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USMLE Step I Pharmacology > Hematology and Oncology Pharmacology > Flashcards

Hematology and Oncology Pharmacology Flashcards

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USMLE® Step 1 flashcards
1
Q

heparin–mechanism

A

lowers the activity of thrombin and factor Xa

short half life

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2
Q

heparin–use

A

immediate anticoagulation for pulmonary embolism (PE), acute coronary syndrome, MI, deep vein thrombosis (DVT),

used during pregnancy–does not cross placenta

follow PTT

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3
Q

heparin–toxicity

A

bleeding

thrombocytopenia (HIT)

osteoporosis

drug-drug interactions

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4
Q

heparin–antidote

A

use protamine sulfate–positively charged mc that binds negatively to heparin

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5
Q

what are the advantages/disadvantages to using low molecular weight heparins?

A

low molecular weight heparins–enoxaparin, dalteparin

advantages:

act more on factor Xa

have better bioavailability

2-4 times longer half life

can be administered subcutaneously and w/o lab monitoring

disadvantage:

not easily reversible

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6
Q

explain heparin induced thrombocytopenia (HIT)

A

development of IgG antibodies against heparin bound platelet factor 4 (PF4)

antibody heparin PF4 complex activates platelets –> thrombosis and thrombocytopenia

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7
Q

name the direct thrombin inhibitor

A

bivalirudin–related to hirudin, the anticoagulant used by leeches

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8
Q

direct thrombin inhibitor–mechanism

A

directly inhibits activity of free and clot-associated thrombin

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9
Q

direct thrombin inhibitor–use

A

venous thromboembolism

atrial fibrillation

can be used in HIT

doe not require lab monitoring

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10
Q

direct thrombin inhibitors–toxicity

A

bleeding

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11
Q

antidote for direct thrombin inhibitors

A

no specific reversal agent

can attempt to use activated prothrombin complex concentrates (PCC) and/or fibrinolytics (eg. transexamic acid)

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12
Q

warfarin–mechanism

A

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

metabolism affected by polymorphisms in the gene for vitamin K epoxide reductase complex (VKORCI)

in lab–effect on EXtrinsic pathway and inc PT, long half life

“the EX-President went to WAR(farin).”

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13
Q

warfarin–use

A

chronic anticoagulation–venous thromboembolism prophylaxis and prevention of stroke in atrial fibrillation

follow PT/INR

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14
Q

can warfarin be used in pregnant women? why?

A

no, b/c crosses placenta (unlike heparin)

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15
Q

warfarin–toxicity

A
  • bleeding
  • teratogenic
  • skin/tissue necrosis
  • drug-drug interactions
  • proteins C and S have shorter half lives than clotting factors II, VII, IX, X which results in early transient hypercoagulability with warfarin use
  • skin/tissue necrosis within first few days of large doses believed to be due ot small vessel microthromboses
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16
Q

antidote for warfarin

A

vitamin K

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17
Q

how would you rapidly reverse warfarin?

A

fresh frozen plasma

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18
Q

explain heparin “bridging”

A
  • heparin frequently used when starting warfarin
  • heparin’s activation of antithrombin enables anticoagulation during initial, transient hypercoagulable state caused by warfarin
  • initial heparin therapy reduces risk of recurrent venous thromboembolism and skin/tissue necrosis
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19
Q

compare and contrast heparin vs. warfarin

A
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20
Q

name direct factor Xa inhibitors

A

ApiXaban

rivatoXaban

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21
Q

direct factor Xa inhibitors–mechanism

A

bind to and directly inhibit factor Xa

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22
Q

direct factor Xa inhibitors–use

A
  • treatment and prophylaxis for DVT and PE (rivaroxaban)
  • prophylaxis in patients with atrial fibrillation
    • oral agents do not require coagulation monitoring
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23
Q

direct factor Xa inhibitors–toxicity

A

bleeding–no reversal agent is available

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24
Q

name the thrombolytics

A

Alteplase (tPA)

Reteplase (rPA)

streptokinase

tenecteplase (TNK-tPA)

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25
Q

thrombolytics–mechanism

A
  • directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots
    • inc PT
    • inc PTT
    • no change in platelet count
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26
Q

thrombolytics–use

A
  • early MI
  • early ischemic stroke
  • direct thrombolysis of severe PE
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27
Q

thrombolytics–toxicity

A
  • bleeding
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28
Q

when are thrombolytics contraindicated?

