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Pharmacology > FA Hematology and Oncology > Flashcards

FA Hematology and Oncology Flashcards

1
Q

Heparin Mechanism

A

Cofactor for the activation of antithrombin, ↓ thrombin, and ↓ factor Xa. Short half-life.

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2
Q

Heparin Use

A

Immediate anticoagulation for PE, acute coronary syndrome, MI, DVT. Used during pregnancy (does not cross placenta). Follow PTT.

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3
Q

Heparin Toxicity

A

Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions. For rapid reversal (antidote), use protamine sulfate (positively charged molecule that binds negatively charged heparin).

Heparin-induced thrombocytopenia (HIT) - development of IgG antibodies against heparin bound to platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets → thrombosis and thrombocytopenia.

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4
Q

Low-Molecular Weight Heparins (LMWHs)

A

Enoxaparin, dalteparin

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5
Q

Enoxaparin, Dalteparin Mechanism

A

Compared to regular heparin, act more on factor Xa, have better bioavailability, and 2-4 times longer half-life. Can be administered subcutaneously and without laboratory monitoring. Not easily reversible.

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6
Q

Argatroban, Bivalirudin Mechanism

A

Derivatives of hirudin, the anticoagulant used by leeches; inhibit thrombin directly.

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7
Q

Argatroban, Bivalirudin Use

A

Used instead of heparin for anticoagulating patients with HIT.

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8
Q

Warfarin (Coumadin) Mechanism

A

Interferes with normal synthesis and γ-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X and proteins C and S. Metabolized by the cytochrome P-450 pathway and ↑ PT. Long half-life.

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9
Q

Warfarin (Coumadin) Use

A

Chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation). Not used in pregnant women (because warfarin, unlike heparin, can cross the placenta). Follow PT/INR values.

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10
Q

Warfarin (Coumadin) Toxicity

A

Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions.
For reversal of warfarin overdose, give vitamin K. For rapid reversal of severe warfarin overdose, give fresh frozen plasma.

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11
Q

Direct Factor Xa Inhibitors

A

Apixaban, rivaroxaban

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12
Q

Apixaban, Rivaroxaban Mechanism

A

Bind and directly inhibit the activity of factor Xa.

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13
Q

Apixaban, Rivaroxaban Use

A

Treatment and prophylaxis of DVT and PE (rivaroxaban), stroke prophylaxis in patients with atrial fibrillation. Oral agents do not usually require coagulation monitoring.

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14
Q

Apixaban, Rivaroxaban Toxicity

A

Bleeding (no specific reversal agent available)

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15
Q

Thrombolytics

A

Alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA)

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16
Q

Thrombolytic Mechanism

A

Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. ↑ PT, ↑ PTT, no change in platelet count.

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17
Q

Thrombolytic Use

A

Early MI, early ischemic stroke, direct thrombolysis of PE

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18
Q

Thrombolytic Toxicity

A

Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis. Fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies.

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19
Q

Aspirin (ASA) Mechanism [Hem.]

A

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation. Platelets cannot synthesize new enzym, so effect lasts until new platelets are produced: ↑ bleeding time, ↓ TXA2 and prostaglandins. No effect on PT or PTT.

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20
Q

Aspirin (ASA) Clinical Use [Hem.]

A

Antipyretic, analgesic, anti-inflammatory, antiplatelet (↓ aggregation).

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21
Q

Aspirin (ASA) Toxicity

A

Gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye syndrome in children with viral infection. Overdose causes respiratory alkalosis initially, which is then superimposed by metabolic acidosis.

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22
Q

ADP Receptor Inhibitors

A

Clopidogrel, Ticlopidine, Prasugrel, Ticagrelor

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23
Q

Clopidogrel Mechanism

A

Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.

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24
Q

Clopidogrel Use

A

Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of thrombotic stroke.

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25
Q

Clopidogrel Toxicity

A

TTP/HUS may be seen.

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26
Q

Ticlopidine Mechanism

A

Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.

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27
Q

Ticlopidine Use

A

Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of thrombotic stroke.

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28
Q

Ticlopidine Toxicity

A

Neutropenia. TTP/HUS may be seen.

