Hem/onc Pharm

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Heparin

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MOA: catalyzes binding of thrombin (IIa) and Factor Xa to Antithrombin III. Dec. levels of both Fact. Xa and Thrombin (IIa)

Use: Immediate anticoagulation (PE, CVA, acute coronary syndrome, MI, DVT). Safe for use during pregnancy.

Toxicity: Heparin Induced Thrombocytopenia (HIT), Bleeding, Osteoporosis

Reversal: Protamine (large pos. charged molecule binds to neg. charged heparin)

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Heparin Induced Thrombocytopenia (HIT)

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Heparin binds platelets via Platelet Factor 4. Causes autoantibody that destroys platelets and activates non-bound platelets. Hypercoagulable state with thrombocytopenia.

Monitoring: Prolongs aPTT.

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Warfarin (Coumadin)

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MOA: Blocks Vitamin K epoxide reductase in Liver. Keeps Vit. K sequestered in epoxide (unusable form). Dec. γ-carboxylation of Factors II, VII, IX, X, and Proteins C and S. Metabolized by cyt-P450 2C9.

Monitoring: Prolongs PT (extrinsic pathway), use INR to monitor.

Use: Chronic Oral Anticoagulation.

Toxicity: Teratogenicity (Do Not Use In Pregnancy), Bleeding, Skin/Tissue Necrosis (Coumadin-induced skin necrosis), Drug-Drug Interactions.

Reversal: Vitamin K

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Low Molecular Weight Heparins (LMWH)

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Less chance of HIT. No monitoring needed, SQ as opposed to IV, not easily reversed with protamine. If you need to monitor, monitor with Factor Xa (Thrombin not as much affected as Xa)

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Lepirudin/Bivalirudin

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MOA: Directly bind and inhibit thrombin

Use: anticoagulation for patients with a history of HIT.

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Streptokinase, Urokinase, tPA, APSAC

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Thrombolytics.
MOA: aid conversion of plasminogen to plasmin (directly or indirectly). Plasminogen cleaves fibrin clots.

Lab: Increases PT and aPTT. Plts: Nml

Use: MI or stroke (CVA) within 4 hours

Toxicity: Bleeding. NEVER use with patient who is or who could be bleeding.

Reversal: aminocaproic acid (inhibits conversion of plasminogen to plasmin)

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Aminocaproic Acid

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MOA: Inhibits conversion of plasminogen to plasmin

Use: Severe bleeding following tPA administration

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Aspirin (ASA)

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Drug Class: NSAIDs, Anti-platelets

MOA: Acetylates COX-1 & 2 to irreversibly inhibit and prevent conversion of arachidonic acid to TxA2.

Use: Antipyretic (fever-reducer), analgesic, anti-inflammatory, anti-platelets

Toxicity: Gastric Ulcers, Bleeding, Hyperventilation, Reye's syndrome (children), and tinnitus (CN VII)

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Clopidogrel, ticlopidine

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Drug Class: Anti-Platelets

MOA: Irreversibly blocks ADP receptors. This blocks GPIIb/IIIa expression and fibrinogen binding. Overall effect: prevent platelet aggregation

Use: Acute coronary syndrome, coronary stenting, dec. incidence of thrombosis

Toxicity: Neutropenia (ticlopidine)

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Abciximab

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Drug Class: Anti-Platelet

MOA: Monoclonal Ab that binds GP IIb/IIIa receptor. Overall effect is to block platelet aggregation

Use: Acute coronary syndromes, coronary angioplasty

Toxicity: Bleeding, thrombocytopenia

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Antineoplastics That Block Nucleotide Synthesis

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MTX, 5-FU: dec. thymidine synthesis

6MP: dec. purine synthesis

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Antineoplastics That Block DNA Synthesis

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Alkylating Agents and cisplatin: cross-link DNA

Dactinomycin, doxorubicin: intercalate DNA

Etoposide: inhibits topoisomerase II

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Antineoplastics That Block Cellular Division

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Vinca alkaloids: inhibit microtubule formation

Paclitaxel: inhibit microtubule disassembly

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Methotrexate (MTX)

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Works In: S-phase

Drug Class: Antimetabolite

MOA: Folic Acid Analog that Inhibits dihydrofolate reductase. Dec. in dTMP and therefore, dec. DNA synthesis.

Use: Leukemia, Lymphoma, choriocarinoma, sarcoma. Abortion, ectopic pregnancy, RA, psoriasis.

Toxicity: Myelosuppression (leucovorin reverses), Macrovesicular fatty change in liver. Folate deficiency --> Megaloblastic anemia

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Leucovorin (Folinic Acid)

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Use: Reverses Methotrexate Myelosuppression.

DOES NOT REVERSE 5-FU MYELOSUPPRESSION

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5-Fluorouracil (5-FU)

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Works in: S-Phase

Drug Class: Antimetabolite

MOA: Pyrimidine analog that covalently binds to folic acid. Complex inhibits thymidylate synthase. Overall effect: dec. dTMP, dec. DNA synthesis

Use: Colon Cancer & Solid Tumors, Basal Cell Carcinoma. Works well with Methotrexate

Toxicity: Myelosuppression. Photosensitivity.

Rescue: Thymidine

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6-Mercaptopurine (6-MP)

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Drug Class: Purine Analog

MOA: Blocks de novo Purine Synthesis. Activated by HGPRTase

Use: Leukemias, Non-Hodgkins Lymphoma.

