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BIIC Cancers and Pharmo > Pharmacology Of Neoplasias > Flashcards

Pharmacology Of Neoplasias Flashcards

1
Q

MOA of Alkylating Agents

A

Alkylation interferes with DNA replication which results in cell death. Cell cycle non-specific.

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2
Q

4 Classes of Alkylating Agents

A
  1. Nitrogen mustards
  2. Nitrosoureas
  3. Platinum analogs
  4. Non-classic alkylating agents
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3
Q

Drugs in Nitrogen Mustard class of Alkylating Agents (6)

A
  1. Mechlorethamine, Melphalan
  2. Cyclophosphamide, Ifosfamide
  3. Chlorambucil
  4. Thiotepa
  5. Busulfan
  6. Altretamine
    Note: Chemoprotective agent - 2% sodium thiosulfate solution - creates water soluble compound for elimination. Addition of a phenyl ring can also decrease reactivity by slowing aziridinium.
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4
Q

Drugs in the Platinum Analog class of Alkylating Agents (2)

A
  1. Cisplatin, Carboplatin
  2. Oxaliplatin
    * These drugs form intra-strand cross-links
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5
Q

MOA of Vinca Alkaloids

A

Binds to tubulin (tubulin is the precursor of microtubulin which is necessary for cell division). M-phase specific.

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6
Q

Drugs in the Vinca Alkaloids class (3)

A
  1. Vincristine
  2. Vinorelbine
  3. Vinblastin
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7
Q

MOA of Taxanes

A

Enhance tubulin polymerization which alters normal tubulin function, preventing cell division. M-phase specific.

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8
Q

Drugs in the Taxanes class (2)

A
  1. Paclitaxel

2. Docetaxel

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9
Q

MOA of Antimetabolites

A

Inhibits enzymes necessary for DNA, RNA or protein synthesis.

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10
Q

3 classes of Antimetabolites

A
  1. Folic acid antagonists
  2. Purine antagonists
  3. Pyrimidine antagonists
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11
Q

Drugs within the Folic Acid Antagonists class of Antimetabolites (3)

A
  1. Methotrexate: directly inhibits dihydrofolate reductase (DHFR) and indirectly inhibits thymidylate synthase.
  2. Pemtrexed
  3. Pralatrexate
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12
Q

Drugs within the Purine Antagonists class of Antimetabolites (4)

A
  1. 6-Mercaptopurine: (ADRs = hepatotoxicity; elevated liver enzymes)
  2. Cladribine
  3. Fludarabine
  4. Pentostatin
    Note: Thiopurines are metabolized by thiopurine methyl transferase (TPMT)
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13
Q
  1. ADR of Fludarabine

2. ADR of Cladribine

A
  1. Cough

2. Stomatitis

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14
Q

Drugs in the Pyrimidine Antagonists class of Antimetabolites (4)

A
  1. 5-Fluorouracil
  2. Capecitabine
  3. Cytarabine
  4. Gemcitabine
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15
Q

ADR of Cytarabine

A

Hand and Foot Syndrome

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16
Q

Drugs in the Antibiotics class (4)

A
  1. Bleomycin
  2. Dactinomycin
  3. Anthracyclines
  4. Mitomycin C
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17
Q

MOA of Bleomycin

A

Binds to iron, creates free radicals, results in DNA strand breaks. G2-phase specific.

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18
Q

MOA of Dactinomycin

A

Inhibits RNA polymerase, binds to DNA.

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19
Q

MOA of Anthracyclines

A

Intercalate into DNA, free radical formation, topoisomerase II inhibitors.

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20
Q

Drugs in the Miscellaneous Agents class (3)

A
  1. L-asparaginase
  2. Arsenic trioxide
  3. Hydroxyurea
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21
Q

MOA of L-asparaginase

A

Enzyme that breaks down L-asparagine, depleting asparagine in cancer cells that cannot produce the amino acid.

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22
Q

MOA of Arsenic Trioxide

A

Inhibits telomerase activity to cause apoptosis and causes DNA strand breaks. Dactinomycin related to this drug.

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23
Q

MOA of Hydroxyurea

A

Inhibits Ribonucleotide reductase. S-phase specific.

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24
Q

Drugs in the Topoisomerase I Inhibitors class (2)

A
  1. Irinotecan

2. Topotecan

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25
Q

MOA of Topoisomerase I Inhibitors

A

Inhibitor of topoisomerase I. S-phase specific.

