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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
What is something to watch out for with **Paclitaxel**, and what is used as pretreatment for this?
**Hypersensitivity allergic** reactions Pretreated with **dexamethasone** and **antihistamines**
26
**Irinotecan** 1. Class 2. Mechanism of Action
1. Topoisomerase Inhibitor 2. Inhibits **topoisomerase I**
27
**Topotecan** 1. Class 2. Mechanism of Action
1. Topoisomerase Inhibitor 2. Inhibits **Topoisomerase I**
28
**Etoposide** 1. Class 2. Mechanism of Action
1. Topoisomerase Inhibitor 2. Inhibits **Topoisomerase II**
29
**Doxorubicin** 1. Class 2. Mechanism of Action (2) 3. Treatment 4. Toxicity
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
What is **Doxorubicin** co-administered with to **reduce cardiotoxicity**?
**Dexrazoxane** (iron chelator - reduces free radicals)
31
**Bleomycin** 1. Class 2. Mechanism of Action 3. Treatment 4. Toxicity
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**\*\*\* 4. **\*\*\*Pulmonary Toxicity\*\*\*** (effects = cumulative/irreversible)
32
Which three **cytotoxic agents** are the _least_ myelosuppressive?
Bleomycin Vin**cris**tine Methotrexate (with leucovorin)
33
What five **cytotoxic agents** are the _most_ myelosuppressive?
Vin**blas**tine Nitrosureas Cyclophosphamide Cytarabine Doxorubicin
34
**Prednisone/Dexamethasone** 1. Class 2. Mechanism of Action 3. Treatment
1. Glucocorticoids 2. Inhibit **Lymphocyte Proliferation** 3. ^^^Treat **Leukemias** and **Lymphomas**^^^, reduce **Intracranial Pressure** (associated w/ brain tumors), reduce **Nausea/Vomiting**
35
**Tamoxifen** 1. Mechanism of Action 2. Treatment 3. Toxicity
1. **SERM** (selective estrogen receptor modulator) which competitively **binds estrogen receptor** 2. **Breast Cancer** (estrogen-dependent) 3. Increased **Endometrial Cancer** risk
36
**Anastrozole** 1. Class 2. Mechanism of Action 3. Treatment
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
**Flutamide** 1. Class 2. Mechanism of Action 3. Treatment
1. Androgen Receptor Inhibitor 2. Prevents **Dihydrotestosterone (DHT)** from binding to androgen receptors 3. **Prostate Cancer**
38
**Leuprolide** and **Goserelin** 1. Class 2. Mechanism of Action 3. Treatment
1. GnRH agonists 2. **Desensitive** GnRH receptor on Pituitary 3. **Prostate Cancer**
39
**Degarelix** 1. Class 2. Mechanism of Action 3. Treatment
1. GnRH antagonist 2. Antagonizes GnRH receptor 3. **Prostate Cancer**
40
**Trastuzu**_mab_**** 1. Class 2. Mechanism of Action 3. Treatment 4. Toxicity
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
**Cetuxi**_mab_**** 1. Class 2. Mechanism of Action 3. Treatment 4. Resistance
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
**Bevacizu**_mab_**** 1. Class 2. Mechanism of Actoin 3. Treatment 4. Toxicity
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
**Lapati**_nib_**** 1. Mechanism of Action 2. Treatment 3. Toxicity
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**\*\*\* 3. **Rashes**, Diarrhea, Cramping, worsening **GERD**
44
**Erloti**_nib_**** 1. Mechanism of Action 2. Treatment 3. Resistance 4. Toxicity
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**) 3. Acquired secondary **mutation** in **EGFR** or **amplification** of **MET** oncogone 4. Diarrhea, Rash, Anorexia, and Fatigue
45
**Imati**_nib_**** 1. Mechanism of Action 2. Treatment 3. Resistance
1. **Small molecule** inhibits **BCR-ABL** (preventing ABL tyrosine kinase activity) 2. **Chronic Myelogenous Leukemia (CML)** \*\*\*Caused by **Philadelphia Chromosome** translocation --\> Contitutive activity\*\*\* 3. **Point Mutations** in BCR-ABL --\> reduced Imatinib affinity, however, analogs (**nilotinib** and **dasatinib**) still able to be effective with many mutations
46
**Asparaginase** 1. Mechanism of Action 2. Treatment 3. Toxicity
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
**Bortezomib** 1. Mechanism of Action 2. Treatment 3. Toxicity
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
**Temsirolimus** 1. Mechanism of Action 2. Treatment 3. Toxicity 4. Resistance
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
What antineoplastic drugs are **Nephrotoxic**? (2)
Cisplatin Methotrexate
50
What antineoplastic drugs are **Neurotoxic** (peripheral neuropathies, cerebellar syndrome, etc.)? (5)
Vin**cris**tine Cytarabine (ara C) Cisplatin Bortezomib Paclitaxel
51
What antineoplastic drugs are **Cardiotoxic**? (2)
Doxorubicin Trastuzumab
52
What antineoplastic drugs show **Pulmonary** toxicity? (3)
Methotrexate Bleomycin Alkylating Agents
53
What antineoplastic drugs show **Bladder Toxicity** (Hemorrhagic Cystitis)? (1)
Cyclophosphamide
54
What antineoplastic drugs cause **Hypersensitivity Reactions**? (2)
Asparaginase Paclitaxel

Pharmacology Exam II (6 decks)

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