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Pharmacology > Hem Onc Drugs > Flashcards

Hem Onc Drugs Flashcards

1
Q

unfractionated heparin mechanism

A
  • activates antithrombin
  • inhibition of IIa (thrombin), Xa –> larger polysaccharides
  • shorter half life
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2
Q

low MW heparin mechanism

A
  • activates antithrombin
  • inhibition of Xa&raquo_space; IIa (thrombin) –> smaller polysaccharides
  • longer half life
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3
Q

fondaparinux mechanism

A
  • activates antithrombin
  • inhibits Xa –> synthetic
  • longer half life
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4
Q

SEs of heparin

A
  • bleeding
  • heparin induced thrombocytopenia (HIT)
  • osteoporosis
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5
Q

heparin antidote

A

protamine (cationic molecule that binds up anionic heparin)

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6
Q

clinical use of heparin

A
  • PE
  • ACS - unstable angina, AMI
  • DVT
  • does not cross placenta, so good for pregnancy
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7
Q

labs to follow for heparin

A

PTT

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8
Q

warfarin mechanism

A
  • interferes with gamma-carboxylation of vit K dependent factors II, VII, IX, X and proteins C and S
  • vit K “antagonist”
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9
Q

labs to monitor for warfarin

A

PT INR (should be 2-3)

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10
Q

clinical use of warfarin

A
  • prophylaxis for venous thromboembolism

- prevent stroke in a fib, a flutter

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11
Q

SEs of warfarin

A
  • fetal warfarin syndrome - hypoplastic nose and limbs, flat face, altered calcification
  • warfarin skin necrosis - since protein C and S have shorter half-lives than the coagulation factors, there will be a state of initial hypercoagulability leading to thromboses in breast, buttocks, penis, extremities (most common in F who receive huge loading doses)
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12
Q

antidote for warfarin

A

vitamin K, fresh frozen plasma if it is urgent

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13
Q

heparin bridging

A
  • heparin given when starting warfarin for anticoagulation during initial hypercoagulable state caused by lack of protein C and S before lack of coagulation factors
  • to prevent warfarin skin necrosis
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14
Q

bivalirudin

A

direct thrombin (IIa) inh

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15
Q

argatroban

A

direct thrombin (IIa) inh

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16
Q

dabigatran

A

direct thrombin (IIa) inh

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17
Q

-aban drugs

A

direct Xa inh

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18
Q

mechanism of aspirin

A
  • irreversible inhibition of COX1 and COX2 by covalent acetylation
  • leading to impaired TXA2 production from arachidonic acid for the entire life of the platelet (platelets cannot synthesize more enzyme)
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19
Q

mechanism of clopidogrel, prasugrel

A

irreversible inhibitor of platelet adenosine (ADP) receptor to prevent platelet aggregation

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20
Q

mechanism of -grelor drugs

A

reversible inhibitor of platelet adenosine (ADP) receptor to prevent platelet aggregation

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21
Q

GPIIb/IIIa inhibitors include:

A

abciximab
eptifibatide
tirofiban

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22
Q

mechanism of -plase drugs/streptokinase

A
  • aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots
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23
Q

Clinical use of direct thrombin inhibitors (argatroban, bivalirudin, dabigatran)

A
  • alternatives to UFH for anticoagulation

- used in the case of heparin-induced thrombocytopenia

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24
Q

mechanism of -aban drugs

A

inhibit Xa

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25
Q

clinical use of -aban drugs

A
  • treatment and prophylaxis for DVT, PE

- stroke prophylaxis for a. fib.

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26
Q

clinical use of -plase drugs/streptokinase

A
  • early MI
  • early ischemic stroke
  • severe acute PE
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27
Q

How to treat -plase drug/streptokinase overdose?

A
  • aminocaproic acid inhibits fibrinolysis

- fresh frozen plasma and cryoprecipitate to correct factor deficiencies

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28
Q

clinical use of aspirin

A
  • antipyretic
  • analgesic
  • anti-inflammatory
  • anti-platelet
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29
Q

SEs of aspirin

A
  • gastric ulceration, tinnitus
  • chronic: renal failure, interstitial nephritis, upper GI bleeding
  • Reye’s syndrome in kids with viral infxns
  • mixed respiratory alkalosis/metabolic acidosis
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30
Q

clinical use of ADP receptor inhibitors

A
  • acute coronary syndrome, coronary stenting

- decrease of recurrence of thrombotic stroke

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31
Q

SEs of ADP receptor inhibitors

A

neutropenia, TTP

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32
Q

mechanism of cilostazol, dipyridamole

A

PDE3 inhibitors raise cAMP in platelets, resulting in inhibition of platelet aggregation and vasodilation

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33
Q

clinical uses of cilostazol, dipyridamole

A
  • intermittent claudication
  • prophylaxis for strokes, TIAs, angina
  • for coronary dilation
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34
Q

clinical use of GP IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban)

A
  • unstable angina

- percutaneous transluminal coronary angioplasty

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35
Q

mechanism of cyclophosphamide, ifosfamide

A
  • alkylating agents
  • strongly cationic drug cross-links negatively charged DNA
  • requires bioactivation by CYP450 in liver
36
Q

SEs of cyclophosphamide, ifosfamide

A
  • myelosuppression
  • immunosuppresion
  • hemorrhagic cystitis - acrolein, a byproduct of metabolism, is toxic (treated with mesna which binds up acrolein covalently)
37
Q

mechanism of 6-mercaptopurine, 6-thioguanine

A
  • require lethal synthesis into 5’ phosphate ribonucleotide (activation by HGPRT)
  • pseudo-feedback to decrease body’s normal purine synthesis (so much of a molecule that is structurally similar, body screws up and recognizes it as endogenous and doesn’t make more)
  • incorporated into DNA&raquo_space; RNA
38
Q

