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120 Cards in this Set

  • Front
  • Back
MOA of Heparin?
Catalyzes the activation of antithrombin III, ↓ thrombin and Xa. Short half-life.
Clinical use of Heparin?
Immediate anticoagulation for pulmonary embolism, stroke, angina, MI, DVT. Used
during pregnancy (does not cross placenta). Follow PTT.
Toxicity of Heparin?
Bleeding, thrombocytopenia, drug-drug interactions. For rapid reversal of
heparinization, use protamine sulfate (positively charged molecule that acts by
binding negatively charged heparin).
Advantages of newer low MW heparins?
Newer low-molecular-weight heparins (enoxaparin) act more on Xa, have better
bioavailability and 2–4 times longer half-life. Can be administered subcutaneously and without laboratory monitoring. Not easily reversible.
MOA of Warfarin (Coumadin)?
Interferes with normal synthesis and γ-carboxylation of vitamin K–dependent clotting factors II, VII, IX, and X and protein C and S. Affects EXtrinsic pathway and ↑ PT.

Remember: "The EX-PaTriot went to WAR(farin)"
The 1/2 life of Warfarin is.......
Clinical use of Warfarin?
Chronic anticoagulation. Not used in pregnant women (because warfarin, unlike heparin, cancross the placenta). Follow PT values.
Toxicity of Warfarin?
Bleeding, teratogenic, drug-drug interactions.
Heparin vs. Warfarin: structure?
H: large anionic polymer, acidic

W: small lipid-soluble molecule
Heparin vs. Warfarin: route of administration?
H: parenteral (IV, SC)

W: oral
Heparin vs. Warfarin: site of action?
H: blood

W: liver
Heparin vs. Warfarin: onset of action?
H: rapid (seconds)

W: slow, limited by half-lives of normal clotting factors
Heparin vs. Warfarin: MOA?
H: activates antithrombin III, which decreases the action of IIa (thrombin) and Xa

W: impairs the synthesis of vitamin K-dependent clotting factors II, VII, IX, and X (vitamin K antagonist)
Heparin vs. Warfarin: duration of action?
H: acute (hours)

W: chronic (weeks to months)
Heparin vs. Warfarin: do they inhibit coagulation in vitro?
H: yes

W: no
Heparin vs. Warfarin: treatment of acute overdose?
H: protamine sulfate

W: IV vitamin K and fresh frozen plasma
Heparin vs. Warfarin: monitoring?
H: PTT (intrinsic pathway)

W: PT (extrinsic pathway)
Heparin vs. Warfarin: crosses placenta?
H: no

W: yes (teratogenic)
What drugs are thrombolytics? (4)
-tPA (alteplase)
-APSAC (anistreplase).
MOA of thrombolytics?
Directly or indirectly aid conversion of plasminogen to plasmin, the major fibrinolytic enzyme, which cleaves thrombin and fibrin clots.
Clinical use of thrombolytics? (2)
Early MI
early ischemic stroke.
Toxicity of thrombolytics?
Bleeding: Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diathesis, or severe hypertension. Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis.
p. 316 figure:

what converts fibrinogen to fibrin?
what activates the breakdown of fibrinogen and fibrin?

what do they become?
plasmin activates the breakdown

fibrinogen --> degradation products
fibrin --> fibrin split products
What things activate the conversion of plasminogen to plasmin?
-streptokinase (via an activator)
What things inhibit the conversion of plasminogen to plasmin?
-aminocaproic acid*
when endothelium is damaged, what platelet factor binds to the exposed collagen?
what molecule binds to GP1b?
what platelet surface glycoprotein allows platelets to aggregate?

what molecule binds them together?

