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Pharmacology Exam II > Antineoplastic Drugs > Flashcards

Antineoplastic Drugs Flashcards

1
Q

Methotrexate

  1. Mechanism of Action
  2. Treatment
  3. Resistance
  4. Toxicity (3)
A
  1. Inhibits Dihydrofolate Reductase
  2. Widespread treatment (Leukemia, Sarcoma, etc.)
  3. DHFR alterations/increased expression
  4. Bone marrow suppression, Lung infections, Nephrotoxicity
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2
Q

5-fluorouracil

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
A
  1. Metabolized into FUTP, FdUMP, FdUTP

FdUMP Inhibits Thymidylate Synthase

FUTP and FdUTP are incorporated into RNA and DNA, respectively

***Given in combination***(rarely used alone)

  1. Widespread Treatment (Breast, Head, Neck, GI)
  2. GI Ulcers, Bone Marrow Suppression
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3
Q

Capecitabine

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
A
  1. Prodrug of 5-FU (So same as 5-FU)
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4
Q

Cyarabine (ara-C)

  1. Mechanism of Action
  2. Treatment
  3. Resistance
  4. Toxicity
A
  1. Ara-C is converted to Ara-CMP by deoxycytidine kinase, Ara-CMP is incorporated into DNA which inhibits DNA polymerase and halts DNA elongation
  2. ***Acute Myelogenous Leukemia*** (AML) and Hematologic Malignancies (No solid tumors)
  3. Loss of Deoxycytidine Kinase, reduced transport in, upregulation of Cytidine Deaminase
  4. Cerebellar Syndrome (dysarthria, nystagmus, ataxia), Kidney/Liver Dysfunction, Advancing Age, Myelosuppression
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5
Q

Gemcitabine

  1. Mechanism of Action
  2. Treatment
  3. Resistance
A
  1. Deoxycytidine Kinase converts Gemcitabine into 2,2-difluorodeoxycytidine, which: 1) is incorporated into DNA and 2) inhibits ribodnucleotide reductase
  2. Treats a Wide Range of cancers (Pancreatic, NSC Lung, Ovarian, Bladder)
  3. Decreased Deoxycytidine Kinase, Increased Deoxycytidine
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6
Q

6-Thioguanine (6-TG) and 6-Mercaptopurine (6-MP)

  1. Mechanism of Action
  2. Treatment
  3. Resistance
  4. Toxicity
A
  1. Converted to Thio-IMP and Thio-GMP by HGPRT (enzyme) and both 1) inhibit purine synthesis and are 2) incorporated into DNA
  2. ***Acute Lymphoblastic Leukemia*** (ALL)
  3. Decreased HGPRT activity
  4. Decreased TPMT activity (due to polymorphisms)

***TPMT inhibits 6-MP***

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7
Q

Fludarabine

  1. Mechanism of Action
  2. Treatment
  3. Resistance
A
  1. Deoxycytidine Kinase activates to triphosphate form, which is incorporated into DNA/RNA and inhibits 1) DNA polymerase, 2) Ribonucleotide Reductase, 3) RNA function (i.e. translation to proteins)
  2. ***Chronic Lymphocytic Leukemia*** (CLL)
  3. Decreased Deoxycytidine Kinase activity, Drug Efflux
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8
Q

Clabridine

  1. Mechanism of Action
  2. Treatment
  3. Resistance
A
  1. Deoxycytidine Kinase activates to tri-phosphate form, which is incorporated into DNA (strand breaks) and inhibits Ribonucleotide Reductase (RNR)
  2. ***Hair Cell Leukemia***
  3. Decreased Deoxycytidine Kinase activity, Drug Efflux, Increased RNR expression
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9
Q

Mechlorethamine

  1. Mechanism of Action
  2. Treatment
A
  1. Administered in combination with Vincristine, Procarbazine, and Prednisone (a combination chemo regimen called MOPP)
  2. MOPP is used to treat ***Hodgkin’s Lymphoma***
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10
Q

Cyclophosphamide

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
A
  1. Liver Cytochrome P450 Oxidase converts to active form Aldophosphamide, which causes DNA cross-linking and strand breakage
  2. Solid Tumors/Hematological Malignancies
  3. ***Hemorrhagic Cystitis*** (if Aldophosphamide is converted to acrolein - 5-10% of pts), Myelosuppression, Nausea, Vomiting
  4. Mechlorethamine
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11
Q

What drug can lead to hemorrhagic cystitis, and what compound prevents this from happening/through what mechanism?

