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piggy > Haematology - Pharmacology > Flashcards

Haematology - Pharmacology Flashcards

1
Q

What is the mechanism by which heparin anticoagulates?

A

It catalyzes the activation of antithrombin III and reduces levels of thrombin and factor Xa

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2
Q

How can you rapidly reverse the anticoagulation induced by heparin administration?

A

Give protamine sulfate, a positively charged molecule that binds negatively charged heparin

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3
Q

Compare enoxaparin and heparin.

A

Enoxaparin is more specific for factor Xa, has higher bioavailability, and 2-4 times longer half-life

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4
Q

What difference between heparin and enoxaparin should be considered when there is a concern of excessive anticoagulation?

A

Enoxaparin is not easily reversible, whereas heparin can be reversed by the administration of protamine sulfate; heparin also has a shorter half-life

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5
Q

What are the benefits of enoxaparin that allow it to be used in the outpatient setting, as opposed to heparin?

A

Enoxaparin can be administered subcutaneously, has a longer half-life, and does not need monitoring

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6
Q

Name four toxicities of heparin.

A

Bleeding, thrombocytopenia, osteoporosis, and drug-drug interactions

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7
Q

During pregnancy, is heparin or warfarin the preferred method of anticoagulation?

A

Heparin; unlike warfarin, which is a teratogen, heparin does not cross the placenta and thus can be used during pregnancy

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8
Q

What laboratory test can be used to determine if the heparin dose is in the therapeutic range?

A

The partial thromboplastin time, because heparin activates antithrombin III, which is involved in the intrinsic coagulation pathway

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9
Q

A 70-year-old woman is given prophylactic heparin while hospitalized for pneumonia. Five days later she develops deep vein thromboses and has a low platelet count. What disease is the likely cause of her sudden thrombocytopenic, hypercoagulable state?

A

Heparin-induced thrombocytopenia; this is an antibody-mediated process that destroys some platelets and overactivates those that remain

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10
Q

Name five clinical uses for heparin.

A

Immediate anticoagulation for pulmonary embolism, stroke, acute coronary syndrome, myocardial infarction, deep vein thrombosis

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11
Q

What is the mechanism of action of lepirudin or bivalirudin?

A

These are hirudin derivatives (an anticoagulant produced by leeches) that directly inhibit thrombin

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12
Q

A patient who was started on heparin therapy develops heparin-induced thrombocytopenia; what change should be made to his treatment regimen?

A

Discontinue the heparin and continue anticoagulation using lepirudin or bivalirudin (direct thrombin inhibitors)

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13
Q

What is the mechanism by which warfarin anticoagulates?

A

It interferes with normal synthesis and the gamma-carboxylation of the vitamin K-dependent clotting factors II, VII, IX, and X and proteins C and S

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14
Q

What laboratory test is used to determine if a patient taking warfarin is in the therapeutic range?

A

The prothrombin time will be increased because warfarin affects the EXtrinsic pathway (factor VII) (remember: the EX-PresidenTwent to WAR(farin))

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15
Q

What is the therapy of choice for patients who require chronic anticoagulation: heparin or warfarin?

A

Warfarin; this is preferred to heparin because it can be administered orally

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16
Q

Name four toxicities of warfarin.

A

Bleeding, teratogenic effects (contraindicated in pregnancy), drug-drug interactions, and skin/tissue necrosis

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17
Q

How is warfarin metabolized?

A

By the cytochrome P450 pathway in the liver

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18
Q

What is the difference in administration between heparin and warfarin?

A

Heparin is administered parenterally (intravenously or subcutaneously) whereas warfarin is given orally

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19
Q

What is the difference in the onset of action between heparin and warfarin?

A

Heparin acts within seconds, whereas warfarin has a slow onset dependent on the half-lives of the normal clotting factors

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20
Q

Describe the treatment of acute warfarin overdose.

A

Intravenous vitamin K and fresh frozen plasma

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21
Q

Name four drugs that can be used to lyse an existing thrombus.

A

Thrombolytics include streptokinase, urokinase, tissue plasminogen activator (alteplase), and anisoylated plasminogen streptokinase activator complex (anistreplase)

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22
Q

Which terminal pathway in the coagulation cascade is enhanced by the administration of thrombolytics?

