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USMLE Step 1 > Heme/Onc Drugs > Flashcards

Heme/Onc Drugs Flashcards

1
Q

Heparin: Mechanism

A
  • cofactor for activation of antithrombrin
  • decreased thrombrin
  • decreased factor Xa
  • Short half life
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2
Q

Heparin: Clinical Use

A

Immediate anticoagulation for pulmonary embolism, 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), osteoporisis, drug-drug interactions.

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4
Q

Antidote for heparin toxicity (not to be confused with HIT)

A

Protamine sulfate - positively charged molecule that binds negatively charged heparin

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5
Q

Low molecular heparin (e.g. enoxaparin, dalteparin)

A

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

Lepirudin, Bivalirudin

A

derivatives of hirudin (anti-coagulant used by leeches)

  • inhibit thrombrin
  • used as an alternative to heparin for anti-coagulating patients with HIT
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7
Q

Heparin-induced thrombocytopenia

A

development of IgG antibodies against heparin bound to platelet factor 4 (PF4).
Antibody-heparin-PF4 activates platelets –> thrombosis and thrombocytopenia

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8
Q

Warfarin: Mechanism

A

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

  • BLOCKS Vitamin K
  • Metabolized by the cytochrome P-450 pathway
  • has effect on EXTRINSIC pathway and increase in PT
  • Long half-life
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9
Q

Warfarin: Clinical Use

A

Chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation).

Follow PT/ INR values

** Don’t use in pregnncy, because unlike heparin, warfarin can cross placents

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10
Q

Warfarin: Toxicity

A

Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions

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11
Q

Treatment to reverse warfarin overdose

A
  • Give vitamin K

- For rapid reversal of severe warfarin overdose, give fresh frozen plasma

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12
Q

Heparin

A
  • large anionic, acidic polymer
  • given parentally (IV, SC)
  • acts on blood
  • rapid onset
  • activates thrombrin, by decreasing action of IIa (thrombrin) and factor Xa
  • lasts for hours
  • inhibits coagulation in vitri
  • overdose treated with protamine sulfate
  • monitor PTT
  • doesn’t cross placenta
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13
Q

Warfarin

A
  • small lipid-soluble molecule
  • given orally
  • acts on liver
  • slow onset, limited by half lives of normal clotting factors
  • impairs synthesis of vitamin K-dependent clotting factors (II, VII, IX, X, proteins C and S)
  • Vitamin K antagonist
  • Lasts for DAYS
  • overdose treated with IV Vitamin K or fresh frozen plasma
  • Monitor extrinsic pathway (PTT/INR)
  • Teratogenic
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14
Q

Thrombolytics

A

Altepase (tPa), reteplase (rPA), tencteplase (TNK-tPA)

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15
Q

Thrombolytic: Mechanism

A

Directly or indirectly aid conversion of plasminogen to plasmi, which cleaves thrombin and fibrin clots.

Increases PT and PTT. NO CHANGE IN PLATELETS

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16
Q

Thrombolytics (“-eplase”): Clinical Use

A

Early MI, early ischemic stroke, direct thrombolysis of severe pulmonary embolism

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17
Q

Thrombolytics (“-eplase”): Toxicity

A

Bleeding.
Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diathesis, or severe hypertension

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18
Q

Tx of thrombolytic (“-eplase”) toxicity:

A

Aminocaproic acid - inhibitor of fibrinolysis

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19
Q

Aspirin: Mechanism

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 produce

  • Increased bleeding time, decreased thromboxane and prostaglandins
  • NO EFFECT on PT and PTT
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20
Q

Aspirin: Clinical Use

A

Antipyretic, analgesic, anti-inflammatory, antiplatelet (decreased aggregation)

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21
Q

Aspirin: Toxicity

A

Gastric ulceration, tinnitus (CN VIII).
Chronic used can lead to acute renal falire, interstitial nephritis, and upper GI bleeding

** Reye’s syndrome in children with with viral effection

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22
Q

Treatment of Apsitin toxicity

A

N-acetylation -

Aspirin toxicity is respiratory alkaltois and metabolic acidosis

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23
Q

ADP receptor inhibitos

A

Clopidogrel, Ticlipidine, Prasugrel, Ticagrelor

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24
Q

ADP Receptor Inhibitor: Mechanism

A

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

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25
Q

ADP receptor inhibitor: Clinical Use

A

Acute coronary syndrome
Coronary stenting
Decreased incidence or recurrence of thrombotic stroke

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26
Q

ADP Receptor Inhibitior: Toxicity

A

Neutropenia (ticlopidine)

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27
Q

Cliostazol, Dipyridamole: Mechanism

A

Phosphodiesterase III inhibitor;
Increased cAMP in platelets, thus inhibiting platelet aggregation
Vasodilators

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28
Q

Cliostazol, Dipyridamole: Clinical Use

A

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

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29
Q

Cliostazol, Dipyridamole: Toxicity

A

Nausea, headache, facial flushing, hypotension, abdominal pain

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30
Q

GP IIb/IIIa inhibitors

A

Abciximab, Eptifibatide, Tirofiban

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31
Q

GP IIb/IIIa Inhibitors (Abciximab, Eptifibatide, Tirofiban): Mechanism

A

Bind to the glycoprotein receptor IIb/IIa on activated platelets, preventing aggregation.