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26
Q

Drugs in the Topoisomerase II class (4)

A
  1. Etoposide
  2. Teniposide
  3. Anthracyclines (Doxorubicin, daunorubicin, idarubicin, epirubicin)
  4. Mitoxantrone
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27
Q

MOA of Topoisomerase II Inhibitors

A

Inhibits complexes with DNA and the enzyme topoisomerase II, which results in DNA strand breaks. S-phase specific.

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28
Q

ADRs of Alkylating Agents (1)

A

Extravasation

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29
Q

ADRs of Cisplatin (5)

A
  1. Severe nausea and vomiting
  2. Electrolyte imbalances
  3. Nephrotoxicity
  4. Ototoxicity
  5. Peripheral neuropathy
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30
Q

ADRs of Anthracyclines [Daunorubicin, doxorubicin] (3)

A
  1. Alopecia
  2. Mucositis
  3. Acute and cumulative cardio toxicity (irreversible CHF)
    There is a total lifetime dose limit due to these side effects.
    Note: Should be treated with a chemoprotective agent- iron chelator (dexrazoxane).
    Mitoxantrone is a synthetic agent related to Anthracyclines that does NOT generate free radicals and avoids cardio toxicity.
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31
Q

ADR for Topoisomerase II Inhibitors

A

Mucositis

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32
Q

ADRs of Methotrexate and 5-fluorouracil (3)

A
  1. Mucositis (mouth sores and diarrhea)
  2. Photosensitivity
  3. Nephrotoxicity
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33
Q

ADRs of Bulsulfan and Bleomycin

A

Pulmonary fibrosis

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34
Q

ADRs of Cyclophosphamide and Ifosfamide

A

Hemorrhagic cystitis
Note: These prodrugs are metabolized to the form acrolein which is urotoxic. Hydration and co-administration with Mesna (chemoprotective agent) can minimize the effects of acrolein.

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35
Q

ADRs of Vinca Alkaloids and Taxanes (3)

A
  1. Alopecia
  2. Neurotoxicity
  3. Peripheral neuropathy
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36
Q

ADRs of Iriontecan

A

Acute and delayed diarrhea

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37
Q

What 2 substances are responsible for stimulating platelet aggregation?

A
  1. Thromboxane A2 (TxA2)

2. ADP

38
Q

MOA of aspirin

A

Irreversibly inhibits COX-1 and COX-2 in platelets. Also inhibits TxA2 and reduces platelet aggregation.

39
Q

Indications for aspirin

A

Thromboembolic disorder, osteoarthritis, RA, fever, pain, prophylaxis for stroke and MI.

40
Q

ADRs for aspirin (6)

A
  1. GI discomfort
  2. Tinnitus
  3. GI ulcer/bleed
  4. Hemorrhage
  5. Reye’s syndrome (usually seen in children recovering from a viral infection that was treated with aspirin)
  6. Possible allergic reaction (hypersensitivity)
41
Q

Difference between COX-1 and COX-2 as pharmacology targets?

A

COX-1 inhibitors (aspirin, ibuprofen) will inhibit or decrease platelet aggregation; aspirin has a 53% greater platelet inhibitor effect in comparison to ibuprofen.
Selective COX-2 inhibitors have NO platelet effect.

42
Q

3 drugs that act as anticoagulants

A
  1. Heparin
  2. Factor Xa Inhibitors
  3. Warfarin
43
Q

MOA of Heparin (HMW: high molecular weight) and Enoxaparin (LMW: low molecular weight)

A

Enhances actions of the protease Anti-thrombin III, which inactivates thrombin and Factor X, slowing the clotting cascade

44
Q

Indications for Heparin and Enoxaparin

A

Anticoagulant therapy and thromboembolic disorders

45
Q

ADRs for Heparin and Enoxaparin (4)

A
  1. Hemorrhage
  2. Easy bruising
  3. GI bleed
  4. Heparin-induced thrombocytopenia (autoimmune activation and destruction of platelets)
46
Q

Considerations for Heparin and Enoxaparin

A
  1. Unfractionated Heparin (HMW) effectively catalyzes the inactivation of both Thrombin and Factor Xa
  2. Enoxaprin increases inactivation of Factor Xa and has LESS of an effect on Thrombin
  3. Protamine sulfate can reverse the effects of heparin
47
Q

Rivaroxaban and Apixaban are inhibitors of ______ ___.