A

Degradation of fibrin and fibrinogen to fibrin-split-products and deactivation of thrombin

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23
Q

What treatment option can potentially reverse the pathology of an early myocardial infarction or ischemic stroke?

A

Prompt administration of thrombolytics

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24
Q

What major complication can be seen from the administration of thrombolytics?

A

Bleeding

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25
Q

Name five contraindications for thrombolytics that are related to increased risk of bleeding.

A

Patients with active bleeding, a history of intracranial bleeding, recent surgery, known bleeding disorders, or severe hypertension

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26
Q

What is the pharmacologic treatment for thrombolytic toxicity?

A

Aminocaproic acid, an inhibitor of fibrinolysis; this medication can also be given to hemophiliacs for dental procedures

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27
Q

What is the primary enzymatic reaction that thrombolytics affect?

A

They either directly or indirectly aid the conversion of plasminogen to plasmin, which initiates fibrinolysis

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28
Q

How do thrombolytics affect the prothrombin time, partial thromboplastin time, and platelet count?

A

There is an increase in both the prothrombin time and partial thromboplastin time due to deactivation of thrombin, and no effect on the platelet count

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29
Q

How does abciximab downregulate platelet aggregation?

A

Abciximab is a monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, thereby preventing aggregation

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30
Q

What is the mechanism of action of aspirin as an anticoagulant?

A

Aspirin acetylates and irreversibly inhibits cyclooxygenase-1 and cyclooxygenase-2 to prevent the conversion of arachidonic acid to thromboxane A2

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31
Q

What is the effect of aspirin on bleeding time, prothrombin time, and partial thromboplastin time?

A

Aspirin increases bleeding time but has no effect on prothrombin time or partial thromboplastin time (it only affects platelets)

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32
Q

Name five common toxicities of aspirin.

A

Gastric ulceration, bleeding, hyperventilation, Reye;s syndrome, and tinnitus (cranial nerve VIII)

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33
Q

Name four clinical effects of aspirin administration.

A

Antipyretic, analgesic, antiinflammatory, and antiplatelet

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34
Q

What is the mechanism of action of clopidogrel and ticlopidine?

A

They inhibit platelet aggregation by irreversibly blocking adenosine diphosphate receptors; without adenosine diphosphate activation there is no glycoprotein IIb/IIIa expressed to bind fibrinogen

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35
Q

Name a potentially life-threatening toxicity of the antiplatelet drug ticlopidine.

A

Neutropenia

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36
Q

What are three common clinical uses of clopidogrel and ticlopidine?

A

Acute coronary syndrome, during coronary stenting, and reducing the incidence or recurrence of thrombotic stroke

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37
Q

Name a monoclonal antibody that binds the glycoprotein IIb/IIIa receptor on activated platelets and that prevents aggregation.

A

Abciximab

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38
Q

What are clinical uses of abciximab?

A

Coronary artery disease: acute coronary syndromes or during percutaneous transluminal coronary angioplasty

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39
Q

Name the two most common toxicities of abciximab.

A

Bleeding and thrombocytopenia

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40
Q

What occurs during stage G1 of the cell cycle?

A

The synthesis of components that are needed for DNA synthesis

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41
Q

What occurs during stage S of the cell cycle?

A

DNA synthesis

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42
Q

What occurs during stage G2of the cell cycle?

A

The synthesis of components that are needed for mitosis

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43
Q

What occurs during stage M of the cell cycle?

A

Mitosis

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44
Q

During which stage of the cell cycle do vinca alkaloids and taxols work?

A

M

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45
Q

During which stage of the cell cycle do antimetabolite drugs work?

A

S

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46
Q

During which stages of the cell cycle does etoposide work?

A

G2

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47
Q

During which stage of the cell cycle does bleomycin work?

A

G2

48
Q

Name three antineoplastic drugs that function by interfering with nucleotide synthesis.

A

Methotrexate, fluorouracil, and 6-mercaptopurine

49
Q

What reaction is inhibited by the administration of either methotrexate or fluorouracil?

A

The synthesis of thymidine, a pyrimidine

50
Q

What reaction is inhibited by the administration of 6-mercaptopurine?