Abciximab is made from monoclonal antibody Fab fragments

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32
Q

GPIIb/IIIa inhibitors (Abciximab, Eptifibatide, Tirofiban): Clinical USe

A

Acute coronary syndromes, percutaneous transluminal coronary angioplasty

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33
Q

GPIIb/IIIa inhibitors (Abciximab, Eptifibatide, Tirofiban)

A

Bleeding, thrombocytopenia

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34
Q

Methotrexate (MTX): Mechanism

A

Folic acid analog that inhibits dihydrofolate reductase –> less dTMP –> less DNA and less protein synthesis

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35
Q

Methotrexate (MTX): Clinical Use

A

Cancers: leukemias, lymphomas, choriocarcinoma, sarcomas

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

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36
Q

Methotrexate (MTX): Toxicity

A

Myelosuppression, which is reversible with leucorvorin (folinic acid) “rescue”

Macrovesicular fatty chain in liver

  • Mucositis
  • Teratogenic
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37
Q

5-Fluorouracil (5-FU): Mechanism

A

Pyrimadine analog bioactivated to 5F-dUMP which covalently complexes folic acid.

This complex inhibits thymidylate synthase –> dTMP –> less DNA and protein synthesis

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38
Q

5-Fluorouracil (5-FU): Clinical Use

A

Colon cancer, basal cell carcinoma (topical)

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39
Q

5-Fluorouracil (5-FU): Toxicity

A

Myelosuppression, which is NOT reversible with leucorvorin

Overdose: “rescue” with thymidine

Photosensitivity

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40
Q

Cytarabine (arabinofuranoysl cytidine): Mechanism

A

Pyrimidine analog –> inhibition of DNA polymerase

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41
Q

Cytarabine: Clinical Use

A

Leukemias, lymphomas

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42
Q

Cytarabine: Toxicity

A

Leukopenia, thrombocytopenia, megaloblastic anemia

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43
Q

Azathoprine ; 6-mercaptopurine; 6-thioguanine : Mechanism

A

Purine (thiol) analogs –> decreased de novo purine synthesis

  • Activated by HGPRT
44
Q

Azathoprine; 6-mercaptopurine; 6-thioguanine: Clinical Use

45
Q

Azathoprine; 5-mercaptopurine; 6-thioguanine: Toxicity

A

Bone marrow, GI, liver

Metabolized by xanthine oxidase –> thus increase toxicity with allopurinol

46
Q

Dactinomycin (actinomycin D): Mechanism

A

Intercalates in DNA

47
Q

Dactinomycin (actinomycin D): Clinical Use

A

Wilm’s tumor, Ewing’s sarcoma, rhabdomyosarcoma

Used for childhood tumors (“children ACT out”)

48
Q

Dactinomycin (actinomycin D): Toxicity

A

Myelosuppression

49
Q

Doxorubicin (Adriamycin), Daunorubicin: Mechanism

A

Generate free radicals

Noncovalently interalate in DNA –> breaks in DNA –> decreased replication

50
Q

Doxorubicin (Adriamycin), Daunorubicin: Clinical Use

A

Solid tumors, leukemias, lymphomas

51
Q

Doxorubicin (Adriamycin), Daunorubicin: Toxicity

A

Cardiotoxicity (dilated cardiomyopathy), myelosuppression, Alopecia

Toxic to tissues following extravasation

Dexrazozane (Fe chelating agent), used to prevent cardiotoxicity

52
Q

Bleomycin: Mechanism

A

Induces free radical formation , which causes breaks in DNA

53
Q

Bleomycin: Clinical Uses

A

Testicular cancer, Hodgkin’s lymphoma

54
Q

Bleomycin: Toxicity

A

Pulmonary fibrosis, skin changes.

Minimal myelosuppression

55
Q

Cyclophosphamide; Ifosfamide: Mechanism

A

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

56
Q

Cyclophosphamide; Ifosfamide: Clinical Use

A

Solid tumors, leukemia, lymphomas, and some brain cancers

57
Q

Cyclophosphamide; Ifosfamide: Toxicity

A

Myelosuppression;

Hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolite)

58
Q

Nitrosoureas (carmustine, lomustine, semustine, streptozocin): Mechanism

A

Alkylating agent
Require bioactivation
Cross blood-brain barrier –> CNS

59
Q

Nitrosoureas (carmustine, lomustine, semustine, streptozocin): Clinical Use

A

Brain tumors (including glioblastoma multiforme)

60
Q

Nitrosoureas (carmustine, lomustine, semusine, streptozocin): Toxicity

A

CNS toxicity (dizziness, ataxia)

61
Q

Bulsulfan: Mechanism

A

Alkylates DNA

62
Q

Bulsulfan: Clinical Use

A

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

63
Q

Bulsulfan: Toxicity

A

Pulmonary fibrosis, hyperpigmentation

64
Q

Vincristine, Vinblastine: Mechanism

A

Alkaloids that bind to tubulin in M phase and block polymerization of microtubules so that mitotic spindle cannot form.

