

Follow by rescue with leucovorin
It is a folinic acid, a fully reduced floated that does not require reduction by DHFR
normal cells have increased capacity to bring in leucovorin relative to normal cells

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16
Q

Fluorouracil (5-FU)

A

Antimetabolite (Pyrimidine Analog)
Mechanism: pyrimidine analog that is activated in cells to FUTP which inhibits RNA synthesis and to Fdump which interferes with thymidylate synthase and ultimately DNA synthesis

S-Phase specific

Side effects; nausea, anorexia, diarrhea, myelosuppression

Broad spectrum uses: carcinoma of stomach, colon, pancreas, ovary, head and neck, breast, bladder and topical for basal cell carcinoma

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17
Q

Cytarabine (Ara-C)

A

Antimetabolite (pyrimidine analog)
Mechanism: pyrimidine (cytidine) analog that competes for phosphorylation of cytidine to dCTP and competes for incorporation into DNA and cause termination
S-Phase specific

Side effects: marked myelosuppression (dose-limiting) and neurotoxicity

Administer: 2 times daily for 5 days because increase probability for killing cells not in s phase and in acute nonlymphocytic leukemia S phase lasts about 18 hours

uses: acute leukemias (acute myelocytic leukemia)

18
Q

Gemcitabine

A

Pyrimidine analog
similar to cyarabine but also inhibit ribonucleotide reductase
Treat: pancreatic cancer

19
Q

Mercaptopurine

A

Antimetabolite (Purine Analog)
Mechanism: purine analog and converted in cells to ribonucleotide that inhibits RNA and DNA synthesis
S -Phase specific

Side effect: bone marrow depression, vomiting, nausea, anorexia, jaundice
Use: acute leukemia

20
Q

Hydroxyurea

A

Antimetabolite

mechanism: inhibit ribonucleotide reductase to block conversion of ribonucleotide to dNTPs thereby preventing DNA synthesis
arrest in G1-S interface (useful in conjunction with radiation)

Use: granulocytic leukemia, head and neck cancer

side effects: hematopoietic depression, GI disturbance

21
Q

Natural Products

A 
Vinca alkaloids: Vincristine, Vinblastine
Texans: Paclitaxel
Epipodophyllotoxins: Etoposide
Monoclonal Ab: Trastuzumab
Antibiotics: Doxorubicin, Bleomycin
22
Q

Vinca Alkaloids

A

Natural Product
Mechanism: binds to tubular, inhibiting proper formation of microtubule and mitotic spindle

Arrest cell in metaphase

Bind to singe tubulin microtubule rather than polymerized

23
Q

Vinblastine

A

Side effects: strongly myelosuppressive (dose-limiting)
epithelial ulceration
Treat: Hodgkin’s and non-Hodgkin’s lymphomas, breast cancer

24
Q

Vincristine

A

side effects: significantly less bone marrow toxicity
Alopecia, neuromuscular abnormalities (peripheral neuropathy)

Treat: acute lymphocytic leukemia, Hodgkin’s and Non-hodgkin’s lymphomas, Wilm’s Tumor, Neuroblastoma, rhabdomyosarcoma

25
Q

Taxanes

A

Mechanism; enhance assembly and stability of microtubules by binding to Beta subunit of tubulin

block in G2 phase later (more sensitive to radiation so placlitaxel may have some use as radio sensitizer)

Bind to polymerized rather than individual microtubule

26
Q

Paclitaxel

A

Uses: refractory ovarian cancer, breast cancer

Interfere with DNA repair, intensifying effect of DNA damage with cisplatin or cyclophosphamide

Side effects: dose-limiting leukopenia, peripheral neuropathy, myalgia, arthralgia

27
Q

Doxorubicin

A 
Natural Product (Antitumor antibiotic)
Cycle-specific/phase non-specific (no Go cells)

Among most active of anti tumor agents

Uses : wide spectrum:most widely prescribed of the class but used specifically for Hodgkin’s and non-Hodgkin’s lymphoma, breast, ovary, small cell lung

Mechanism: intercalate in DNA, distort DNA helix, cause lipid peroxidation and free radical generation, and it bind to DNA and topoisomerase 2 (prevent DNA strand break)
Side effects: cardiomyopathy, bone marrow depression, alopecia, GI problems

