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Hem Onc Drugs Flashcards

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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
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

Pharmacology (22 decks)

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