“Microtubules are the vines of your cells”

65
Q

Vincristine, Vinblastine: Clinical Use

A

Solid tumors, leukemias, and lymphomas

66
Q

Vincristine, Vinblastine: Toxicity

A

Vincristine - nephrotoxicity ( areflexia, peripheral neuritis), paralytic ileus

Vinblastine - myelosuppression

67
Q

Paclitaxel, other taxols: Mechanism

A

Hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot breakdown (anaphase cannot occur)

68
Q

Paclitaxel, other taxols: Clinical Use

A

Ovarian and breast carcinomas

69
Q

Paclitaxel, other taxols: Toxicity

A

Myelosuppression and hypersensitivity

70
Q

Cisplatin, carboplatin: Mechanism

A

Cross-link DNA

71
Q

Cisplatin, carboplatin: Clinical Use

A

Testicular, bladder, ovary, and lung carcinomas

72
Q

Cisplatin, carboplatin: Toxicity

A

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

73
Q

Etoposide, Tenoposide: Mechanism

A

Inhibit DNA topoisomerase II –> increased DNA degradation

74
Q

Etoposide: Tenoposide: Clinical Use

A

Solid tumors, leukemias, lymphomas

75
Q

Etoposide, Tenoposide: Toxicity

A

Myelosuppression, GI irritation

76
Q

Hydroxyurea: Mechanism

A

Inhibits ribonucleotide reductase –> less DNA Synthesis (S phase specific)

77
Q

Hydroxyurea: Clinical Use

A

Melanoma, CML, sickle cell disease (increase HbF)

78
Q

Hydroxyurea: Toxicity

A

Bone marrow suppression, GI upset

79
Q

Prednisone, Prenisolone: Mechanism

A

May trigger apoptosis. May even work on non-dividing cells.

80
Q

Prednisone, Prenisolone: Clinical Use

A

Most commonly used glucocorticoid in cancer chemotherapy. Used in CLL, non-Hodgkin’s lymphoma (part of combination chemotherapy regimen).

  • Also used as an immunosuppressant (e.g. autoimmune disease)
81
Q

Prednisone, Prenisolone: Toxicity

A

Cushing-like symptoms; immunosuppression, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis

82
Q

Tamoxifen, Raloxifene: Mechanism

A

SERMs- receptor antagonist in breast and antagonist in bone. Block the binding of estrogen to estrogen-positive cells

83
Q

Tamoxifen, Raloxifene: Clinical Use

A

Breast cancer treatment and prevention. Also useful to prevent osteoporosis

84
Q

Tamoxifen Toxicity

A

Partial agonist in endometrium, which increases risk of endometrial cancer , “hot flashes”

85
Q

Raloxifene: Toxicity

A

No increased risk of endometrial cancer because it is an endometrial antagonist

86
Q

Trastuzumab (Herceptin): Mechanism

A

Monoclonal antibody against HER-2 (cerbB2), tyrosine kinase. Helps kill breast cancer that overexpress HER-2, possibly through antibody-dependent cytotoxicity

87
Q

Trastuzumab (Herceptin): Clinical Use

A

HER-2 positive breast cancer

88
Q

Trastuzumab (Herceptin): Toxicity

A

Cardiotoxicity

89
Q

Imatinib (Gleevac): Mechanism

A

Philadelpha chromosome bcl-acr tyrosine kinase inhibitor

90
Q

Imatinib (Gleevac): Clinical Use

A

CML, GI stromal tumors

91
Q

Imatinib (Gleevac): Toxicity

A

Fluid retention

92
Q

Rituximab: Mechanism

A

Monoclonal antibody against CD20, which is found in B cell neoplasms

93
Q

Rituximab: Clinical Use

A

Non-Hodgkin’s lymphoma, rheumatoid arthritis (with methotrexate)

94
Q

Vemurafenib: Mechanism

A

Small molecule inhibitor of forms of B-RAF kinase with V600E mutation

95
Q

Vemurafenib: Clinical Use

A

Metastatic melanoma

96
Q

Bevacizumab: Mechanism

A

Monoclonal antibody against VEGF angiogenesis

97
Q

Bevacizumab: Clinical Use

A

Solid tumors

98
Q

Cisplatin/Carboplatin Toxicity

A

Acoustic nerve damage (and nephrotoxicity)

99
Q

Vinecristine: toxicity

A

Peripheral neuropathy

100
Q

Belomycin, Busulfan: Toxicity

A

Pulmonary fibrosis

101
Q

Doxorubicin: Toxicity

A

Cardiotoxicity

102
Q

Trastuzumab: Toxicity

A

Cardiotoxicity

103
Q

Cyclophosphamide

A

Hemorrhagic cystitis

104
Q

5-FU and 6-MP: Toxicity

A

Myelosuppression

105
Q

Methotrexate: Toxicity

A

Myelosuppression

USMLE Step 1 (34 decks)

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