28
Q

Bleomycin

A

Mechanism: mixture of iron containing glycopeptides that bind to DNA and cause oxidative like damage to DNA which leads to DNA stand breaks (forms site specific ds DNA breaks)
phase specific for G2

Uses: germ cell tumors of testes and ovaries, head, neck, lung, lymphomas

Side effects: minimal myelosuppression, pulmonary toxicity (dose-related and cumulative and potentially fatal), skin vesiculation and hyper pigmentation

29
Q

Etoposide

A

Mechanism: stabilizes DNA topoisomerase 2 complex which results in dsDNA breaks that cannot be repaired

Block in late G2 phase at M interface

Use: lymphoma, acute nonlymphocytic leukemia, small cell lung, testis, Kaposi’s sarcoma

Side effects: leukopenia (dose-limiting), nausea, vomiting, diarrhea, alopecia

30
Q

Biological Response modifier

A

Natural Product
Intent: alter patient’s own biological response to a tumor or to treatment regimens
limitation: responseis variable

31
Q

Filgrastin (G-CSF)

A

Goal: limit chemotherapy induced neutropenia
promotes progenitors of neutrophils and expands the absolute population of neutrophils (granulocyte production by marrow)
quick recovery with bone marrow suppression (neutropenia)
side effect: bone pain

32
Q

Trastuzumab

A

Mechanism: monoclonal antibody that binds to HER2 receptor
Use: breast cancers that overexpress HER2
side effects: cardiomyopathy, hypersensitivity, infusion reactions

33
Q

Cisplatin

A

Mechanism: platinum coordinated complex
hydrolysis yields activated species which causes DNA cross link
Cycle-specific/phase-nonspecific (no Go)

Wide anti tumor spectrum
Use: testicular cancer and ovarian, head, neck, bladder, small cell lung, colon, esophagus

Side effects: nephrotoxicity, ototoxicity, peripheral neuropathy, electrolyte disturbance, nausea and vomiting, myelosuppression

34
Q

Procarbazine

A

Mechanism: activate in vivo to a methylating agent which causes a chromosomal damage

Use: Hodgkin’s lymphoma (G1 and S phase)

side effects : myelosuppression, nausea, vomiting, maybe secondary malignancy (DnA damage)

35
Q

Prednisone

A

Hormone (Adrenocorticosteroid)
Mechanism: bind to steroid receptor which depress RNa synthesis of many growth related genes
also induce nucleases which modulate cell lysis

arrest cells in G1

Use: acute and chronic lymphocytic leukemia,
breast cancer, Hodgkin’s and non-Hodgkins’ disease

Palliative effects: anti-emetics, stimulate appetite, anti-inflammatory

Complication: immunosuppression but limited myelosuppression, weight gain, fluid retention, psychologic effect

36
Q

Tamoxifen

A

MOA: Non steroidal anti estrogen that competitively blocks estrogen receptor activity in breast tissue

Cytostatic: held in Go/G1 phase and tumor regrows when tamoxifen removed
stops cell growth without killing the cells

Uses: advanced post menopausal breast cancer and pre-menopausal metastatic breast cancer
breast cancer prophylaxis for women at high risk

Activation : Activated by CYP2D6 (cancer recurrence if using CYP 2D6 inhibitor)

Side effects: nausea, hot flashes, fatigue, bone and musculoskeletal pain, increase rates of uterine/endometrial cancer

37
Q

Raloxifene

A

Treat: uterine and endometrial cancer

38
Q

Letrozole

A

mechanism: block conversion of androgen to estrogen by inhibing aromatase

Use: first line treatment of post-menopause advanced or metastatic breast cancer

side effect: hot flush, nausea, fatigue, bone and other musculoskeletal pain

39
Q

Leuprolide

A

analog of GnRH
after 2-4 weeks it desensitizes GnRH signaling, decreasing LH/FSH and decreasing testosterone to castration levels

Use: advanced hormonally responsive prostate cancer

Side effects: hot flash and impotence

40
Q

Flutamide

A

non steroidal androgen MOA: blocker of androgen receptor
Treat: metastatic prostate cancer
side effect: gynecomastia, diarrhea, hepatotoxicity

41
Q

Vincristine and Prednisone and Doxorubicin

A

Acute Lymphocytic Leukemia

FPP-MSS (1 decks)

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