A

The synthesis of purines

51
Q

Name five antineoplastic drugs that function by damaging DNA.

A

Alkylating agents, cisplatin, dactinomycin, doxorubicin, etoposide

52
Q

How do alkylating agents and cisplatin exert an antineoplastic effect?

A

These agents introduce cross-links in the DNA structure

53
Q

Which antineoplastic drugs interfere with DNA by intercalating into the double helix?

A

Doxorubicin, dactinomycin

54
Q

How does etoposide exert its antineoplastic effect?

A

Etoposide inhibits topoisomerase II, which is needed to relieve DNA supercoils

55
Q

Name two antineoplastic drugs that function by interfering with cellular division.

A

Vinca alkaloids, paclitaxel

56
Q

How do vinca alkaloids exert their antineoplastic effect?

A

They inhibit microtubule formation, which results in an inability of the cell to perform mitosis

57
Q

How does paclitaxel exert its antineoplastic effect?

A

Paclitaxel inhibits microtubule disassembly, which interrupts the dynamic process required for cell division

58
Q

What drug, used as an antineoplastic agent, is a folic acid analog that works by inhibiting dihydrofolate reductase?

A

Methotrexate; inhibiting dihydrofolate reductase results in less deoxythymidine monophosphate, which is needed for DNA and protein synthesis

59
Q

Name four cancers that methotrexate can be used to treat.

A

Leukemias, lymphomas, choriocarcinomas, and sarcomas (all have many dividing tumor cells)

60
Q

Name three nonneoplastic conditions in which methotrexate can be used.

A

Abortion in ectopic pregnancy (blocks cell proliferation), rheumatoid arthritis, and psoriasis (decreased immune proliferation and response)

61
Q

What agent can be administered to reverse the bone marrow suppression seen with methotrexate use?

A

Leucovorin (folinic acid) can be used to rescue the bone marrow by competing with methotrexate for binding sites; however, it does not reverse the effects of fluorouracil

62
Q

Other than myelosuppression, what are three toxicities of treatment with methotrexate?

A

Patients can develop a painful mucositis and microvesicular fatty changes in the liver, and it is a teratogen (remember: used for abortion in ectopic pregnancy)

63
Q

How does fluorouracil, a pyrimidine, interact with folic acid?

A

Fluorouracil is converted to 5F-dUMP, which covalently binds folic acid rendering it ineffective (noncompetitive inhibition)

64
Q

What enzyme is inhibited by the 5F-dUMP/folic acid complex?

A

This complex inhibits thymidylate synthase, which is needed to form deoxythymidine monophosphate for DNA and protein synthesis

65
Q

Often given in conjunction with methotrexate, fluorouracil is administered in the treatment of which tumors?

A

Colon cancer and solid tumors (it is a part of the FOLFOX regimen); it is applied topically for basal cell carcinoma

66
Q

A patient is given an excessive dose of fluorouracil; what can be administered to the patient to reduce toxicity?

A

Thymidine (remember: folinic acid will not reverse fluorouracil)

67
Q

What precaution should patients on fluorouracil take, especially in the summer?

A

Sun protection; fluorouracil can cause photosensitivity

68
Q

What is the mechanism by which 6-mercaptopurine and 6-thioguanine exert an antineoplastic effect?

A

These are purine analogs, which inhibit de novo purine synthesis; they are activated by hypoxanthine-guanine phosphoribosyltransferase

69
Q

6-mercaptopurine is used in the treatment of what types of cancers?

A

Leukemias and lymphomas (although not used in chronic lymphocytic leukemia or Hodgkin;s lymphoma)

70
Q

Which disease is treated using 6-thioguanine?

A

Acute lymphoblastic leukemia

71
Q

You are treating a patient with leukemia and are considering using either 6-mercaptopurine or 6-thioguanine. Which should be used if you are also going to treat with allopurinol to prevent tumor lysis syndrome?

A

6-thioguanine; 6-mercaptopurine is metabolized by xanthine oxidase, the enzyme blocked by allopurinol and may thus reach toxic levels if given together

72
Q

What adverse effects are seen in patients treated using 6-mercaptopurine or 6-thioguanine?