SEs of 6-MP, 6-TG

A
  • myelosuppression, GI and liver toxicity

- 6-MP metabolized by xanthine oxidase, so don’t give this drug with allopurinol for gout

39
Q

mechanism of 5-fluorouracil (5-FU)

A
  • requires lethal synthesis into 5’ phosphate ribonucleotide
  • covalently complexes folic acid, and this complex inhibits thymidylate synthase –> inhibits pyrimidine synthesis
  • incorporates into RNA&raquo_space; DNA
40
Q

SEs of 5-FU

A

myelosuppression

41
Q

mechanism of cytarabine

A

pyrimidine analogue –> inhibits DNA pol

42
Q

SEs of cytarabine

A

leukopenia, thrombocytopenia ,megaloblastic anemia

43
Q

mechanism of doxorubicin, daunorubicin, anthracyclin

A

intercalates DNA causing expansion and warping –> DNA breaks

44
Q

SEs of doxorubicin, daunorubicin, anthracyclin

A
  • dilated cardiomyopathy (dexrazoxane can prevent cardiotoxicity)
  • myelosuppression
  • alopecia
45
Q

mechanism of bleomycin

A

binds to DNA to cause ss, ds DNA breaks

46
Q

SEs of bleomycin

A
  • pulmonary fibrosis
  • skin hyperpigmentation
  • mucositis
  • mild myelosuppression
47
Q

mechansim of dactinomycin

A

intercalates DNA

48
Q

mechanism of -platin drugs

A

electrophilic molecules that cross-link DNA

49
Q

clinical use of -platin drugs

A

testicular, bladder, ovary, lung carcinomas

50
Q

SEs of -platin drugs

A
  • nephrotoxicity (prevent with amifostine and saline diuresis)
  • ototoxicity
51
Q

mechanism of vincristine, vinblastine

A

vinca alkaloids that bind B-tubulin and inhibit its polymerization into microtubules, preventing mitotic spindle formation (M phase arrest –> apoptosis)

52
Q

SEs of vincristine, vinblastine

A

neurotoxicity, paralytic ileus

53
Q

mechanism paclitaxel

A

prevents mitotic spindle breakdown, prevents depolymerization of tubulin after M phase

54
Q

clinical use of paclitaxel

A

ovarian, breast carcinomas

55
Q

SEs of paclitaxel

A
  • myelosuppression
  • alopecia
  • stocking/glove neuropathy
56
Q

mechanism of -poside drugs

A

inhibition of topoisomerase II –> dsDNA breaks

57
Q

SEs of -poside drugs

A

myelosuppression, GI upset, alopecia

58
Q

mechanism of -tecan drugs

A

inhibition of topoisomerase I –> ssDNA breaks

prevents unwinding/replication

59
Q

toxicity of -tecan drugs

A
  • myelosuppression

- diarrhea

60
Q

mechanism of hydroxyurea

A

inhibits ribonucleotide reductase - decrease in DNA synthesis (S phase specific)

61
Q

SEs of hydroxyurea

A
  • myelosuppression
  • GI upset
  • birth defects
  • skin hyperpigmentation
62
Q

mechanism of prednisone

A

anti-inflammatory glucocorticoid that alters gene transcription, suppresses lymphocytes

63
Q

SEs of prednisone

A

Cushings symptoms - weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, HTN, peptic ulcers, hyperglycemia, psychosis, immunosuppression, pancreatitis

64
Q

mechanism of bevacizumab

A

monoclonal antibody against VEGF - inhibits angiogenesis

65
Q

SEs of bevacizumab

A

hemorrhage, blood clots, impaired wound healing, flu-like symptoms

66
Q

mechanism of imatinib

A

tyrosine kinase inhibitor of BCR-ABL (Philly chromosome fusing gene in CML) and c-kit (gI stromal tumors)

67
Q

clinical use of imatinib

A
  • CML with 9:22 translocation

- GI stromal tumors

68
Q

SEs of imatinib

A

fluid retention, fever, nausea

69
Q

mechanism of rituximab

A

monoclonal ab. against CD20

70
Q

SEs of rituximab

A
  • progressive multifocal leukoencephalopathy

- activation of latent infections - run TB, HIV, hep tests before starting

71
Q

mechanism of tamoxifen

A

selective estrogen receptor modulator - ER antagonist in breast

72
Q

clinical use of tamoxifen

A

ER+ breast cancer

73
Q

SEs of tamoxifen

A
  • endometrial cancer
  • hot flashes, mood swings
  • risk of thromboembolism
74
Q

mechanism of bortezomib

A

reversible proteasome inhibitor - accumulation of unwanted proteins in cells –> apoptosis

75
Q

mechanism of trastuzumab

A

monocloncal antibody against HER-2, a tyrosine kinase receptor

76
Q

clinical use of trastuzumab

A

HER-2+ breast cancer and gastric cancer

77
Q

SEs of trastuzumab

A

cardiotoxicity

78
Q

GnRH agonists include:

A

leuprolide, histerelin, nafarelin

79
Q

mechanism of GnRH agonists

A

flare of testosterone production such that feedback prevents further production (chemical castration)

80
Q

clinical use of GnRH agonists

A

prostate cancer

81
Q

GnRH antagonists include:

A

abarelix, triptorelin

82
Q

mechanism of GnRH antagonists

A

no pituitary stimulation, so ultimately underproduction of testosterone

83
Q

clinical use of GnRH antagonists

A

prostate cancer

84
Q

mechanism of anastrozole

A

aromatase inhibitor, so less estrogen/testosterone production

85
Q

clinical use of anastrozole

A

ER+, PR+ breast cancer

86
Q

SEs of anastrozole

A

thromboembolism, osteoporosis

Pharmacology (22 decks)

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