pharm3-drug-chart by dandanhuanghuang

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									                 DRUG                                      MECHANISM
antimetabolites
folate antagonists
                                         1. inhibition of dihydrofolate reductase 2.
                                         decreased tetrahydrofolate              3.
e.g. methotrexate
                                         decreased purine/thymidine synthesis


purine antagonists
                                     1. inhibit enzyme activity catalyzing de novo
                                     purine synthesis                      2. act as
e.g. 6-mercaptopurine, 6-thioguanine
                                     purine base analogs

pyrimidine antagonists                   1. uracil analog converted to 5-FdUMP 2.
                                         FdUMP inhibits thymidylate synthase, inhibiting
e.g. 5-fluorouracil
                                         dTMP synthesis
ribonucleotide reductase inhibitor
                                         1. inhibition of ribonucleotide reductase,
e.g. hydroxyurea                         inhibiting DNA synthesis


DNA modifiers
alkylating agents
                                         1. cause DNA cross-linking                    2.
e.g. cyclophosphamide (nitrogen          results in DNA strand breakage
mustard)
platinum compounds                       1. converted to cytotoxic form                2.
e.g. cisplatin, carboplatin              cause DNA cross-linking
DNA intercalaters
                                         1. drugs insert between paired bases    2.
e.g. doxorubicin (anthrocyclin),
                                         inhibition of topoisomerase II       3. free
daunorubicin, bleomycin
                                         radical formation


topoisomerase inhibitors
                                         1. interfere with enzyme function        2.
e.g. irinotecan (Top I), toptecan (Top   block ligation of damaged DNA, causing
I), etoposide (Top II)                   permanent strand breaks          3. S phase-
                                         specific

microtubule inhibitors
vinca alkaloids
                                         1. inhibit tubulin polymerization
e.g. vincristine, vinblastine
taxanes                                  1. inhibit tubulin depolymerization      2. arrest
                                         cells in M phase
e.g. paclitaxel, docetaxel
hormonal agents
                               1. block estrogen receptors                 2.
estrogen antagonists
                               transcriptionally inactive -- cell growth &
e.g. tamoxifen                 proliferation inhibited
aromatase inhibitors           1. inhibit aromatase enzymatic activity 2.
e.g. anastrozole, letrozole    decrease estrogen production

androgen antagonists           1. competitive inhibition of androgen receptors
                               2. inhibit cell growth/proliferation
e.g. flutamide

                               1. inhibit lutenizing hormone (LH) secretion
GnRH receptor modulators
                               2. suppress testosterone production & cancer
                               growth
e.g. leuroprolide, goserelin


corticosteroids                1. inhibit lymphocyte proliferation        2.
                               induce atrophy of lymphoid tissues

e.g. prednisone

targeted anticancer agents
                               1. interferes with downstream signalling
tyrosine kinase inhibitors     pathways                               2.
                               impedes tumor growth
e.g. imatinib
                               1. inhibit enzymatic activity & downstream
                               pathways                       2. impede tumor
monoclonal antibodies
                               growth

e.g. rituximab                 1. inhibition/downregulation of GF-receptor
                               interaction-induced signaling
        INDICATIONS                     ADVERSE EFFECTS


ALL, head/neck carcinomas,
pediatric Burkitt's lymphoma, bone marrow suppression, GI
choriocarcinoma, breast       distress, alopecia, nephrotoxicity
cancer



                                 hepatotoxicity,
AML, ALL, CML
                                 myelosuppression, GI distress


breast, colorectal, GI, & skin   myeolosuppression, GI distress,
cancers                          alopecia


CML, ovarian cancer,
                                 myeolosuppression
melanoma




                                 hemorrhagic cystitis


                                 nephrotoxicity

ALL, AML, SCC, myeloma,          organ-specific:
neuroblastoma, various soft      doxorubicin/daunorubicin
tissue cancers, Hodgkin's        cardiotoxicity, bleomycin-
lymphoma                         induced pulmonary fibrosis




ovarian, testicular, colorectal, alopecia, myelosuppression,
& lung cancer, leukemia          diarrhea




hematologic cancers, lung
                                 neurotoxicity
cancers
breast, ovarian, prostate, &
                                 neurotoxicity
non-small cell lung cancers
breast cancer                hot flashes, nausea, vomiting




                             impotence, gynecomastia, GI
prostate cancer
                             distress




hematologic malignancies
(lymphocytic leukemias,
                             immunosuppression
lymphomas, multiple
myeloma)




CML, GI stromal tumor, Ph+   myelosuppression, nausea,
ALL                          vomiting, fluid retention



B-cell non-Hodgkin's         IV-related reactions,
lymphoma                     myelosuppression
                DRUG                                                         MECHANISM
adrenal corticosteroids
glucocorticoids

                                     METABOLIC EFFECTS
e.g. cortisol (hydrocortisone),
                                     1. increase blood glucose level           2.
prednisolone, methylpredisolone,
                                     increase amino acid level                3.
predisone, triamcinolone,
                                     promote lipolysis (increased activity of
beclomethasone, betamethasone,
                                     hormone-sensitive lipase)
dexamethasone, fluticasone


mineralocorticoids                   1. regulate Na reabsorption in kidney, colon,
                                     sweat/salivary glands                   2.
                                     promotes Na retention & K excretion by
e.g. aldosterone (endogenous, non-
                                     increasing Na channels in apical membrane
therapeutic), fludrocortisone
                                     & Na/K ATPase pumps in basolateral
                                     membrane
MECHANISM                                                                             INDICATIONS


    ANTI-INFLAMMATORY EFFECTS               1.
                                                                              Adrenal insufficiency
    suppress T cell activation & cytokine
                                                 receptors broadly            replacement, Cushing's
    production                            2.
                                                 distributed thru tissue,     sydrome diagnosis,
    decrease release of inflammatory mediators
                                                 high affinity for cortisol   Inflammation, allergy,
    (histamine, PGs, leukotrienes)
                                                 ONLY                         autoimmune disease,
    3. decrease capillary permeability &
                                                                              dermatologic conditions
    promote vasoconstriction



                                                 receptors specific to
                                                                            adrenal insufficiency
                                                 excretory organs, high
                                                                            replacement therapy
                                                 affinity for both cortisol
                                                                            (Addison's disease)
                                                 & aldosterone
      ADVERSE EFFECTS


iatrogenic Cushing's,
hyperglycemia/diabetes, HTN,
Na retention, hypokalemia,
increased susceptibility to
infection, osteoporosis, growth
retardation, mood change,
cataracts/glaucoma




HTN, hypokalemia, heart
failure

								
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