fibrinogen binds them
what drug is a monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets and thus prevent aggregation?
....see bottom right corner of figure on p.316...
Acetylates and irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) to prevent conversion of arachidonic acid to prostaglandins. ↑ bleeding time. No effect on PT,
Clinical use of ASA? (4)
-antiplatelet drug
Toxicity of ASA? (5)
-gastric ulceration
-Reye's syndrome
-tinnitus (CN VIII)
MOA of Clopidogrel and Ticlopidine?
Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogenbinding by preventing glycoprotein IIb/IIIa expression.
Clinical use of Clopidogrel and Ticlopidine?
Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of
thrombotic stroke.
Toxicity of Ticlopidine?
MOA of Abciximab?
Monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated
platelets, preventing aggregation
Clinical use of Abciximab? (2)
-acute coronary syndromes
-percutaneous transluminal coronary angioplasty
Toxicity of Abciximab? (2)
CA drugs -- site of action: Methotrexate + 5-FU
↓ thymidine synthesis
CA drugs -- site of action: 6-MP
↓ purine synthesis
CA drugs -- site of action: Cytarabine???
CA drugs -- site of action: Alkylating agents + cisplatin?
DNA cross-linkage
CA drugs -- site of action: Dactinomycin + Doxorubicin
DNA intercalation
CA dugs -- site of action: Bleomycin?
strand breakage + DNA intercalation
CA dugs -- site of action: Etoposide?
strand breakage
CA dugs -- site of action: steroids???
CA dugs -- site of action: Tamoxifen?
CA dugs -- site of action: Vinca alkaloids?
inhibit microtubule formation
CA drugs -- site of action: Paclitaxel?
inhibits microtubule disassembly
What CA drugs are cell cycle specific?
-antimetabolites (MTX, 5-FU, 6-MP)
-vinca alkaloids
What drugs are cell cycle nonspecific?
-alkylating agents
-antibiotics: dactinomycin, doxorubicin, bleomycin
What CA drugs inhibit the cell cycle at M phase?
-vinca alkaloids and toxols
Where do antimetabolites (anti-CA drugs) inhibit the cell cycle?
S phase: DNA synthesis
Where does Etoposide inhibit the cell cycle?
S phase (DNA synthesis) and G2 (synthesis of components needed for mitosis)
Where does Bleomycin inhibit the cell cycle?
G2: synthesis of components needed for mitosis
What happens during G1 phase of cell cycle?
synthesis of components needed for DNA synthesis
What happens during S phase of cell cycle?
DNA synthesis
What happens during G2 phase of cell cycle?
synthesis of components needed for mitosis
MOA of Methotrexate?
S-phase-specific antimetabolite.

Folic acid analog that inhibits dihydrofolate reductase, resulting in ↓ dTMP and therefore ↓ DNA and protein synthesis.
Clinical use of Methotrexate? (8)
ectopic pregnancy
rheumatoid arthritis
Toxicity of Methotrexate?
Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue.”

Macrovesicular fatty change in the liver.
MOA of 5-fluorouracil (5-FU)?
S-phase-specific antimetabolite.

Pyrimidine analog bioactivated to 5F-dUMP, which
covalently complexes folic acid. This complex inhibits thymidylate synthase, resulting in ↓ dTMP and same effects as MTX.
Clinical use of 5-fluorouracil?

Synergisitic with what?
Colon cancer and other solid tumors, basal cell carcinoma (topical).

Synergy with MTX.
Toxicity of 5-fluorouracil? (2)
Myelosuppression, which is NOT reversible with leucovorin.

What drug inhibits thymidylate synthase?
What is the action of thymidylate synthase?
converts dUMP --> dTMP
What drug inhibits DHF reductase?

What does this enzyme do?

DHF reductase converts DHF --> THF
MOA of 6-mercaptopurine (6-MP)?

What activates it?
Blocks de novo purine synthesis.

Activated by HGPRTase.
Clinical use of 6-MP?
-lymphomas (not CLL or Hodgkin's)
Toxicity of 6-MP?

What enzyme metabolizes it and, thus, what drug should it not be used with?
-bone marrow

Metabolized by xanthine oxidase; thus ↑ toxicity with allopurinol.
MOA of Cytarabine (ara-C)?
inhibits DNA polymerase
Clinical use of Cytarabine?
toxicity of Cytarabine?
-megaloblastic anemia
MOA of Cyclophosphamide and Ifosfamide?

How are these drugs activated?
Alkylating agents; covalently x-link (interstrand) DNA at guanine N-7.

Require bioactivation by liver.
Clinical uses of Cyclophosphamide and Ifosfamide?
-Non-Hodgkin’s lymphoma
-breast carcinomas
-ovarian carcinomas