48
Q

Indications for Rivaroxaban and Apixaban

A

Treatment or prophylaxis for DVT

49
Q

ADRs of Rovaroxaban and Apixaban

A
  1. Hemorrhage
  2. Easy bruising
  3. GI bleed
50
Q

Considerations for Rivaroxaban and Apixaban (3)

A
  1. Given as a fixed dose and no monitoring is required
  2. More rapid onset and shorter half-life than warfarin
  3. Andexanet alfa approved as a reversal agent for Xa inhibitors in 2018
51
Q

MOA of warfarin

A

Inhibits liver Vitamin K Reductase: inhibits regeneration of Vitamin K, an essential cofactor for synthesis of clotting factors in the liver: factors II, VIII, IX, and X

52
Q

Warfarin pharmokinetics considerations

A

Genetic variants in:

  1. CYP2C9 will cause varying rates of drug activity as warfarin is metabolized by this enzyme
  2. Vitamin K epoxide reductase (VKOR) will cause varying responses to warfarin
53
Q

ADRs of warfarin (2)

A
  1. Hemorrhage

2. GI bleed

54
Q

Warfarin considerations (5)

A
  1. Reversal agents: Vitamin K, fresh-frozen plasma, three- or four-factor prothrombin complex concentrate
  2. Should be monitored regularly by PTT and INR
  3. Highly protein bound and may interact with other medications (aspirin, NSAIDs)
  4. Metabolized by CYPs and should be used with caution with other CYP inducers or inhibitors
  5. Avoid foods high in Vitamin K (collard greens, kale, spinach)
55
Q

Allopurinol (Xanthine Oxidase Inhibitor) MOA

A

Inhibits xanthine oxidase, which converts hypoxanthine to xanthine and xanthine to uric acid; decreased uric acid levels lead to reduced urate crystal formation

56
Q

ADRs of Allopurinol (5)

A
  1. Pruritus
  2. Rash
  3. GI upset
  4. Agranulocytosis
  5. Aplastic anemia
57
Q

Ruxolitinib (Tyrosine Kinase Inhibitor) MOA

A

A kinase inhibitor which selectively inhibits JAKs 1 and 2: particularly targets dysregulated JAK signaling associated with myelofibrosis and polycythemia vera and their unregulated cell proliferation.

58
Q

ADRs of Ruxolitinib (7)

A
  1. Edema
  2. Bruising
  3. Dizziness
  4. Headache
  5. Anemia
  6. Herpes zoster
  7. Hepatitis
59
Q

Pegylated interferon alpha MOA

A

Enhances host immune system to increase activated T lymphocytes, NK cells, and macrophages

60
Q

ADRs of Pegylated interferon alpha (4)

A
  1. Fever
  2. Headache
  3. Chills
  4. Generalized aches and pains
61
Q

MOA of Hydroxyurea

A

Inhibits ribonucleotide reductase and inhibits DNA synthesis

62
Q

Indications for hydroxyurea

A

Sickle cell anemia, essential thrombocythemia, polycythemia vera

63
Q

ADRs of hydroxyurea (7)

A
  1. Nausea/vomiting
  2. Myelosuppression
  3. Neutropenia
  4. Decreased platelet count
  5. Decreased reticulocyte count
  6. Lower extremity ulcers
  7. Skin cancer risk
64
Q

Prednisone and methylprednisolone MOA

A

Anti-inflammatory corticosteroids with potent glucocorticoid and weak mineralocorticoid activity.
Broad range of active inhibition against multiple cell types and mediators involved in inflammation.

65
Q

ADRs of prednisone and methylprednisolone (8)

A
  1. Infections, striae, delayed wound healing
  2. Osteopenia, osteoporosis
  3. Adrenal insufficiency
  4. Avascular necrosis
  5. Weight gain
  6. Insomnia
  7. Mood changes, delirium
  8. Cataracts, glaucoma
66
Q

MOA of low-dose thalidomide

A

Exhibits immunomodulatory and anti-angiogenic characteristics; immunologic effects mary vary based on conditions
TERATOGENIC
Pregnancy Category: X

67
Q

ADRs of low-dose thalidomide (2)

A
  1. Nausea/vomiting

2. Fatigue

68
Q

Treatments of erythromelalgia of Essential Thrombocytosis (ET)

A
  1. COX-1 inhibitors (aspirin, ibuprofen)

2. If no response to salicylates, hydroxyurea, pegylated interferon alpha, or anagrelide

69
Q

MOA of Anagrelide

A

A phosphodiesterase-3 enzyme (PDE-3) inhibitor that inhibits platelet aggregation and causes a dose-related reduction in platelet production

