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Step 1 Pharmacology > Hematology and Oncology > Flashcards

Hematology and Oncology Flashcards

1
Q

What is the mechanism of Heparin?

A

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

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2
Q

What is the clinical use of Heparin?

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

What is the toxicity of Heparin?

A

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

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4
Q

What are some additional key facts about Heparin?

A

Low-molecular-weight heparins (e.g., enoxaparin, dalteparin) 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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5
Q

Describe Heparin-induced thrombocytopenia (HIT).

A

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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6
Q

What are the key features of Argatroban and bivalirudin?

A

Derivatives of hirudin, the anticoagulant used by leeches; inhibit thrombin directly. Used instead
of heparin for anticoagulating patients with HIT.

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7
Q

What is the mechanism of Warfarin (Coumadin)?

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. In laboratory assay, has effect on Extrinsic pathway and ↑ PT. Long half-life.

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8
Q

What is the clinical use of Warfarin (Coumadin)?

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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9
Q

What are the toxicities of Warfarin (Coumadin)?

A

Bleeding, teratogenic, skin/tissue necrosis A, 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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10
Q

What are the direct factor Xa inhibitors?

A

Apixaban and rivaroxaban

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11
Q

What is the mechanism of direct factor Xa inhibitors?

A

Bind and directly inhibit the activity of factor Xa.

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12
Q

What is the clinical use of direct factor Xa inhibitors?

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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13
Q

What is the toxicity of direct factor Xa inhibitors?

A

Bleeding (no specific reversal agent available)

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14
Q

Compare the structure of Heparin to Warfarin.

A

Heparin - Large anionic, acidic polymer

Warfarin - Small lipid-soluble molecule

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15
Q

Compare the route of administration of Heparin to Warfarin.

A

Heparin - Parenteral (IV, SC)

Warfarin - Oral

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16
Q

Compare the site of action of Heparin to Warfarin.

A

Heparin - Blood

Warfarin - Liver

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17
Q

Compare onset of the of Heparin to Warfarin.

A

Heparin - Rapid (seconds)

Warfarin - Slow, limited by half-lives of normal clotting factors

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18
Q

Compare the mechanism of action of Heparin to Warfarin.

A

Heparin - Activates antithrombin, which ↓ the action of IIa (thrombin) and factor Xa
Warfarin - Impairs the synthesis of vitamin K–dependent clotting factors II, VII, IX, and X (vitamin K antagonist)

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19
Q

Compare the duration of action of Heparin to Warfarin.

A

Heparin - Acute (hours)

Warfarin - Chronic (days)

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20
Q

Do Heparin and Warfarin inhibit coagulation in vitro?

A

Heparin - Yes

Warfarin - No

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21
Q

Compare the treatment of acute overdose of Heparin to Warfarin.

A

Heparin - Protamine sulfate

Warfarin - IV vitamin K and fresh frozen plasma

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22
Q

Compare how Heparin and Warfarin are monitored.

A

Heparin - PTT (intrinsic pathway)

Warfarin - PT/INR (extrinsic pathway)

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23
Q

Do Heparin and Warfarin cross the placenta?

A

Heparin - No

Warfarin - Yes (teratogenic)

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24
Q

What are the Thrombolytics?

A

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

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25
Q

What is the mechanism of the thrombolytics?

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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26
Q

What is the clinical use of thrombolytics?

A

Early MI, early ischemic stroke, direct thrombolysis of severe PE.

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27
Q

What is the toxicity of thrombolytics?

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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28
Q

What is the mechanism of Aspirin (ASA)?

A

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

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29
Q

What is the clinical use of Aspirin (ASA)?

A

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

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30
Q

What is the toxicity of Aspirin (ASA)?

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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31
Q

What are the ADP receptor inhibitors?

A

Clopidogrel, ticlopidine, prasugrel, ticagrelor

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32
Q

What is the mechanism of ADP receptor inhibitors?

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

What is the clinical use of ADP receptor inhibitors?

A

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

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34
Q

What is the toxicity of ADP receptor inhibitors?

A

Neutropenia (ticlopidine). TTP/HUS may be seen.

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35
Q

What is the mechanism of Cilostazol and Dipyridamole?

A

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

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36
Q

What is the clinical use of Cilostazol and Dipyridamole?

A

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

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37
Q

What is the toxicity of Cilostazol and Dipyridamole?

A

Nausea, headache, facial flushing, hypotension, abdominal pain

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38
Q

What are the GP IIb/IIIa inhibitors?

