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Boards Antibiotics > Heme/Onc Pharm > Flashcards

Heme/Onc Pharm Flashcards

1
Q

What is the mechanism of Heparin?

A

Catalyzes the activation of AT3 which decreases Fx 2 and Xa

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2
Q

Half life of Heparin:

A

SHORT

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3
Q

What is heparin used for clinically?

A

IMMEDIATE anticoagulation for

  • PE
  • Stroke
  • Angina
  • MI
  • DVT
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4
Q

When can heparin be used/why?

A

Pregnancy - does not cross placenta

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5
Q

How is Heparin therapy monitored?

A

PTT

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6
Q

3 toxic side effects of heparin:

A

-Bleeding

-Thrombocytopenia (HIT)

-Drug interactions

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7
Q

Antidote for rapid reversal of Heparin; mechanism?

A

Protamine sulfate - pos charged molecule; binds highly neg charged Heparin

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8
Q

What is a LMWH?

A

Enoxaparin, Daltaparin

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9
Q

How do the LMWH’s act differently from Heparin?

A

More action on Xa than Thrombin; better bioavailability and 2-4 times longer half life

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10
Q

How can LMWH’s be administered?

A

Subcutaneously instead of only IV

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11
Q

What is the good thing about better bioavailability and half life of LMWH’s?

A

Don’t require lab monitoring with PTT

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12
Q

What is Warfarin’s clinical use?

A

CHRONIC longterm anticoagulation

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13
Q

When CAN’T Warfarin be used?

A

Pregnancy - teratotenic

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14
Q

Site of action of

  • Heparin
  • Warfarin
A

Heparin - blood

Warfarin - Liver

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15
Q

Onset of action of:

  • Heparin
  • Warfarin
A

Heparin - seconds

Warfarin - takes several days until the pre-existing clotting fxs are removed - half lives limit

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16
Q

4 Thrombolytic agents

A

Streptokinase
Urokinase
tPA
APSAC

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17
Q

Mechanism of thrombolytics:

A

Help convert Plasminogen to Plasmin to cleave Fibrin clots

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18
Q

2 clinical uses of thrombolytic agents:

A

-Early MI

-Early ischemic stroke

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19
Q

Toxicity of Thrombolytics:

A

Bleeding

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20
Q

What is the antidote for Thrombolytic TOXICITY?

A

Aminocaproic acid - fibrinolysis inhibitor

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21
Q

What is the rec on platelets for

  • collagen
  • vWF
  • Fibrinogen
  • TxA2/ADP/5-HT
A

Collagen is GP1a
vWF is GP1b
Fibrinogen is GP2b3a
Txa2/ADP/5HT all bind GP’s

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22
Q

What 2 drugs inhibit platelet synthesis of thromboxane?

A

Aspirin

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23
Q

What 3 drugs block GP2b/3a to prevent Fibrinogen crosslinking the platelet plug?

A
  • Abciximab
  • Eptifabatide
  • Tirofiban
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24
Q

What 4 drugs irreversibly block ADP receptors on platelets?

A
  • Clopidogrel
  • Ticlopidine
  • Prasugrel
  • Ticagrelor

(Note: these also block GP2b/3a to prevent Fibrinogen crosslinking the platelet plug)

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25
Q

What effect does blocking ADP receptors on Platelets have?

A

It inhibits the expression of GP2b/3a hence no fibrinogen crosslinking!

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26
Q

What are 2 clinical uses of Ticlopidine and Clopidogrel?

A

Acute coronary syndorme

Cardiac stenting

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27
Q

What toxic side effect does Ticlopidine have?

A

Neutropenia

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28
Q

What are the 3 antimetabolite cancer drugs?

A
  • Methotrexate
  • 5-Fluorouracil
  • 6-Mercaptopurine
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29
Q

How do MTX and 5-FU work?

A

Synergistically

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30
Q

What cell cycle phase are MTX and 5-FU both specific for?

A

S-phase - DNA synthesis

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31
Q

What is the mechanism of MTX?

A

-Folate analog

-Inhibits Di-HF reductase, Inhibits dTMP synth, DNA synth, and protein synthesis

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32
Q

What 4 cancers is MTX used for?

A

-Lymphomas

-Leukemias

-Choriocarcinoma

-Sarcomas

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33
Q

What are 4 non-neoplastic clinical uses of Methotrexate?

A

PEAR

  • Psoriasis
  • Ectopic pregnancy
  • Abortion
  • Rheumatoid arthritis
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34
Q

What are 2 toxic side effects of MTX and how is one treated?

A

-Macrovesicular Fatty Liver

-Myelosuppression - rescued with Leucovorin

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35
Q

What is the mechanism of 5-FU?

A

-Pyrimidine analog; bioactivated to 5F-Dump; covalently complexes Folate which inhibits Thymidylate Synthase.

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36
Q

And what is the effect of inhibiting thymidylate synthease?

A

Inhibits dTMP synth, DNA, and protein synthesis.