A
  • patients with:
    • active bleeding
    • history of intracranial bleeding
    • recent surgery
    • known bleeding diatheses
    • severe hypertension
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29
Q

how to treat toxicity of thrombolytics

A
  • aminocaproic acid, an inhibiotr or fibrinolysis
  • can also use fresh frozen plasma and cryoprecipitate to correct factor deficiencies
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30
Q

name the ADP receptor inhibitors

A

clopidogrel

prasugrel

ticagrelor (reversible)

ticlopidine

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31
Q

ADP receptor inhibitors–mechanism

A
  • inhibit platelet aggregation by irreversibly blocking ADP receptors
  • prevent expression of glycoproteins IIb/IIIa on platelet surface
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32
Q

ADP receptor inhibitors–use

A
  • acute coronary syndrome
  • coronary stenting
    • decrease incidence or recurrence of thrombotic stroke
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33
Q

ADP receptor inhibitors–toxicity

A
  • neutropenia (ticlopidine)
    • TTP may be seen
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34
Q

cilostazol, dipyridamole–mechanism

A
  • phosphodiesterase III inhibitor
  • inc cAMP in platelets
    • results in inhibition of platelet aggregation
  • vasodilators
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35
Q

cilostazol, dipyridamole–use

A
  • intermittent claudication
  • coronary vasdilation
  • prevention of stroke or TIAs (combined with aspirin)
  • angina prophylaxis
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36
Q

cilostazol, dipyridamole–toxicity

A
  • nausea
  • headache
  • facial flushing
  • hypotension
  • abdominal pain
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37
Q

name the glycoprotein IIb/IIIa inhibitors

A
  • abciximab
  • eptifibatide
  • tirofiban
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38
Q

glycoprotein IIb/IIIa inhibitors–mechanism

A
  • bind to the glycoprotein receptor IIb/IIIa on activated platelets
    • prevent aggregation
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39
Q

what is abciximab made from?

A

(glycoprotein IIb/IIIa inhibitors)

monoclonal antibody Fab fragments

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40
Q

glycoprotein IIb/IIIa inhibitors–use

A
  • unstable angina
  • percutaneous transluminal coronary angioplasty
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41
Q

glycoprotein IIb/IIIa inhibitors–toxicity

A
  • bleeding
  • thrombocytopenia
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42
Q

what are the anti-metabolite drugs?

A
  • azathiprine and 6-mercaptopurine
  • cladribine
  • cytarabine
  • 5-fluorouracil
  • methotrexate
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43
Q

azathiprine, 6-mercaptopurine–mechanism

A
  • purine analogs –> dec de novo purine synthesis
  • activated by HGPRT
    • azathioprine is metabolized into 6-MP
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44
Q

azathiprine, 6-mercaptopurine–use

A
  • prevent organ rejection
  • rheumatoid arthritis
  • IBD
    SLE
  • used to wean patients off steroids in chronic dz and to treat steroid refractory chronic disease
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45
Q

azathiprine, 6-mercaptopurine–toxicity

A
  • myelosuppression
  • GI
  • liver
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46
Q

how are azathiprine and 6-mercaptopurine metabolized, and how does this affect toxicity?