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29
Q

Prasugrel Mechanism

A

Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.

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30
Q

Prasugrel Use

A

Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of thrombotic stroke.

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31
Q

Prasugrel Toxicity

A

TTP/HUS may be seen.

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32
Q

Ticagrelor Mechanism

A

Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.

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33
Q

Ticagrelor Use

A

Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of thrombotic stroke.

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34
Q

Ticagrelor Toxicity

A

TTP/HUS may be seen.

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35
Q

Cilostazol Mechanism

A

Phosphodiesterase III inhibitor; ↑ cAMP in platelets, thus inhibiting platelet aggregation; vasodilator.

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36
Q

Cilostazol Use

A

Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis.

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37
Q

Cilostazol Toxicity

A

Nausea, headache, facial flushing, hypotension, abdominal pain.

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38
Q

Dipyridamole Mechanism

A

Phosphodiesterase III inhibitor; ↑ cAMP in platelets, thus inhibiting platelet aggregation; vasodilator.

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39
Q

Dipyridamole Use

A

Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis.

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40
Q

Dipyridamole Toxicity

A

Nausea, headache, facial flushing, hypotension, abdominal pain.

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41
Q

GPIIb/IIIa Inhibitors

A

Abciximab, eptifibatide, tirofiban

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42
Q

GPIIb/IIIa Inhibitors Mechanism

A

Bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation. Abciximab is made from monoclonal antibody Fab fragments.

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43
Q

GPIIb/IIIa Inhibitor Use

A

Unstable angina, percutaneous transluminal coronary angioplasty

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44
Q

GPIIb/IIIa Inhibitor Toxicity

A

Bleeding, thrombocytopenia

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45
Q

Antimetabolites

A

Methotrexate, 5-fluorouracil, Cytarabine (arabinofuranosyl cytidine), Azathioprine, 6-mercaptopurine, 6-thioguanine

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46
Q

Methotrexate (MTX) Mechanism

A

Folic acid analog that inhibits dihydrofolate reductase → ↓ dTMP → ↓ DNA and ↓ protein synthesis

47
Q

Methotrexate (MTX) Use

A

Cancers: leukemias, lymphomas, choriocarcinoma, sarcomas.

Non-neoplastic: abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis, IBD.

48
Q

Methotrexate (MTX) Toxicity

A

Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue.”
Macrovesicular fatty change in liver.
Mucositis.
Teratogenic.

49
Q

5-fluorouracil (5-FU) Mechanism

A

Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid.
This complex inhibits thymidylate synthase → ↓ dTMP → ↓ DNA and ↓ protein synthesis.

50
Q

5-fluorouracil (5-FU) Use

A

Colon cancer, pancreatic cancer, basal cell carcinoma (topical).

51
Q

5-fluorouracil (5-FU) Toxicity

A

Myelosuppression, which is not reversible with leucovorin. Overdose: “rescue” with uridine. Photosensitivity.

52
Q

Cytarabine (arabinofuranosyl cytidine) Mechanism

A

Pyrimidine analog → inhibition of DNA polymerase.

53
Q

Cytarabine (arabinofuranosyl cytidine) Use

A

Leukemias, lymphomas

54
Q

Cytarabine (arabinofuranosyl cytidine) Toxicity

A

Leukopenia, thrombocytopenia, megaloblastic anemia.

CYTarabine causes panCYTopenia.

55
Q

Azathioprine, 6-mercaptopurine (6-MP), 6-thioguanine (6-TG) Mechanism

A

Purine (thiol) analogs → ↓ de novo purine synthesis. Activated by HGPRT.

56
Q

Azathioprine, 6-mercaptopurine (6-MP), 6-thioguanine (6-TG) Use

A

Preventing organ rejection, RA, SLE (azathioprine).

Leukemia, IBD (6-MP, 6-TG).

57
Q

Azathioprine, 6-mercaptopurine (6-MP), 6-thioguanine (6-TG) Toxicity

A

Bone marrow, GI, liver.
Azathioprine and 6-MP are metabolized by xanthine oxidase; thus both have ↑ toxicity with allopurinol, which inhibits their metabolism.