A

Bone marrow suppression and liver disease; patients on 6-mercaptopurine also often have gastrointestinal complaints

73
Q

How does cytarabine exert its antineoplastic effect?

A

It is a pyrimidine antagonist, which inhibits DNA polymerase (needed in S phase)

74
Q

What neoplasms are commonly treated using cytarabine?

A

Cytarabine is used to treat leukemias and lymphomas (acute myelogenous leukemia, acute lymphoblastic leukemia, and high-grade non-Hodgkin;s lymphoma)

75
Q

What are three adverse effects seen in the use of cytarabine?

A

Leukopenia, thrombocytopenia, and megaloblastic anemia

76
Q

Name three antineoplastic drugs that function by intercalating into DNA strands.

A

Dactinomycin (actinomycin D), daunorubicin, and doxorubicin work by intercalating in DNA strands, causing structural and functional distortions

77
Q

What are three neoplasms in which dactinomycin is commonly used?

A

Ewing sarcoma, Wilms; tumor, and rhabdomyosarcoma (think of childhood tumors: ACTinomycin D because children ACT out)

78
Q

Which of the antitumor antibiotics has the least myelosuppression as an adverse effect?

A

Bleomycin; myelosuppression is a common adverse effect of all other antitumor antibiotics

79
Q

What common mechanism is seen in the antineoplastic drugs bleomycin, daunorubicin, and doxorubicin?

A

These drugs generate free radicals, which can cause DNA strand breaks and halt cell replication

80
Q

Which malignancies are commonly treated with doxorubicin or daunorubicin?

A

Hodgkin;s lymphoma (the A in the ABVD regimen), myeloma, sarcoma, and solid tumors like breast, lung, or ovarian cancer

81
Q

A patient presents late in the course of chemotherapy treatments with new symptoms of heart failure; what antineoplastic drug was likely a part of his regimen?

A

Doxorubicin and daunorubicin are notorious for dose-dependent cardiotoxicity; patients may also develop alopecia or other tissue toxicity

82
Q

Name two neoplasms commonly treated with bleomycin.

A

Testicular cancer and Hodgkin;s lymphoma (the B in the ABVD regimen)

83
Q

After several rounds of chemotherapy, a patient complains of severe dyspnea and your exam fails to find symptoms of heart failure; what antitumor antibiotic is likely a part of his chemotherapy regimen?

A

Bleomycin, an antineoplastic agent that has the well-documented adverse effect of pulmonary fibrosis; you may also see skin changes as an adverse effect

84
Q

When does etoposide interfere with the cell cycle?

A

Between G2 and S phase; etoposide inhibits topoisomerase II, which is needed to uncoil DNA strands and synthesize a sister chromatid

85
Q

Name three neoplasms commonly treated using etoposide.

A

Small-cell carcinoma of the lung, small-cell carcinoma of the prostate, and testicular cancer

86
Q

Which chemotherapeutic drugs are most likely to cause alopecia as an adverse effect?

A

Doxorubicin, daunorubicin, and etoposide

87
Q

Which alkylating agent requires activation by the liver (and thus might not be effective in a patient with liver failure)?

A

Cyclophosphamide or ifosfamide; these cause DNA crosslinks at the 7 position of guanine

88
Q

Which alkylating agents are effective at penetrating the blood-brain barrier to access the central nervous system?

A

Nitrosoureas, including carmustine, lomustine, semustine, and streptozotocin

89
Q

Cyclophosphamide and ifosfamide are commonly used to treat which conditions?

A

These are used in breast cancer, ovarian cancer, and non-Hodgkin;s lymphoma; they are also used at lower doses as immunosuppressants

90
Q

A patient who has been receiving chemotherapy for breast cancer presents with dark urine and is found to have many red blood cells in urine; this could have been avoided using what medication?

A

Mesna; this patient has hemorrhagic cystitis from cyclophosphamide use

91
Q

Which alkylating agents are used especially in treating central nervous system neoplasms?

A

Nitrosoureas; since they penetrate the blood-brain barrier they are used to treat brain tumors like glioblastoma multiforme, but also have central nervous system toxicities like dizziness and ataxia

92
Q

Which alkylating agent would you choose in a patient about to undergo hematopoietic stem cell transplantation?