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37
Q

And what does giving MTX and 5-FU together allow for?

A

Synergistic inhibition of the same biochemical pathway (inhibiting dTMP syn, DNA, & protein synth)

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38
Q

What are 3 cancers that 5-Fluorouracil is used for?

A

-Colon cancers

-Other solid tumors

-Cream for Basal cell carcinoma

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39
Q

What are 2 side effects of 5-Fluorouracil?

A

-Photosensitivity

-Irreversible Myelosuppression

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40
Q

What has to be given to ‘rescue’ the myelosuppression due to 5-FU?

A

Thymidine

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41
Q

What is the other antimetabolite?

A

6-Mercaptopurine

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42
Q

How is 6-MP activated and what is its effect?

A

-Activated by HGPRTase

-Blocks de Novo Purine synthesis

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43
Q

What cancers can/can’t 6-MP be used for treating?

A

CAN treat Leukemia/Lymphoma

CAN’T treat CLL/Hodgkin lymphoma

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44
Q

What are 3 tissues that 6-MP has toxic effects on?

A

-Bone marrow

-GI tract

-Liver

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45
Q

What metabolizes 6-MP to its inactive form?

A

Xanthine oxidase

46
Q

So what can prevent 6-MP metabolism?

A

Allopurinol - careful!

47
Q

Drug for treating AML:

A

Cytarabine; ara-C

48
Q

What is the mechanism of Cytarabine?

A

INhibits DNA polymerase

49
Q

What are 3 toxic side effects of Cytarabine?

A

-Leukopenia

-Thrombocytopenia

-Megaloblastic anemia

50
Q

What type of agents are Cyclophosphamide and Ifosfamide?

A

Alkylating agents

51
Q

What is the mechanism of Cyclophosphamide and Ifosfamide? How are they activated?

A

-X-link DNA (interstrand) at Guanine-7 - Activated by Liver bioactivation

52
Q

What are the 4 clinical uses of Cyclophosphamide and Ifosfamide?

A

-NHL

-Breast cancer

-Ovarian cancer

-Immunosuppressant

53
Q

What are 2 toxic side effects of Cyclophosphamide and Ifosfamide?

A

-Myelosuppression

-Hemorrhagic cystitis

54
Q

How can the Hemorrhagic cystitis caused by Cyclophosph and Ifosfamide be prevented?

A

With MESNA

55
Q

What are the Nitrosoureas? 4

A

-Carmustine

-Lomustine

-Semustine

-Streptozocin

56
Q

What is the mechanism of the Nitrosoureas? What are they especially useful for?

A
  • Alkylate DNA

- Cross the BBB - so treat BRAIN TUMORS!

57
Q

What brain tumor do the nitrosoureas like Carmustine especially treat?

A

Glioblastoma multiforme

58
Q

What are the main toxic side effects of the Nitrosoureas?

A

CNS - toxicity and Ataxia

59
Q

How do Cisplatin and Carboplatin work?

A

LIKE alkylating agents

60
Q

What are the 4 cancers treated by Cisplatin and Carboplatin?

A

OBLT

  • Ovarian
  • Breast
  • Lung
  • Testicular
61
Q

What are 2 toxic side effects of Cisplatin and Carboplatin?

A

-Nephrotoxicity

-Acoustic nerve damage

62
Q

What drug is used for treating CML?

A

Busulfan

63
Q

What is the mechanism of Bulsulfan?

A

Alkylates DNA

64
Q

What are 2 toxic side effects of Busulfan?

A

-Pigmentation

-PULMONARY FIBROSIS

65
Q

So what are the 4 alkylating agents?

A

-Cyclophosphamide/Ifosfamide

-Nitrosoureas (Carmustine)

-Cisplatin/Carboplatin

-Busulfan

66
Q

What is Doxorubicin aka?

A

Adriamycin

67
Q

What is the mechanism of Doxorubicin and Daunorubicin? (3 steps)

A

-Generate FREE RADICALS

-INTERCALATE DNA

-CREATE BREAKS in DNA strand to inhibit replication

68
Q

What is Adriamycin used for?

A
  • ABVD regimen - Hodgkin lymphoma
  • Sarcomas
  • Myelomas
  • Other solid tumors (brst/ovary)
69
Q

What are 3 toxic side effects of Adriamycin/doxorubicin/daunorubicin?

A

-CARDIOtoxicity

-Marked Alopecia

-Myelosuppression

70
Q

What intercalator just intercalates and doesn’t cause strand breaks?

A

Dactinomycin

71
Q

What is Dactinomycin used for clinically?

A

CHILDHOOD tumors

  • Wilms tumor
  • Ewing’s sarcoma
  • Rhabdomyosarcoma
72
Q

What is the toxic side effect Dactinomycin can have?

A

Myelosuppression

73
Q

What drug is the B in the ABVD regimen for Hodgkin lymphoma?

A

Bleomycin

74
Q

What is Bleomycin’s mechanism?