58
Q

Antitumor Antibiotics

A

Dactinomycin, Doxorubicin (Adriamycin), Daunorubicin, Bleomycin

59
Q

Dactinomycin (actinomycin D) Mechanism

A

Intercalates in DNA.

60
Q

Dactinomycin (actinomycin D) Use

A

Wilms tumor, Ewing sarcoma, rhabdomyosarcoma. Used for childhood tumors (“children act out”).

61
Q

Dactinomycin (actinomycin D) Toxicity

A

Myelosuppression.

62
Q

Doxorubicin (Adriamycin), Daunorubicin Mechanism

A

Generate free radicals. Intercalate in DNA → breaks in DNA → ↓ replication.

63
Q

Doxorubicin (Adriamycin), Daunorubicin Use

A

Solid tumors, leukemias, lymphomas.

64
Q

Doxorubicin (Adriamycin), Daunorubicin Toxicity

A

Cardiotoxicity (dilated cardiomyopathy), myelosuppression, alopecia. Toxic to tissues following extravasation.
Dexrazoxane (iron chelating agent), used to prevent cardiotoxicity.

65
Q

Bleomycin Mechanism

A

Induces free radical formation, which causes breaks in DNA strands.

66
Q

Bleomycin Use

A

Testicular cancer, Hodgkin lymphoma.

67
Q

Bleomycin Toxicity

A

Pulmonary fibrosis, skin changes, mucositis. Minimal myelosuppression.

68
Q

Alkylating Agents

A

Cyclophosphamide, Ifosfamide, Nitrosoureas (Carmustine, Lomustine, Semustine, Streptozocin), Busulfan

69
Q

Cyclophosphamide, Ifosfamide Mechanism

A

Covalently X-link (interstrand) DNA at guanine N-7. Require bioactivation by liver.

70
Q

Cyclophosphamide, Ifosfamide Use

A

Solid tumors, leukemia, lymphomas, and some brain cancers.

71
Q

Cyclophosphamide, Ifosfamide Toxicity

A

Myelosuppression; hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolites).

72
Q

Nitrosoureas

A

Carmustine, lomustine, Semustine, Streptozocin

73
Q

Carmustine, lomustine, Semustine, Streptozocin Mechanism

A

Require bioactivation. Cross blood-brain barrier → CNS. Cross-links DNA.

74
Q

Carmustine, lomustine, Semustine, Streptozocin Use

A

Brain tumors (including glioblastoma multiforme).

75
Q

Carmustine, lomustine, Semustine, Streptozocin Toxicity

A

CNS toxicity (convulsions, dizziness, ataxia).

76
Q

Busulfan Mechanism

A

Cross-links DNA.

77
Q

Busulfan Use

A

CML. Also used to ablate patient’s bone marrow before bone marrow transplantation.

78
Q

Busulfan Toxicity

A

Severe myelosuppression (in almost all cases), pulmonary fibrosis, hyperpigmentation.

79
Q

Microtubule Inhibitors

A

Vincristine, Vinblastine, Paclitaxel, Other Taxols

80
Q

Vincristine, Vinblastine Mechanism

A

Vinca alkaloids that bind β-tubulin, inhibit its polymerization into microtubules, thereby preventing mitotic spindle formation (M-phase arrest).

81
Q

Vincristine, Vinblastine Use

A

Solid tumors, leukemias, and lymphomas.

82
Q

Vincristine, Vinblastine Toxicity

A

Vincristine—neurotoxicity (areflexia, peripheral neuritis), paralytic ileus.
Vinblastine blasts bone marrow (suppression).

83
Q

Cisplatin, Carboplatin Mechanism

A

Cross-link DNA.

84
Q

Cisplatin, Carboplatin Use

A

Testicular, bladder, ovary, and lung carcinomas.

85
Q

Cisplatin, Carboplatin Toxicity

A

Nephrotoxicity and acoustic nerve damage. Prevent nephrotoxicity with amifostine (free radical scavenger) and chloride diuresis.

86
Q

Etoposide, Teniposide Mechanism

A

Etoposide inhibits topoisomerase II → ↑ DNA degradation.