A

Abciximab, eptifibatide, tirofiban

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39
Q

What is the mechanism of GP IIb/IIIa inhibitors?

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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40
Q

What is the clinical use of GP IIb/IIIa inhibitors?

A

Unstable angina, percutaneous transluminal coronary angioplasty.

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41
Q

What is the toxicity of GP IIb/IIIa inhibitors?

A

Bleeding, thrombocytopenia

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42
Q

Cancer drugs (cell cycle) - What part of the cell cycle does Bleomycin block?

A

G2 (synthesis of components needed for mitosis)

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43
Q

Cancer drugs (cell cycle) - What part of the cell cycle do Vinca alkaloids and taxols block?

A

M

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44
Q

Cancer drugs (cell cycle) - What part of the cell cycle do Antimetabolites block?

A

S (DNA synthesis)

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45
Q

Cancer drugs (cell cycle) - What parts of the cell cycle does Etoposide block?

A

G2 (synthesis of components needed for mitosis) and S (DNA synthesis)

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46
Q

Cancer drugs (cell cycle) - What drug blocks G1 (synthesis of components needed for DNA synthesis?

A

None

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47
Q

Antineoplastics - What drugs inhibit Nucleotide synthesis?

A

MTX, 5-FU: ↓ thymidine synthesis

6-MP: ↓ purine synthesis

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48
Q

Antineoplastics - What drugs block DNA?

A

Alkylating agents, cisplatin: cross-link DNA
Dactinomycin, doxorubicin: DNA intercalators
Etoposide: inhibits topoisomerase II

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49
Q

Antineoplastics - What drugs inhibit cell division?

A

Vinca alkaloids: inhibit microtubule formation

Paclitaxel: inhibits microtubule disassembly

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50
Q

Antimetabolites - What is the mechanism of Methotrexate (MTX)?

A

Folic acid analog that inhibits dihydrofolate reductase → ↓ dTMP → ↓ DNA and ↓ protein synthesis.
All anti-metabolites are S-phase specific.

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51
Q

Antimetabolites - What is the clinical use of Methotrexate (MTX)?

A

Cancers: leukemias, lymphomas, choriocarcinoma, sarcomas.

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

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52
Q

Antimetabolites - What are the toxicities of Methotrexate (MTX)?

A

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

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53
Q

Antimetabolites - What is the mechanism of 5-fluorouracil (5-FU)?

A

Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid.
This complex inhibits thymidylate synthase → ↓ dTMP → ↓ DNA and ↓ protein synthesis.
All anti-metabolites are S-phase specific.

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54
Q

Antimetabolites - What is the clinical use of 5-fluorouracil (5-FU)?

A

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

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55
Q

Antimetabolites - What are the toxicities of 5-fluorouracil (5-FU)?

A

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

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56
Q

Antimetabolites - What is the mechanism of Cytarabine (arabinofuranosyl cytidine)?

A

Pyrimidine analog → inhibition of DNA polymerase.

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57
Q

Antimetabolites - What is the clinical use of Cytarabine (arabinofuranosyl cytidine)?

A

Leukemias, lymphomas

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58
Q

Antimetabolites - What are the toxicities of Cytarabine (arabinofuranosyl cytidine)?

A

Leukopenia, thrombocytopenia, megaloblastic anemia. Cytarabine causes pancytopenia.

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59
Q

Antimetabolites - What is the mechanism of Azathioprine, 6-mercaptopurine (6-MP), and 6-thioguanine (6-TG)?

A

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

Activated by HGPRT.

60
Q

Antimetabolites - What is the clinical use of Azathioprine, 6-mercaptopurine (6-MP), and 6-thioguanine (6-TG)?

A

Preventing organ rejection, RA, SLE (azathioprine).

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

61
Q

Antimetabolites - What is the toxicity of Azathioprine, 6-mercaptopurine (6-MP), and 6-thioguanine (6-TG)?

A

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

62
Q

Antitumor antibiotics - What is the mechanism of Dactinomycin (actinomycin D)?

A

Intercalates in DNA

63
Q

Antitumor antibiotics - What is the clinical use of Dactinomycin (actinomycin D)?

A

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

64
Q

Antitumor antibiotics - What is the toxicity of Dactinomycin (actinomycin D)?

A

Myelosuppression.

65
Q

Antitumor antibiotics - What is the mechanism of Doxorubicin (Adriamycin) and daunorubicin?

A

Generate free radicals.