A

Busulfan, which will ablate the host bone marrow before transplantation; it is also used in the treatment of chronic myelogenous leukemia

93
Q

What toxicity is common to both busulfan and bleomycin?

A

Pulmonary fibrosis; both busulfan and bleomycin can result in lung disease

94
Q

Which antineoplastic drugs bind to tubulin during the M phase, inhibiting the formation of microtubules?

A

Vincristine or vinblastine; microtubules are the vines of your cells, and without them the mitotic spindle cannot form

95
Q

Name three neoplasms commonly treated using a vinca alkaloid (vincristine or vinblastine).

A

Hodgkin;s lymphoma (the MOPP regimen contains vincristine), Wilms; tumor, and choriocarcinoma

96
Q

What toxicities are associated with vincristine treatment?

A

Neurotoxicity, including areflexia and peripheral neuritis, as well as paralytic ileus

97
Q

What toxicity is associated with vinblastine treatment?

A

Bone marrow suppression (remember: vinBLASTine BLASTs Bone marrow)

98
Q

What antineoplastic drug functions by hyperstabilizing the mitotic spindle so that tumor cells are unable to complete anaphase?

A

PacliTAXel or other TAXols (remember: it is TAXing to stay polymerized [the microtubule stays polymerized])

99
Q

Which neoplasms are commonly treated using taxols?

A

Breast and ovarian carcinomas

100
Q

What are the clinical uses of cisplatin and carboplatin?

A

Testicular, bladder, ovary, and lung carcinomas

101
Q

Name two major toxicities of cisplatin and carboplatin.

A

Nephrotoxicity and acoustic nerve damage

102
Q

Which drug inhibits ribonucleotide reductase, acting during the S phase to decrease DNA synthesis?

A

Hydroxyurea

103
Q

What are the three clinical uses for hydroxyurea?

A

Melanoma, chronic myelogenous leukemia, and sickle cell disease (hydroxyurea increases concentration of hemoglobin F)

104
Q

What is the most commonly used glucocorticoid in cancer chemotherapy?

A

Prednisolone

105
Q

Which cancers have prednisone as part of their treatment regimen?

A

Chronic lymphocytic leukemia, Hodgkin;s lymphoma (MOPP regimen)

106
Q

How is prednisone thought to exert an antineoplastic effect?

A

Prednisone is thought to induce apoptosis, and may even affect nondividing cells

107
Q

Name two selective estrogen receptor modulators that are used to treat breast cancer.

A

Tamoxifen and raloxifene

108
Q

What is the primary mechanism of action of tamoxifen and raloxifene?

A

They are selective estrogen receptor modulators that block binding of estrogen to estrogen-receptor-positive cells

109
Q

A postmenopausal woman who recently started on a selective estrogen receptor modulator for breast cancer complains of vaginal spotting; what condition should you be concerned about?

A

Endometrial carcinoma; because of its partial agonist effects, tamoxifen increases the risk of endometrial carcinoma; raloxifene does not increase the risk of endometrial carcinoma

110
Q

Why is raloxifene not associated with an increased risk of endometrial carcinoma?

A

Raloxifene acts as an antagonist at the level of the endometrium; tamoxifen acts as an agonist (increasing endometrial cancer risk)

111
Q

The presence of what tumor marker would prompt you to use tamoxifen in the treatment of breast cancer?

A

Selective estrogen receptor modulators, like tamoxifen, act on the estrogen receptor, so the tumor should be estrogen receptor positive

112
Q

What treatment option is available in a patient who has metastatic breast cancer that is HER-2/erb-B2 positive?

A

Trastuzumab, a monoclonal antibody against HER-2

113
Q

What is the proposed mechanism of action of trastuzumab?

A

Helps kills breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity

114
Q

What organ should be monitored closely for adverse effects in a patient taking trastuzumab?

A

The heart; an adverse effect of trastuzumab therapy is cardiotoxicity

115
Q

What is the mechanism of action of imatinib?

A

This molecule binds to and inhibits the tyrosine kinase formed by the bcr-abl translocation found in chronic myelogenous leukemia

116
Q

What are the clinical uses for imatinib?

A

Chronic myelogenous leukemia and gastrointestinal stromal tumors (both express the bcr-abl tyrosine kinase)

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