A

Induces formation of free radicals - causes DNA strand breaks!

75
Q

What are 2 uses of Bleomycin then?

A

-Hodgkin lymphoma

-Testicular cancer

76
Q

What are 2 toxic effects of Bleomycin?

A

-PULMONARY FIBROSIS (bab)

-Skin changes

77
Q

What does Bleomycin cause MINIMALLY?

A

Myelosuppression

78
Q

What cell cycle phase is Bleomycin specific for?

A

G2

79
Q

What drug works on S and G2?

A

Etoposide

80
Q

What is Etoposide’s mechanism?

A

-Inhibits Topoisomerase II

-Increases DNA degradation

81
Q

What are 3 cancers Etoposide is used for?

A

-SCC of lung

-SCC of prostate

-Testicular cancer

82
Q

SE’s of Etoposide?

A

Normal

-GI upset, myelosuppress, alopecia

83
Q

What is the most commonly used Glucocorticoid in cancer therapy?

A

PREDNISONE

84
Q

What is Prednisone’s mechanism?

A

Triggers Apoptosis

85
Q

What are 2 cancers Prednisone is used for treating?

A
  • CLL

- Hodgkin’s lymphoma

86
Q

What are 9 side effects of Prednisone?

A

COACHH PIP

  • Cushing’s syndrome
  • Osteoporosis, Acne, Cataracts
  • Hypertension/Hyperglycemia
  • Peptic ulcers, Immunosuppress, Psychosis
87
Q

What are the main drugs for treating Estrogen receptor pos breast cancer?

A

Tamoxifen/Raloxifene

88
Q

How do Tamoxifen and Raloxifene work on the breast? Bone?

A

Breast Est antagonist

Bone Est agonist!

89
Q

So what are the 2 useful effects of Tamox/Raloxifene?

A
  • Slow Br cancer growth

- Slow osteoporosis!

90
Q

What are 2 toxic side effects of Tamoxifen specifically?

A

-Hot flashes

-May increase risk of endometrial carcinoma - agonist properties in the uterus

91
Q

Why doesn’t Raloxifene have this risk?

A

It’s an antagonist in the uterus

92
Q

What is Herceptin and what is it aka?

A

Trastuzumab - anti Her-2 (erb-B2)

93
Q

What is Trastuzumab used for?

A

HER-2 expressive Breast cancer

94
Q

What is a possible side effect of Trastuzumab?

A

Cardiotoxicity

95
Q

What is Imatinib aka?

A

Gleevac!

96
Q

What is Gleevac used for?

A

Inhibition of the Ph’ chromosome brc-abl fusion protein tyrosine kinase product

97
Q

So what 2 cancers are treated with Gleevac?

A

-CML

-GI stromal tumors

98
Q

What is a toxic side effect of Gleevac?

A

Fluid retention

99
Q

What are the ‘Vinca alkaloids’?

A

Vincristine and Vinblastine

100
Q

What is the mechanism of Vincristine/blastine; what cell cycle phase are they specific for?

A
  • Bind tubulin, block MT polymerization - mitotic spindle can’t form!
  • M-phase specific! Mitotic
101
Q

What are 3 clinical uses of Vincristine/blastine?

A
  • Wilm’s tumor
  • Lymphoma
  • Choriocarcinoma
102
Q

What are 2 side effects of:
-Vincristine

-Vinblastine

A

Cristine Neurotoxic/Paralytic ileus

Blastine Bone marrow suppression

103
Q

What is Paclitaxel?

A

A Taxol!

104
Q

What is the mechanism of Paclitaxel and other Taxols?

A

Bind tubulin and HYPERSTABILIZE polymerized MT’s so the mitotic spindle can’t BREAK DOWN!

105
Q

What cell cycle phase are the taxols specific for?

A

M-phase - prevent progression to anaphase

106
Q

What are 2 cancers for which the Taxols/Paclitaxel are used?

A

-Breast

-Ovarian

107
Q

What are 2 side effects of the Taxols?

A

-Myelosuppresion

-Hypersensitivity

108
Q

What are the drugs that act on MIcrotubules?

A

Maybe Taxes on Grease Vindicate Coalworkers!

  • Mabendazole
  • Taxols (Paclitaxel)
  • Griseofulvin
  • Vincristine/blastine
  • Colchicine
109
Q

What 2 drugs are the Phosphodiesterase III inhibitors?

A

Cilostazol & Dipyridamole

increase cAMP in platelets, thus inhibiting platelet aggregation; vasodilators

110
Q

MOA of Cilostazol & Dipyridamole?

A

Phosphodiesterase III inhibitors

- increase cAMP in platelets, thus inhibiting platelet aggregation; vasodilators

111
Q

Clinical use of Cilostazol & Dipyridamole?

A

Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined w/ Aspirin), angina prophylaxis

112
Q

Cilostazol & Dipyridamole – Toxicities?

A

Nausea, headache, facial flushing, hypotension, abdominal pain

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