Intercalate in DNA → breaks in DNA → ↓ replication.

66
Q

Antitumor antibiotics - What is the clinical use of Doxorubicin (Adriamycin) and daunorubicin?

A

Solid tumors, leukemias, lymphomas.

67
Q

Antitumor antibiotics - What are the toxicities of Doxorubicin (Adriamycin) and daunorubicin?

A

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

68
Q

Antitumor antibiotics - What is the mechanism of Bleomycin?

A

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

69
Q

Antitumor antibiotics - What is the clinical use of Bleomycin?

A

Testicular cancer, Hodgkin lymphoma

70
Q

Antitumor antibiotics - What are the toxicities of Bleomycin?

A

Pulmonary fibrosis, skin changes, mucositis. Minimal myelosuppression.

71
Q

Alkylating agents - What is the mechanism of Cyclophosphamide and ifosfamide?

A

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

72
Q

Alkylating agents - What is the clinical use of Cyclophosphamide and ifosfamide?

A

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

73
Q

Alkylating agents - What are the toxicities of Cyclophosphamide and ifosfamide?

A

Myelosuppression; hemorrhagic cystitis, partially

prevented with mesna (thiol group of mesna binds toxic metabolites).

74
Q

Alkylating agents - What is the mechanism of Nitrosoureas (carmustine, lomustine, semustine,
streptozocin)?

A

Require bioactivation.

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

75
Q

Alkylating agents - What is the clinical use of Nitrosoureas (carmustine, lomustine, semustine,
streptozocin)?

A

Brain tumors (including glioblastoma multiforme).

76
Q

Alkylating agents - What are the toxicities of Nitrosoureas (carmustine, lomustine, semustine,
streptozocin)?

A

CNS toxicity (convulsions, dizziness, ataxia).

77
Q

Alkylating agents - What is the mechanism of Busulfan?

A

Cross-links DNA.

78
Q

Alkylating agents - What is the clinical use of Busulfan?

A

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

79
Q

Alkylating agents - What are the toxicities of Busulfan?

A

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

80
Q

Microtubule inhibitors - What is the mechanism of Vincristine and vinblastine?

A

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

81
Q

Microtubule inhibitors - What is the clinical use of Vincristine and vinblastine?

A

Solid tumors, leukemias, and lymphomas.

82
Q

Microtubule inhibitors - What are the toxicities of Vincristine and vinblastine?

A

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

83
Q

Microtubule inhibitors - What is the mechanism of Paclitaxel and other taxols?

A

Hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down (anaphase cannot occur).

84
Q

Microtubule inhibitors - What is the clinical use of Paclitaxel and other taxols?

A

Ovarian and breast carcinomas

85
Q

Microtubule inhibitors - What are the toxicities of Paclitaxel and other taxols?

A

Myelosuppression, alopecia, hypersensitivity.

86
Q

What is the mechanism of Cisplatin and carboplatin?

A

Cross-link DNA

87
Q

What is the clinical use of Cisplatin and carboplatin?

A

Testicular, bladder, ovary, and lung carcinomas

88
Q

What are the toxicities of Cisplatin and carboplatin?

A

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

89
Q

What is the mechanism of Etoposide and teniposide?

A

Etoposide inhibits topoisomerase II → ↑ DNA degradation

90
Q

What is the clinical use of Etoposide and teniposide?

A

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

91
Q

What are the toxicities of Etoposide and teniposide?

A

Myelosuppression, GI irritation, alopecia

92
Q

What is the mechanism of Irinotecan and topotecan?

A

Inhibit topoisomerase I and prevent DNA unwinding and replication

93
Q

What is the clinical use of Irinotecan and topotecan?

A

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

94
Q

What are the toxicities of Irinotecan and topotecan?

A

Severe myelosuppression, diarrhea

95
Q

What is the mechanism of Hydroxyurea?

A

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

96
Q

What is the clinical use of Hydroxyurea?

A

Melanoma, CML, sickle cell disease (↑ HbF)

97
Q

What are the toxicities of Hydroxyurea?

A

Bone marrow suppression, GI upset

98
Q

What is the mechanism of Prednisone and prednisolone?

A

May trigger apoptosis. May even work on nondividing cells.

99
Q

What is the clinical use of Prednisone and prednisolone?

A

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

100
Q

What are the toxicities of Prednisone and prednisolone?

A

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

101
Q

What is the mechanism of Tamoxifen and raloxifene?

A

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

102
Q

What is the clinical use of Tamoxifen and raloxifene?