A
  • they are metabolized by xanthine oxidase
    • so, they have inc toxicity with allopurinol or febuxostat
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47
Q

cladribine–mechanism

A
  • purine analog
  • multiple mechanisms–inhibition of DNA polymerase, DNA strand breaks
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48
Q

cladribine–use

A
  • hairy cell leukemia
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49
Q

cladribine–toxicity

A
  • myelosuppression
  • nephrotoxicity
  • neurotoxicity
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50
Q

cytarabine (arabinofuranosyl cytidine)–mechanism

A
  • pyrimidine analog
  • inhibition of DNA polymerase
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51
Q

cytarabine (arabinofuranosyl cytidine)–use

A
  • leukemias (AML)
  • lymphomase
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52
Q

cytarabine (arabinofuranosyl cytidine)–toxicity

A
  • myelosuppression with megaloblastic anemia
  • CYTarabine causes panCYTopenia
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53
Q

5-fluorouracil–mechanism

A
  • pyrimidine analog bioactivated to 5-FdUMP–covalently complexes folic acid
    • this complex inhibits thymidylate synthase –> dec dTMP –> dec DNA synthesis
54
Q

5-fluorouracil–use

A
  • colon cancer
  • pancreatic cancer
  • basal cell carcinoma (topical)
    • effects enhanced with the addition of leucovorin
55
Q

5-fluorouracil–toxicity

A
  • myelosuppression
    • worsened with addition of leucovorin (folinic acid)
56
Q

methotrexate–mechanism

A
  • folic acid analog–competitively inhibits dihydrofolate reductase –> dec dTMP –> dec DNA synthesis
57
Q

methotrexate–use

A
  • cancers:
    • leukemias (ALL)
    • lymphomas
    • choriocarcinoma
    • sarcomas
  • non-neoplastic:
    • ectopic pregnancy
    • medical abortion (with misoprostol)
    • rheumatoid arthritis
    • psoriasis
    • IBD
    • vasculitis
58
Q

methotrexate–toxicity

A
  • myelosuppression
    • reversible with leucovorin “rescue”
  • hepatotoxicity
  • mucositis (ie. mouth ulcers)
  • pulmonary fibrosis
59
Q

name the antitumor antibiotics

A
  • bleomycin
  • dantinomycin (antinomycin D)
  • doxorubicin, daunorubicin
60
Q

bleomycin–mechanism

A

induces free radical formation –> breaks in DNA strands

61
Q

bleomycin–use

A
  • testicular cancer
  • Hodgkin lymphoma
62
Q

bleomycin–toxicity

A
  • pulmonary fibrosis
  • skin hyperpigmentation
  • minimal myelosuppression
63
Q

dactinomycin (actinomycin D)–mechanism

A

intercalates in DNA

64
Q

dactinomycin (ACTinomycin D)–use

A
  • Wilms tumor
  • Ewing sarcoma
  • rhabdomyosarcoma
  • used for childhood tumors
    • “children ACT out”
65
Q

dactinomycin (actinomycin D)–toxicity

A

myelosuppression

66
Q

doxorubicin, daunorubicin–mechanism

A
  • generate free radicals
  • intercalate in DNA –> breaks in DNA –> dec replication
67
Q

doxorubicin, daunorubicin–use

A
  • solid tumors
  • leukemias
  • lymphomas
68
Q

doxorubicin, daunorubicin–toxicity

A
  • cardiotoxicity (dilated cardiomyopathy)
  • myelosuppression
  • alopecia
69
Q

what can be used to prevent cardiotoxicity that may result from using doxorubicin, daunorubicin?

A

dexrazoxane–iron chelating agent

70
Q

name the alkylating agents

A
  • busulfan
  • cyclophosphamide, ifosfamide
  • nitrosoureas
    • carmustine
    • lomustine
    • semustine
    • streptozocin
71
Q

busulfan–mechanism

A

crosslinks DNA

72
Q

busulfan–use

A
  • CML
  • also used to ablate patient’s bone marrow before bone marrow transplantation
73
Q

busulfan–toxicity

A
  • severe myelosuppression–in almost all cases
  • pulmonary fibrosis
  • hyperpigmentation
74
Q

cyclophosphamide, ifosfamide–mechanism

A
  • cross link DNA at guanine N-7
    • require bioactivation by the liver
75
Q

cyclophosphamide, ifosfamide–use

A
  • solid tumors
  • leukemia
  • lymphomas
76
Q

cyclophosphamide, ifosfamide–toxicity

A
  • myelosuppression
  • hemorrhagic cystitis
77
Q

how can you prevent hemorrhagic cystitis that may result from using cyclophosphamide, ifosfamide?