70
Q

ADRs of Anagrelide (6)

A
  1. Headache
  2. Edema
  3. Diarrhea
  4. Palpitations
  5. Prolonged QT interval
  6. Hemorrhage
71
Q

ALL induction treatment regimen (2):

A
  1. Vincristine + glucocorticoid + anthracycline +/- pegaspargase
  2. If Ph+, add imatinib or another tyrosine kinase inhibitor if resistant to imatinib
72
Q

ALL CNS prophylaxis goal of therapy

A

Eradicate undetectable leukemia cells in CNS and minimize neurotoxicity

73
Q

ALL CNS prophylaxis treatment

A

Intrathecal methotrexate +/- cranial irradiation

74
Q

ALL Maintenance Therapy

A

12-week course of POMP regimen

Purinethol, Oncovin, Methotrexate, Prednisone

75
Q

Relapsed ALL Treatment

A

Blinatumomab is a monoclonal antibody that binds to both CD19 (an antigen present during B cell development) and CD3 (T-cell receptor), which results in lysis of CD19 cells

76
Q

Rituximab (CD20 antibody) MOA and Indications

A

Targets CD20 found on surface of normal and malignant B cells. Binds to CD20 and recruits immune effector functions to mediate B-cell lysis (via CDC and ADCC) and cause apoptosis.
Used to treat Non-Hodgkin’s Lymphoma and CLL.

77
Q

ADR of Rituximab

A

Steven-Johnson Syndrome

78
Q

AML Post-remission Therapy

A

Purine Antagonists of Antimetabolites: Fludarabine, Cladribine, Clofarabine (adenosine analogs).
DNA polymerase and chain elongation inhibitors.

79
Q

Acute Myeloid Leukemia (AML) Induction Treatment

A

Pyrimidine Antagonists of Antimetabolites: Cytarabine and gemcitabine (cytidine analogs).
DNA polymerase and chain elongation inhibitors.

80
Q

Dasatinib (Tyrosine Kinase Inhibitor) MOA and Indications

A

Targets multiple defective tyrosine kinases (SRC tyrosine kinase, platelet-derived growth factor receptor, BCR-ABL, C-KIT kinase).
More potent inhibitor of ABL than imatinib.
Has activity against imatinib-resistant leukemia.
Used for Philadelphia chromosome positive CML (Ph+CML) and ALL (Ph+ALL).

81
Q

ADRs of Dasatinib (2)

A
  1. Edema and pleural effusion

2. Hemorrhage

82
Q

Nilotinib (Tyrosine Kinase Inhibitor) MOA and Indications

A

BCR-ABL selective tyrosine kinase inhibitor. Acts as a competitive inhibitor of the ATP-binding site of BCR-ABL. Inhibits cellular proliferation and induces apoptosis.
Higher affinity for BCR-ABL than imatinib and dasatinib.
Used for Ph+CML.

83
Q

ADR of Nilotinib

A

Electrolyte abnormalities

84
Q

Hodgkin’s Lymphoma Treatment Overview

A

ABVD (Adriamycin, Bleomycin, Vinblastine, Dacarbazine)

85
Q

Brentuximab vedotin MOA and Indications

A

Targets CD30 found on Hodgkin’s Lymphoma and Anaplastic Large Cell Lymphoma (ALCL)

86
Q

ADRs of Brentuximab vedotin (4)

A
  1. Neutropenia
  2. Peripheral neuropathy
  3. Fatigue
  4. Nausea/vomiting/diarrhea
  5. Anemia
  6. URIs
87
Q

Non-Hodgkin Lymphomas Indolent Subtype Treatment

A

Not curable with chemotherapy.

Bendamustine: DNA alkylation and antimetabolite (S-phase specific). ADR = increased bilirubin levels.

88
Q

Non-Hodgkin Lymphomas Aggressive Subtype Treatment

A

Potentially curable with chemotherapy.

89
Q

Non-Hodgkin Lymphomas Highly Aggressive Subtype Treatment

A

Potentially curable with chemotherapy

95
Q

Imatinib (Tyrosine Kinase Inhibitor) MOA and Indications

A

Inhibition of proliferation which results in apoptosis.

Used to treat BCR-ABL mutation in CML, GI stromal tumors, and platelet-derived growth factor receptor mutations.

96
Q

ADRs of Imatinib (4)

A
  1. Nausea/vomiting
  2. Edema
  3. Arthralgia/myalgias
  4. Myelosuppression

BIIC Cancers and Pharmo (10 decks)

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