Also immunosuppressants.
Toxicity of Cyclophophamide and Ifosfamide?
-hemorrhagic cystitis (can be partially prevented with mesna)
MOA of Nitrosoureas?
-what's required?
-do they enter the CNS?
Alkylate DNA.
Require bioactivation.
Cross blood-brain barrier → CNS.
Clinical use of Nitrosoureas?
brain tumors (including glioblastoma multiforme)
Toxicity of Nitrosoureas?
CNS toxicity (dizziness, ataxia)
MOA of Cisplatin and Carboplatin?
Act like alkylating agents.
Clinical uses of Cisplatin and Carboplatin? (4)
-Testicular CA
-Bladder CA
-Ovary CA
-Lung CA
Toxicity of Cisplatin and Carboplatin?
Nephrotoxicity and acoustic nerve damage.
MOA of Busulfan?
alkylates DNA
clinical use of Busulfan?
toxicity of Busulfan?
-pulmonary fibrosis
MOA of Doxorubicin (Adriamycin) and Daunorubicin?
Generate free radicals and noncovalently intercalate in DNA (creating breaks in DNA strand to ↓ replication).
Clinical use of Doxorubicin (Adriamycin) and Daunorubicin?
Part of the ABVD combination regimen for Hodgkin’s and for myelomas, sarcomas, and solid tumors (breast, ovary, lung).
Toxicity of Doxorubicin (Adriamycin) and Daunorubicin?
-also myelosuppression and marked alopecia

-toxic extravasation
MOA of Dactinomycin (actinomycin D)?
intercalates in DNA
Clinical use of Dactinomycin (actinomycin D)?
-Wilm's tumor
-Ewing's sarcoma
Toxicity of Dactinomycin (actinomycin D)?
mnemonic for Dactinomycin?
ACTinomycin D is used for childhood tumors (b/c children ACT out)
MOA of Bleomycin?
Induces formation of free radicals, which cause breaks in DNA strands.
Clinical use of Bleomycin?
-testicular cancer
-lymphomas (part of ABVD regimen for Hodgkin's)
Toxicity of Bleomycin?
-pulmonary fibrosis
-skin changes, but minimal myelosuppression
MOA of Etoposide (VP-16)?
G2-phase-specific agent that inhibits topoisomerase II and ↑ DNA degradation.
Clinical use of Etoposide (VP-16)? (3)
Small cell carcinoma of the lung and prostate

Testicular carcinoma.
Toxicity of Etoposide (VP-16)?
-GI irritation
MOA of Prednisone?
May trigger apoptosis. May even work on nondividing cells.
Clinical use of Prednisone?
Most commonly used glucocorticoid in cancer chemotherapy.

Used in CLL, Hodgkin’s lymphomas (part of the MOPP regimen).

Also an immunosuppressant used in autoimmune diseases.
Toxicity of Predisone? (9)
Cushing-like symptoms
peptic ulcers
MOA of Tamoxifen and Raloxifene?
Estrogen receptor mixed agonist/antagonists (“SERMs”) that block the binding of estrogen to estrogen receptor–positive cells.
Clinical uses of Tamoxifen and Raloxifen? (2)
Breast cancer.

Also useful to prevent osteoporosis.
Toxicity of Tamoxifen and Raloxifen?
-Tamoxifen may ↑ the risk of endometrial carcinoma via partial agonist effects

-“hot flashes.”
MOA of Trastuzamab (Herceptin)?
Monoclonal antibody against HER-2 (erb-B2).

Helps kill breast cancer cells that
overexpress HER-2, possibly through antibody-dependent cytotoxicity.
Clinical use?
metastatic breast CA
Clinical use of Trastuzamab (Herceptin)?
metastatic breast CA
Toxicity of Trastuzamab (Herceptin)?
MOA of Imatinib (Gleevec)?
myoclonal antibody against the Philadelphia chromosome brc-abl tyrosine kinase
Clinical uses of Imatinib (Gleevec)? (2)
-GI stromal tumors
Toxicity of Imatinib (Gleevec)?
fluid retention
MOA of Vincristine and Vinblastine?
M-phase-specific alkaloids that bind to tubulin and block polymerization of microtubules so that mitotic spindle cannot form.
Clinical use of Vincristine and Vinblastine? (3)
Part of the MOPP (Oncovin [vincristine]) regimen for lymphoma, Wilms’ tumor,
Toxicity of Vincristine and Vinblastine?
Vincristine––neurotoxicity (areflexia, peripheral neuritis), paralytic ileus.

VinBLASTine BLASTs Bone marrow (suppression).
MOA of Paclitaxel and other taxols?
M-phase-specific agents that bind to tubulin and hyperstabilize polymerized
microtubules so that mitotic spindle cannot break down (anaphase cannot occur).
Clinical use of Paclitaxel and other taxols?
ovarian and breast carcinomas
Toxicity of Paclitaxel and other taxols? (2)
What drugs are Nitrosoureas? (4)