A
  • prevented by using mesna (thiol group of mesna binds toxic metabolites) or N acetylcysteine
78
Q

nitrosoureas–mechanism

A
  • requires bioactivation
  • cross blood brain barrier –> CNS
    • cross link DNA
79
Q

nitrosoureas–use

A

brain tumors–including glioblastoma multiforme

80
Q

nitrosoureas–toxicity

A
  • CNS toxicity
    • convulsions
    • dizziness
    • ataxia
81
Q

name the microtubule inhibitors

A
  • paclitaxel, other taxols
  • vincristine, vinblastine
82
Q

paclitaxel, other taxols–mechanism

A
  • hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down
    • anaphase cannot occur
83
Q

paclitaxel, other taxols–use

A
  • ovarian carcinomas
  • breast carcinomas
84
Q

paclitaxel, other taxols–toxicity

A
  • myelosuppression
  • neuropathy
  • hypersensitivity
85
Q

vincristine, vinblastine–mechanism

A
  • vinca alkaloids that bind beta tubulin and inhibit its polymerization into microtubules –> prevent mitotic spindle formation
    • M phase arrest
86
Q

vincristine, vinblastine–use

A
  • solid tumors
  • leukemias
  • Hodgkin (vinblastine) lymphomas
  • non Hodgkin (vincristine) lymphomas
87
Q

vincristine, vinblastine–toxicity

A
  • vincristine
    • neurotoxicity–areflexia, peripheral neuritis
    • consipation–including paralytic ileus
88
Q

cisplatin, carboplatin–mechanism

A

cross link DNA

89
Q

cisplatin, carboplatin–use

A
  • testicular carcinomas
  • bladder carcinomas
  • ovary carcinomas
  • lung carcinomas
90
Q

cisplatin, carboplatin–toxicity

A
  • nephrotoxicity
  • peripheral neuropathy
  • ototoxicity
91
Q

how would you prevent nephrotoxicity that may result from use of cisplatin, carboplatin?

A
  • use amifostine (free radical scavenger) and chloride (saline) diuresis
92
Q

etoposide, teniposide–mechanism

A

eTOPOside inhibits topoisomerase II –> inc DNA degradation

93
Q

etoposide, teniposide–use

A
  • solid tumors
    • particularly testicular and small cell lung cancer
  • leukemias
  • lymphomas
94
Q

etoposide, teniposide–toxicity

A
  • myelosuppression
  • alopecia
95
Q

Irinotecan, topotecan–mechanism

A
  • inhibits topoisomerase I
  • prevents DNA unwinding and replication
96
Q

Irinotecan, topotecan–use

A
  • colon cancer (irinotecan)
  • ovarian and small cell lung cancers (topotecan)
97
Q

Irinotecan, topotecan–toxicity

A
  • severe myelosuppression
  • diarrhea
98
Q

hydroxyurea–mechanism

A

inhibits ribonucleotide reductase –> dec DNA Synthesis (S phase specific)

99
Q

hydroxyurea–use

A
  • melanoma
  • CML
  • sickle cell disease (inc HbF)
100
Q

hydroxyurea–toxicity

A

severe myelosuppression

101
Q

prednisone, prednisolone–mechanism

A
  • various
    • bind intracytoplasmic steroid receptor
    • alter gene transcription
102
Q

prednisone, prednisolone–use

A
  • most commonly used as glucocorticoids in cancer chemotherapy
  • used in CLL, non Hodgkin lymphomas
    • part of combination chemotherapy regimen
  • used as immunosuppressants
    • ie. in autoimmune diseases
103
Q

prednisone, prednisolone–toxicity

A
  • cushing like symptoms
    • weight gain
    • central obesity
    • muscle breakdown
    • cataracts
    • acne
    • osteoporosis
    • HTN
    • peptic ulcers
    • hyperglycemia
    • psychosis
104
Q