87
Q

Etoposide, Teniposide Use

A

Solid tumors (particularly testicular and small cell lung cancer), leukemias, lymphomas.

88
Q

Etoposide, Teniposide Toxicity

A

Myelosuppression, GI irritation, alopecia.

89
Q

Irinotecan, Topotecan Mechanism

A

Inhibit topoisomerase I and prevent DNA unwinding and replication.

90
Q

Irinotecan, Topotecan Use

A

Colon cancer (irinotecan); ovarian and small cell lung cancers (topotecan).

91
Q

Irinotecan, Topotecan Toxicity

A

Severe myelosuppression, diarrhea.

92
Q

Hydroxyurea Mechanism

A

Inhibits ribonucleotide reductase → ↓ DNA Synthesis (S-phase specific).

93
Q

Hydroxyurea Use

A

Melanoma, CML, sickle cell disease (↑HbF).

94
Q

Hydroxyurea Toxicity

A

Bone marrow suppression, GI upset.

95
Q

Prednisone, Prednisolone Mechanism (Oncology)

A

May trigger apoptosis. May even work on nondividing cells.

96
Q

Prednisone, Prednisolone Use (Oncology)

A

Most commonly used glucocorticoids in cancer hemotherapy. Used in CLL, non-Hodgkin lymphomas (part of combination chemotherapy regimen). Also used as immunosuppressants (e.g., autoimmune diseases).

97
Q

Prednisone, Prednisolone Toxicity (Oncology)

A

Cushing-like symptoms; weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis.

98
Q

Tamoxifen, Raloxifene Mechanism (Oncology)

A

Selective estrogen receptor modulators (SERMs) receptor antagonists in breast and agonists in bone. Block the binding of estrogen to ER+ cells.

99
Q

Tamoxifen, Raloxifene Use (Oncology)

A

Breast cancer treatment (tamoxifen only) and prevention. Raloxifene also useful to prevent osteoporosis.

100
Q

Tamoxifen, Raloxifene Toxicity (Oncology)

A

Tamoxifen—partial agonist in endometrium, which ↑ the risk of endometrial cancer; “hot flashes.” Raloxifene—no ↑ in endometrial carcinoma because it is an endometrial antagonist.

101
Q

Trastuzumab (Herceptin) Mechanism

A

Monoclonal antibody against HER-2 (c-erbB2), a tyrosine kinase receptor. Helps kill breast cancer cells that overexpress HER-2, through inhibition of HER2-initiated cellular signaling and antibody-dependent cytotoxicity.

102
Q

Trastuzumab (Herceptin) Use

A

HER-2+ breast cancer and gastric cancer (tras2zumab).

103
Q

Trastuzumab (Herceptin) Toxicity

A

Cardiotoxicity.

104
Q

Imatinib (Gleevec) Mechanism

A

Tyrosine kinase inhibitor of bcr-abl (Philadelphia chromosome fusion gene in CML) and c-Kit (common in GI stromal tumors).

105
Q

Imatinib (Gleevec) Use

A

CML, GI stromal tumors.

106
Q

Imatinib (Gleevec) Toxicity

A

Fluid retention.

107
Q

Rituximab Mechanism

A

Monoclonal antibody against CD20, which is found on most B-cell neoplasms.

108
Q

Rituximab Use

A

Non-Hodgkin lymphoma, rheumatoid arthritis (with MTX), ITP.

109
Q

Rituximab Toxicity

A

↑ risk of progressive multifocal leukoencephalopathy

110
Q

Vemurafenib Mechanism

A

Small molecule inhibitor of forms of the B-Raf kinase with the V600E mutation.

111
Q

Vemurafenib Use

A

Metastatic melanoma.

112
Q

Bevacizumab Mechanism

A

Monoclonal antibody against VEGF. Inhibits angiogenesis.

113
Q

Bevacizumab Use

A

Solid tumors (colorectal cancer, renal cell carcinoma).

114
Q

Bevacizumab Toxicity

A

Hemorrhage and impaired wound healing.

Pharmacology (14 decks)

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