A
  • Cyclophosphamide
  • Prevented with Mesna, which inactivates acrolein
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12
Q

Carmustine (BCNU)

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
A
  1. Lipophilic (crosses BBB) and leads to DNA cross-linking and Strand Breakage

***Carmustine Wafers***

  1. ***Brain Tumors, Hodgkin’s/Non-Hodgkin’s Lymphoma***
  2. Myelosuppression

Mnemonic: BrainCancerNon-Hodgkin’s

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13
Q

General Adverse Effects of Alkylating Agents

(e.g. Cyclophosphamide, Mechlorethamide, Carmustine (BCNU))

(4)

A
  1. Mutagenic, Teratogenic, and Myelosuppressive
  2. Dose-limiting toxicity = Bone Marrow Suppression and Damage to Intestinal Mucosa
  3. Can cause Leukemia (peak at approx 4 yrs. post therapy)
  4. Blistering of veins with repeated use
    (i. e. Vesicant properties)
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14
Q

Resistance to Alkylating Agents

(e.g. Cyclophosphamide, Mechlorethamide, Carmustine (BCNU))

(4)

A
  1. Inactivation by Glutathione and other nucleophiles (increased Glutathione production)
  2. Reduced uptake
  3. Accelerated DNA repair
  4. Increased expression of MGMT (O6-methylguanine-DNA methyltransferase)
    - Removes alkyl groups from guanine before cross-links form (preventing further DNA damage)
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15
Q

Platinum Compounds (Non-Classical Alkylating Agents)

  1. Mechanism of Action
  2. Treatment
  3. Drugs (3)
A
  1. Platinum group allows for DNA cross-linkages to form (specifically targets nucleophilic center (Guanine-N7)
  2. Widespread Treatment
  3. Cisplatin** (1st gen.), Carboplatin** (2nd gen.), Oxaliplatin** (3rd gen.)
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16
Q

Cisplatin

  1. Key Side Effects
A

Peripheral motor and sensory neuropathy

Tinnitus and high-frequency hearing loss

Nephrotoxicity (reduced by IV saline)

Anaphylactic-like reactions (Hypersensitivity Reactions)

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17
Q

Carboplatin

  1. Key Side Effects
A

Dose-limiting toxicity is Myelosuppression

Anaphylactic-like reactions (Hypersensitivity Reactions)

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18
Q

Procarbazine

  1. Class
  2. Treatment
A
  1. Non-classical alkylating agents (MoA –> DNA cross-linking/damage)
  2. Hodgkin’s Disease
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19
Q

Dacarbazine

  1. Class
  2. Treatment
A
  1. Non-classical alkylating agents (MoA –> DNA cross-linking/damage)
  2. Component of curative combination therapy for Hodgkin’s Lymphoma

-Melanomas and Sarcomas

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20
Q

Temozolomide

  1. Class
  2. Treatment
A
  1. Non-classical alkylating agents (MoA –> DNA cross-linking/damage)
  2. Glioblastomas and Metastatic Melanoma
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21
Q

Vinblastine

  1. Class
  2. Mechanism of Action
  3. Toxicity
A
  1. Antimicrotubule Agent
  2. Prevents microtubules from forming
  3. Significant Myelosuppression
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22
Q

Vincristine

  1. Class
  2. Mechanism of Action
  3. Toxicity
A
  1. Antimicrotubule Agent
  2. Prevent microtubules from forming
  3. Neurological (numbness/tingling of extremities, motor weakness), Limited Myelosuppression
23
Q

Paclitaxel (taxol)

  1. Class
  2. Mechanism of Action
  3. Toxicity
  4. Other Drug in Class
A
  1. Antimicrotuble Agent (Taxane)
  2. Prevents depolymerization of microtubules
  3. Bone Marrow Toxicity (dose-limiting), Peripheral Neuropathy
  4. Docetaxel
24
Q

What drug is given with filgrastim (granulocyte colony stimulating factor) to reduce myelosuppression?