bevacizumab–mechanism

A
  • monoclonal antibody against VEGF
  • inhibits angiogenesis
105
Q

bevacizumab–use

A
  • solid tumors
    • colorectal cancer
    • renal cell carcinoma
106
Q

bevacizumab–toxicity

A
  • hemorrhage
  • blood clots
  • impaired wound healing
107
Q

erlotinib–mechanism

A
  • EGFR tyrosine kinase inhibitor
108
Q

erlotinib–use

A
  • non small cell lung carcinoma
109
Q

erlotinib–toxicity

A
  • rash
110
Q

cetuximab–mechanism

A
  • monoclonal antibody against EGFR
111
Q

cetuximab–use

A
  • stage IV colorectal cancer–wild type KRAS
  • head and neck cancer
112
Q

cetuximab–toxicity

A
  • rash
  • elevated LFTs
  • diarrhea
113
Q

imatinib–mechanism

A
  • tyrosine kinase inhibitor of BCR-ABL
    • Philadelphia chromosome fusion gene in CML
  • c-kit
    • common in GI stromal tumors
114
Q

imatinib–use

A
  • CML
  • GI stromal tumors
115
Q

imatinib–toxicity

A
  • fluid retention
116
Q

rituximab–mechanism

A
  • monoclonal antibody against CD20
    • found on most B cell neoplasms
117
Q

rituximab–use

A
  • non Hodgkin lymphoma
  • CLL
  • ITP
  • rheumatoid arthritis
118
Q

rituximab–toxicity

A
  • inc risk of progressive multifocal leukoencephalopathy
119
Q

tamoxifen, raloxifene–mechanism

A
  • selective estrogen receptor modulators (SERMs)
    • receptor antagonists in breast
    • receptor agonists in bone
  • block the binding of estrogen in ER + cells
120
Q

tamoxifen, raloxifene–use

A
  • breast cancer treatment (tamoxifen only) and prevention
  • raloxidene also used to prevent osteoporosis
121
Q

tamoxifen, raloxifene–toxicity

A
  • both drugs increase risk of thromboembolic events (ie. DVT, PE)
122
Q

tamoxifen–toxicity

A
  • partial agonist in endometrium
    • inc the risk of endometrial cancer
  • causes hot flashes
123
Q

raloxifene–toxicity

A
  • no in in endometrial carcinoma b/c it is an estrogen receptor antagonist in endometrial tissue
124
Q

trastuzumab (herceptin)–mechanism

A
  • monoclonal antibody against HER-2 (c-erbB2)–a tyrosine kinase receptor
    • helps kill cancer cells that overexpress HER-2 through inhibition of HER2-initiated cellular signaling and antibody dependent cytotoxicity
125
Q

trastuzumab (herceptin)–use

A

HER-2 + breast cancer and gastric cancer

(trans2zumab)

126
Q

trastuzumab (herceptin)–toxicity

A
  • cardiotoxicity
    • HEARTceptin damages the heart
127
Q

vemurafenib–mechanism

A
  • small molecule inhibitor of BRAF oncogene + melanoma
    • VEmuRAF-enib is for V600E-mutated BRAF inhibition
128
Q

vemurafenib–use

A
  • metastatic melanoma
129
Q

know the common chemotoxicities of the following:

  1. Cisplatin/Carboplatin
  2. Vincristine
  3. Bleomycin, Busulfan
  4. Doxorubicin
  5. Trastuzumab
  6. Cisplatin/Carboplatin
  7. CYclophosphamide
  8. 5-FU
  9. 6-MP
  10. Methotrexate
A
  1. Cisplatin/Carboplatin –> ototoxicity (and nephrotoxicity)
  2. Vincristine –> peripheral neuropathy
  3. Bleomycin, Busulfan –> pulmonary fibrosis
  4. Doxorubicin –> cardiotoxicity
  5. Trastuzumab –> cardiotoxicity
  6. Cisplatin/Carboplatin –> nephrotoxic (and acoustic nerve damage)
  7. CYclophosphamide –> hemorrhage cystitis
  8. 5-FU –> myelosuppression
  9. 6-MP –> myelosuppression
  10. Methotrexate –> myelosuppression
130
Q
A

USMLE Step I Pharmacology (17 decks)

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