Toxicity: Myelosuppression, GI, Liver. Metabolized by xanthine oxidase --> toxicity increased by allopurinol
**Not active against Hodgkin's lymphoma or CLL

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Cytarabine (ara-C)

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MOA: Inhibit DNA Polymerase

Use: AML, ALL, high-grade Non-Hodgkin's Lymphoma (NHL)

Toxicity: Leukopenia, thrombocytopenia, megaloblastoid anemia

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Cyclophosphamide, ifosfamide

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Active In: S-Phase

Drug Class: Alkylating Agents

MOA: Crosslinking of DNA (guanine N-7). Require bioactivation by liver.

Use: Non-Hodgkin's lymphoma, breast/ovarian carcinomas. Also used as an immunosuppressant.

Toxicity: HEMORRHAGIC CYSTITIS, Myelosuppression

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Cisplatin, Carboplatin

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Active In: S-Phase

Drug Class: Platinum Agents

MOA: Cross-link DNA (like alkylating agents)

Use: Testicular, Bladder, Ovary, and Lung Carcinomas.

Toxicity: Nephrotoxicity, ACOUSTIC NERVE DAMAGE

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Nitrosureas (Carmustine, lomustine, semustine, strtozocin)

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Active In: S-Phase

Drug Class: Alkylating Agents

MOA: Alkylate DNA. Require bioactivation in liver, CROSS BLOOD BRAIN BARRIER --> CNS

Use: Brain tumors

Toxicity: CNS toxicity

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Busulfan

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Active In: S-Phase

Drug Class: Alkylating Agents

MOA: Alkylates DNA

Use: CML or stem cell transplants

Toxicity: Pulmonary Fibrosis, Hyperpigmentation

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Doxorubicin (adriamycin), daunorubicin

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MOA: Generates Free Radicals. Intercalates in DNA (causes breaks in DNA & dec. DNA synthesis)

Use: Hodgkin's Lymphoma (Adriamycin is part of ABVD treatment regimen), also used for myelomas, sarcomas, and solid tumors (breast, ovary, lung)

Toxicity: CARDIOTOXICITY, myelosuppression, and marked alopecia.

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Dactinomycin (Actinomycin-D)

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MOA: Intercalates in DNA

Use: Wilm's tumor, Ewing's sarcoma, rhabdomyosarcoma

Toxicity: Myelosuppression

Mnemonic: ACTinomycin is used for children's tumors. (Children ACT out)

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Bleomycin

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Active in: G2 phase!

MOA: Free radical formation leads to breaks in DNA strands

Use: Testicular cancer, Hodgkin's Lymphoma (B of the ABVD treatment regimen)

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Hydroxyurea

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Active In: S-Phase

MOA: Inhibits Ribonucleotide Reductase (ribonucleotides to deoxynucleotides). Therefore, decreases DNA synthesis

Use: Melanoma, CML, SICKLE CELL DISEASE (inc. HbF)

Toxicity: Myelosuppression, GI irritation

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Etoposide

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Active in: G2 Phase!

Drug Class: Topoisomerase II Inhibitor

MOA: Topo-II Inhibitor and inc. DNA degradation

Use: Small cell carcinoma (lung and prostate), testicular carcinoma

Toxicity: Myelosuppression, GI irritation, alopecia

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Prednisone

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Drug Class: Corticosteroid

MOA: May trigger apoptosis. May work on non-dividing cells

Use: Most commonly used glucocorticoid in cancer cheotherapy and autoimmune diseases

Toxicity: Cushing's syndrome, immunosuppression, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis

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Tamoxifen, raloxifene

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Drug Class: Selective Estrogen Receptor Modulator (SERM)

MOA: Estrogen receptor antagonist in breast, estrogen receptor agonist in bone.

Use: Breast Cancer, Prevention of Osteoporosis

Toxicity: Inc. Risk of Endometrial carcinoma with Tamoxifen (not in raloxifene)

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Trastuzumab (Herceptin)

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Drug Class: Directed Antibody

MOA: Monoclonal Ab against HER-2 (erb-2). Helps kill breast cancer cells that overexpress HER-2 (ADCC).

Use: Metastatic Breast Cancer

Toxicity: Cardiotoxicity

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Imatinib (Gleevec)

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Drug Class: Targeted Antibody

MOA: bcr-abl Tyrosine Kinase Inhibitor

Use: CML, GI stromal tumors

Toxicity: Fluid Retention

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Vincristine, Vinblastine

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Active In: M-Phase

Drug Class: Vinca Alkaloids

MOA: Bind Tubulin and Block Microtubule Polymerization. Overall Effect: Block Mitotic Spindle Formation

Use: Hodgkin's Lymphoma (MOPP regimen (Oncovin)), Wilm's tumor, Choriocarcinoma

Toxicity: Vincristine: Neurotoxicity, Ileus; Vinblastine: Blasts Bone Marrow (Myelosuppression)

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Paclitaxel, other Taxols

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Active in: M-Phase

Drug Class: taxols

MOA: Bind Tubulin and Hyperstabilize. Overall effect: Mitotic Spindle can't break down. So cells are stuck in metaphase

Use: Ovarian/Breast Cancers

Toxicity: Myelosuppression