A

Paclitaxel

25
Q

What is something to watch out for with Paclitaxel, and what is used as pretreatment for this?

A

Hypersensitivity allergic reactions

Pretreated with dexamethasone and antihistamines

26
Q

Irinotecan

  1. Class
  2. Mechanism of Action
A
  1. Topoisomerase Inhibitor
  2. Inhibits topoisomerase I
27
Q

Topotecan

  1. Class
  2. Mechanism of Action
A
  1. Topoisomerase Inhibitor
  2. Inhibits Topoisomerase I
28
Q

Etoposide

  1. Class
  2. Mechanism of Action
A
  1. Topoisomerase Inhibitor
  2. Inhibits Topoisomerase II
29
Q

Doxorubicin

  1. Class
  2. Mechanism of Action (2)
  3. Treatment
  4. Toxicity
A
  1. Cytotoxic Antibiotic
  2. Inhibits DNA polymerase (intercalates w/ DNA), Inhibits Topoisomerase II
  3. Widespread Treatment
  4. Binds iron which generates free radicals leading to ***Irreversible Cardiomyopathy***, another SE is Severe Myelosupprssion
30
Q

What is Doxorubicin co-administered with to reduce cardiotoxicity?

A

Dexrazoxane (iron chelator - reduces free radicals)

31
Q

Bleomycin

  1. Class
  2. Mechanism of Action
  3. Treatment
  4. Toxicity
A
  1. Cytotoxic Antibiotic
  2. Small peptide that binds to DNA and induces single/double strand breaks and arrests cells in G2 phase
  3. Testicular Cancer and Hodgkin’s Disease

***Minimally Myelo/Immunosuppressive so used in combination***

  1. ***Pulmonary Toxicity*** (effects = cumulative/irreversible)
32
Q

Which three cytotoxic agents are the least myelosuppressive?

A

Bleomycin

Vincristine

Methotrexate (with leucovorin)

33
Q

What five cytotoxic agents are the most myelosuppressive?

A

Vinblastine

Nitrosureas

Cyclophosphamide

Cytarabine

Doxorubicin

34
Q

Prednisone/Dexamethasone

  1. Class
  2. Mechanism of Action
  3. Treatment
A
  1. Glucocorticoids
  2. Inhibit Lymphocyte Proliferation
  3. ^^^Treat Leukemias and Lymphomas^^^, reduce Intracranial Pressure (associated w/ brain tumors), reduce Nausea/Vomiting
35
Q

Tamoxifen

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
A
  1. SERM (selective estrogen receptor modulator) which competitively binds estrogen receptor
  2. Breast Cancer (estrogen-dependent)
  3. Increased Endometrial Cancer risk
36
Q

Anastrozole

  1. Class
  2. Mechanism of Action
  3. Treatment
A
  1. Aromatase Inhibitor
  2. Inibits Aromatase activity, which prevents testosterone from being converted to estrogen and lowers estrogen levels
  3. Breast Cancer (estrogen-dependent)
37
Q

Flutamide

  1. Class
  2. Mechanism of Action
  3. Treatment
A
  1. Androgen Receptor Inhibitor
  2. Prevents Dihydrotestosterone (DHT) from binding to androgen receptors
  3. Prostate Cancer
38
Q

Leuprolide and Goserelin

  1. Class
  2. Mechanism of Action
  3. Treatment
A
  1. GnRH agonists
  2. Desensitive GnRH receptor on Pituitary
  3. Prostate Cancer
39
Q

Degarelix

  1. Class
  2. Mechanism of Action
  3. Treatment
A
  1. GnRH antagonist
  2. Antagonizes GnRH receptor
  3. Prostate Cancer
40
Q

Trastuzumab**

  1. Class
  2. Mechanism of Action
  3. Treatment
  4. Toxicity
A
  1. Monoclonal Antibody
  2. Blocks HER-2 (HER-2/neu (ErbB2)), a member of the EGFR family, mediated signaling/induces antibody-dependent cytotoxicity
  3. Invasive Breast Cancer (only the kind with amplified HER-2)
  4. Cardiotoxicity
41
Q