A

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

103
Q

What are the toxicities of Tamoxifen and raloxifene?

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.

104
Q

What is the mechanism of Trastuzumab (Herceptin)?

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.

105
Q

What is the clinical use of Trastuzumab (Herceptin)?

A

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

106
Q

What are the toxicities of Trastuzumab (Herceptin)?

A

Cardiotoxicity.

107
Q

What is the mechanism of Imatinib (Gleevec)?

A

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

108
Q

What is the clinical use of Imatinib (Gleevec)?

A

CML, GI stromal tumors.

109
Q

What are the toxicities of Imatinib (Gleevec)?

A

Fluid retention

110
Q

What is the mechanism of Rituximab?

A

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

111
Q

What is the clinical use of Rituximab?

A

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

112
Q

What are the toxicities of Rituximab?

A

↑ risk of progressive multifocal leukoencephalopathy

113
Q

What is the mechanism of Vemurafenib?

A

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

114
Q

What is the clinical use of Vemurafenib?

A

Metastatic melanoma

115
Q

What is the mechanism of Bevacizumab?

A

Monoclonal antibody against VEGF. Inhibits angiogenesis

116
Q

What is the clinical use of Bevacizumab?

A

Solid tumors (colorectal cancer, renal cell carcinoma)

117
Q

What are the toxicities of Bevacizumab?

A

Hemorrhage and impaired wound healing

118
Q

What is the common toxicity of Cisplatin/Carboplatin?

A

Acoustic nerve damage (and nephrotoxicity)

119
Q

What is the common toxicity of Vincristine?

A

Peripheral neuropathy

120
Q

What is the common toxicity of Bleomycin and Busulfan?

A

Pulmonary fibrosis

121
Q

What is the common toxicity of Doxorubicin?

A

Cardiotoxicity

122
Q

What is the common toxicity of Trastuzumab?

A

Cardiotoxicity

123
Q

What is the common toxicity of Cisplatin/Carboplatin?

A

Nephrotoxic (and acoustic nerve damage)

124
Q

What is the common toxicity of Cyclophosphamide?

A

Hemorrhagic cystitis

125
Q

What is the common toxicity of 5-FU?

A

Myelosuppression

126
Q

What is the common toxicity of 6-MP?

A

Myelosuppression

127
Q

What is the common toxicity of Methotrexate?

A

Myelosuppression

128
Q

What prevents mast cell degranulation?

A

Cromolyn sodium (used for asthma prophylaxis)

129
Q

What is given to and Rh- mother during every pregnancy to prevent initial sensitization to Rh antigen?

A

Rho(D) immune globulin

130
Q

Thrombogenesis - What drug inhibits cyclooxygenase (TXA2 synthesis)?

131
Q

What drops inhibit ADP induced expression of GpIIb/IIIa?

A

Ticlopidine and clopidogrel

132
Q

What drug inhibits GpIIb/IIIa directly?

133
Q

What drug activates vWF to bind to GpIb?

A

Ristocetin

134
Q

What is the 1st lien of treatment for lead poisoning?

A

Dimercaprol and EDTA

135
Q

What is the treatment for Sideroblastic anemia?

A

Pyridoxine (B6, cofactor for δ-ALA synthase)

136
Q

What drugs cause folate deficiency?

A

Antifolates (e.g., methotrexate, trimethoprim, phenytoin)

137
Q

What drugs cause B12 deficiency (cobalamin)?

A

Proton pump inhibitors

138
Q

What is the treatment for Orotic aciduria?

A

Uridine monophosphate to bypass mutated enzyme

139
Q

What drugs cause Nonmegaloblastic macrocytic anemias?

A

5-FU, zidovudine, hydroxyurea

140
Q

What drugs cause aplastic anemia?

A

Benzene, chloramphenicol, alkylating agents, antimetabolites

141
Q

What drugs are used to treat aplastic anemia?

A

Antithymocyte globulin; cyclosporine

142
Q

What drugs treat Paroxysmal nocturnal hemoglobinuria?

A

Eculizumab

143
Q

What is seen with α-methyldopa?

A

Autoimmune hemolytic anemia

144
Q

What is Hairy cell leukemia treated with?

A

Cladribine (2-CDA), and adenosine analog (inhibits adenosine deaminase)

145
Q

What does Chronic myelogenous leukemia (CML) respond to?

A

Imatinib (a small-molecule inhibitor of the bcr-abl tyrosine kinase)

Step 1 Pharmacology (18 decks)

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