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Flashcards in Hem Onc Drugs Deck (86):
1

unfractionated heparin mechanism

- activates antithrombin
- inhibition of IIa (thrombin), Xa --> larger polysaccharides
- shorter half life

2

low MW heparin mechanism

- activates antithrombin
- inhibition of Xa >> IIa (thrombin) --> smaller polysaccharides
- longer half life

3

fondaparinux mechanism

- activates antithrombin
- inhibits Xa --> synthetic
- longer half life

4

SEs of heparin

- bleeding
- heparin induced thrombocytopenia (HIT)
- osteoporosis

5

heparin antidote

protamine (cationic molecule that binds up anionic heparin)

6

clinical use of heparin

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

7

labs to follow for heparin

PTT

8

warfarin mechanism

- interferes with gamma-carboxylation of vit K dependent factors II, VII, IX, X and proteins C and S
- vit K "antagonist"

9

labs to monitor for warfarin

PT INR (should be 2-3)

10

clinical use of warfarin

- prophylaxis for venous thromboembolism
- prevent stroke in a fib, a flutter

11

SEs of warfarin

- 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)

12

antidote for warfarin

vitamin K, fresh frozen plasma if it is urgent

13

heparin bridging

- 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

14

bivalirudin

direct thrombin (IIa) inh

15

argatroban

direct thrombin (IIa) inh

16

dabigatran

direct thrombin (IIa) inh

17

-aban drugs

direct Xa inh

18

mechanism of aspirin

- 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)

19

mechanism of clopidogrel, prasugrel

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

20

mechanism of -grelor drugs

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

21

GPIIb/IIIa inhibitors include:

abciximab
eptifibatide
tirofiban

22

mechanism of -plase drugs/streptokinase

- aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots

23

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

- alternatives to UFH for anticoagulation
- used in the case of heparin-induced thrombocytopenia

24

mechanism of -aban drugs

inhibit Xa

25

clinical use of -aban drugs

- treatment and prophylaxis for DVT, PE
- stroke prophylaxis for a. fib.

26

clinical use of -plase drugs/streptokinase

- early MI
- early ischemic stroke
- severe acute PE

27

How to treat -plase drug/streptokinase overdose?

- aminocaproic acid inhibits fibrinolysis
- fresh frozen plasma and cryoprecipitate to correct factor deficiencies

28

clinical use of aspirin

- antipyretic
- analgesic
- anti-inflammatory
- anti-platelet

29

SEs of aspirin

- gastric ulceration, tinnitus
- chronic: renal failure, interstitial nephritis, upper GI bleeding
- Reye's syndrome in kids with viral infxns
- mixed respiratory alkalosis/metabolic acidosis

30

clinical use of ADP receptor inhibitors

- acute coronary syndrome, coronary stenting
- decrease of recurrence of thrombotic stroke

31

SEs of ADP receptor inhibitors

neutropenia, TTP

32

mechanism of cilostazol, dipyridamole

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

33

clinical uses of cilostazol, dipyridamole

- intermittent claudication
- prophylaxis for strokes, TIAs, angina
- for coronary dilation

34

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

- unstable angina
- percutaneous transluminal coronary angioplasty

35

mechanism of cyclophosphamide, ifosfamide

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

36

SEs of cyclophosphamide, ifosfamide

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

37

mechanism of 6-mercaptopurine, 6-thioguanine

- 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 >> RNA

38

SEs of 6-MP, 6-TG

- myelosuppression, GI and liver toxicity
- 6-MP metabolized by xanthine oxidase, so don't give this drug with allopurinol for gout

39

mechanism of 5-fluorouracil (5-FU)

- requires lethal synthesis into 5' phosphate ribonucleotide
- covalently complexes folic acid, and this complex inhibits thymidylate synthase --> inhibits pyrimidine synthesis
- incorporates into RNA >> DNA

40

SEs of 5-FU

myelosuppression

41

mechanism of cytarabine

pyrimidine analogue --> inhibits DNA pol

42

SEs of cytarabine

leukopenia, thrombocytopenia ,megaloblastic anemia

43

mechanism of doxorubicin, daunorubicin, anthracyclin

intercalates DNA causing expansion and warping --> DNA breaks

44

SEs of doxorubicin, daunorubicin, anthracyclin

- dilated cardiomyopathy (dexrazoxane can prevent cardiotoxicity)
- myelosuppression
- alopecia

45

mechanism of bleomycin

binds to DNA to cause ss, ds DNA breaks

46

SEs of bleomycin

- pulmonary fibrosis
- skin hyperpigmentation
- mucositis
- mild myelosuppression

47

mechansim of dactinomycin

intercalates DNA

48

mechanism of -platin drugs

electrophilic molecules that cross-link DNA

49

clinical use of -platin drugs

testicular, bladder, ovary, lung carcinomas

50

SEs of -platin drugs

- nephrotoxicity (prevent with amifostine and saline diuresis)
- ototoxicity

51

mechanism of vincristine, vinblastine

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

52

SEs of vincristine, vinblastine

neurotoxicity, paralytic ileus

53

mechanism paclitaxel

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

54

clinical use of paclitaxel

ovarian, breast carcinomas

55

SEs of paclitaxel

- myelosuppression
- alopecia
- stocking/glove neuropathy

56

mechanism of -poside drugs

inhibition of topoisomerase II --> dsDNA breaks

57

SEs of -poside drugs

myelosuppression, GI upset, alopecia

58

mechanism of -tecan drugs

inhibition of topoisomerase I --> ssDNA breaks
prevents unwinding/replication

59

toxicity of -tecan drugs

- myelosuppression
- diarrhea

60

mechanism of hydroxyurea

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

61

SEs of hydroxyurea

- myelosuppression
- GI upset
- birth defects
- skin hyperpigmentation

62

mechanism of prednisone

anti-inflammatory glucocorticoid that alters gene transcription, suppresses lymphocytes

63

SEs of prednisone

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

64

mechanism of bevacizumab

monoclonal antibody against VEGF - inhibits angiogenesis

65

SEs of bevacizumab

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

66

mechanism of imatinib

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

67

clinical use of imatinib

- CML with 9:22 translocation
- GI stromal tumors

68

SEs of imatinib

fluid retention, fever, nausea

69

mechanism of rituximab

monoclonal ab. against CD20

70

SEs of rituximab

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

71

mechanism of tamoxifen

selective estrogen receptor modulator - ER antagonist in breast

72

clinical use of tamoxifen

ER+ breast cancer

73

SEs of tamoxifen

- endometrial cancer
- hot flashes, mood swings
- risk of thromboembolism

74

mechanism of bortezomib

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

75

mechanism of trastuzumab

monocloncal antibody against HER-2, a tyrosine kinase receptor

76

clinical use of trastuzumab

HER-2+ breast cancer and gastric cancer

77

SEs of trastuzumab

cardiotoxicity

78

GnRH agonists include:

leuprolide, histerelin, nafarelin

79

mechanism of GnRH agonists

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

80

clinical use of GnRH agonists

prostate cancer

81

GnRH antagonists include:

abarelix, triptorelin

82

mechanism of GnRH antagonists

no pituitary stimulation, so ultimately underproduction of testosterone

83

clinical use of GnRH antagonists

prostate cancer

84

mechanism of anastrozole

aromatase inhibitor, so less estrogen/testosterone production

85

clinical use of anastrozole

ER+, PR+ breast cancer

86

SEs of anastrozole

thromboembolism, osteoporosis