Cetuximab**

  1. Class
  2. Mechanism of Action
  3. Treatment
  4. Resistance
A
  1. Monoclonal Antibody
  2. Binds EGFR and blocks signaling
  3. Colorectal Tumors (EGFR-expression) in combination w/ other drugs
  4. Activating Ras mutations (leads to no effect by Cetuximab, as Ras is downstream from EGRF receptor)
42
Q

Bevacizumab**

  1. Class
  2. Mechanism of Actoin
  3. Treatment
  4. Toxicity
A
  1. Monoclonal Antibody
  2. Binds to VEGF and prevents it from binding VEGFR
  3. Colorectal Cancer (w/ capecitabine and oxaliplatin) and metastatic Breast Cancer
  4. Hypertension, Increased risk of Thrombosis or Bleeding, Decreased Wound Healing
43
Q

Lapatinib**

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
A
  1. Small molecule that inhibits EGFR and HER-2 kinase activity via action inside the cell
  2. Breast Cancer (HER-2 amplified, Trastuzumab-refractory)

***2nd line treatment to Trastuzumab to avoid resistance***

  1. Rashes, Diarrhea, Cramping, worsening GERD
44
Q

Erlotinib**

  1. Mechanism of Action
  2. Treatment
  3. Resistance
  4. Toxicity
A
  1. Oral small molecule EGRF inhibitor/ATP competitive inhibitor
  2. 1st line treatment of metastatic non-small cell lung cancer (NSCLC)

***Need to determin mutation status w/ FDA approved test (know this is the direction treatment is going)

  1. Acquired secondary mutation in EGFR or amplification of MET oncogone
  2. Diarrhea, Rash, Anorexia, and Fatigue
45
Q

Imatinib**

  1. Mechanism of Action
  2. Treatment
  3. Resistance
A
  1. Small molecule inhibits BCR-ABL (preventing ABL tyrosine kinase activity)
  2. Chronic Myelogenous Leukemia (CML)

***Caused by Philadelphia Chromosome translocation –> Contitutive activity***

  1. Point Mutations in BCR-ABL –> reduced Imatinib affinity, however, analogs (nilotinib and dasatinib) still able to be effective with many mutations
46
Q

Asparaginase

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
A
  1. Enzyme that hydrolyzes L-asparagine to L-aspartate (Tumor cells cannot synthesize L-asparagine, and therefore are starved)
  2. Acute Lymphoblastic Leukemia (ALL)
  3. Allergic Hypersensitivity Reactions (fever, chills, rash, hives) which can become severe causing respiratory failure and hypotension
47
Q

Bortezomib

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
A
  1. Inhibits proteasome leading to increased p53 ; also decreases NF-kappa B (which noramly inhibits apoptosis)
  2. Relapsed/Refractory Multiple Myeloma
  3. Peripheral Neuropathy, Thrombocytopenia, Neutropenia, Anemia
48
Q

Temsirolimus

  1. Mechanism of Action
  2. Treatment
  3. Toxicity
  4. Resistance
A
  1. Inhibits mTOR complex 1 (mTORC1) which causes decreased protein translation, increased cell cycle inhibition, and increased apoptosis
  2. Renal Cell Carcinoma
  3. Hyperglycemia, Hypertriglyceridemia, Rash, Mucositis, Aemia, Leukopenia and Thrombocytopenia
  4. mTOR forms a complex called mTOR complex 2 (mTORC2) which is not inhibited by Temsirolimus
49
Q

What antineoplastic drugs are Nephrotoxic?

(2)

A

Cisplatin

Methotrexate

50
Q

What antineoplastic drugs are Neurotoxic (peripheral neuropathies, cerebellar syndrome, etc.)?

(5)

A

Vincristine

Cytarabine (ara C)

Cisplatin

Bortezomib

Paclitaxel

51
Q

What antineoplastic drugs are Cardiotoxic?

(2)

A

Doxorubicin

Trastuzumab

52
Q

What antineoplastic drugs show Pulmonary toxicity?

(3)

A

Methotrexate

Bleomycin

Alkylating Agents

53
Q

What antineoplastic drugs show Bladder Toxicity (Hemorrhagic Cystitis)?

(1)

A

Cyclophosphamide

54
Q

What antineoplastic drugs cause Hypersensitivity Reactions?

(2)

A

Asparaginase

Paclitaxel

Pharmacology Exam II (6 decks)

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