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Drugs coumarin

T]ie active principles of there drugs are benzo-a-pyrones, which are further classified as  [Pg.125]


The orally effective anticoagulant drugs are fat-soluble derivatives of 4-hydroxycoumarin or indan-l,3-dione, and they resemble vitamin K. Warfarin is the oral anticoagulant of choice. The indandione anticoagulants have greater toxicity than the coumarin drugs. [Pg.260]

Unlike heparin, the primary advantage of coumarin drugs is that they are administered orally.72 However, because of the nature of their action, there is often a lag time of several days before the decreased production of clotting factors is sufficient to interrupt the clotting cascade and an anticoagulant effect is ap-... [Pg.351]

Commonly prescribed drugs can potentiate or antagonize the anticoagulant effect of coumarin drugs in several ways ... [Pg.989]

Feder W, Auerbach R. Purple toes an uncommon sequela of oral coumarin drug therapy. Ann Intern Med 1961 55 911-17. [Pg.994]

Born SL, Hu JK, and Lehman-McKeeman LD (2000) o-hydroxyphenylacetaldehude is a toxic metabolite of coumarin. Drug Metabolism and Disposition 28(2) 218-223. [Pg.676]

Laboratory tests can identify a faulty component of clotting or whether an elderly patient is required to alter coumarin drug or vitamin K dosages before a tooth is extracted. Samples of the patient s blood are taken and treated in various ways to allow the observation of the appropriate steps in the hemostasis pathways. For example, tissue factor is added to the blood sample for the prothrombin time (PT) test. Alternatively, certain clotting system components in the blood sample are removed or inactivated. These tests can be run quickly on small samples of blood. [Pg.200]

Since the epoxidized form of vitamin K is inactive, and the coumarin drugs therefore hinder the carboxylation reaction (Eq. 11.1) indirectly, it is theoretically incorrect to refer to them as vitamin K antagonists. On the other hand, it can be assumed that it is the structural congruity between the coumarin drugs and the K vitamins that enable them to inhibit the reducing enzyme diaphorase. [Pg.505]

Remark Coumarin drugs often contain phenol carboxylic acids, e.g. ferulic acid and caffeic acid, which also show blue fluorescence... [Pg.134]

Figure 3 Vitamin K oxidalion-reduclion ( de during Gla formation. Oxidation of vitamin K hydroquinone (reduced vitamin) to vitamin K epoxide by molecular oxygen provides the energy needed to drive the carboxylation of peptidyl-Glu to pepddyl-Gla (i.e., gamma-carboxy glutamate). The vitamin K epoxide is then recycled by reduction with dithiols in two stages. The first stage requires a reductase enzyme that is coumarin drug (e.g., warfarin) inhibitable. The second stage can be catalyzed by either of two reductases, one of which is NAD(P)H dependent and is not warfarin inhibited. Figure 3 Vitamin K oxidalion-reduclion ( de during Gla formation. Oxidation of vitamin K hydroquinone (reduced vitamin) to vitamin K epoxide by molecular oxygen provides the energy needed to drive the carboxylation of peptidyl-Glu to pepddyl-Gla (i.e., gamma-carboxy glutamate). The vitamin K epoxide is then recycled by reduction with dithiols in two stages. The first stage requires a reductase enzyme that is coumarin drug (e.g., warfarin) inhibitable. The second stage can be catalyzed by either of two reductases, one of which is NAD(P)H dependent and is not warfarin inhibited.

See other pages where Drugs coumarin is mentioned: [Pg.604]    [Pg.223]    [Pg.351]    [Pg.351]    [Pg.1202]    [Pg.95]    [Pg.96]    [Pg.506]    [Pg.506]    [Pg.507]    [Pg.125]    [Pg.127]    [Pg.129]    [Pg.131]    [Pg.139]    [Pg.141]    [Pg.143]    [Pg.145]    [Pg.147]    [Pg.354]    [Pg.616]    [Pg.222]    [Pg.95]    [Pg.1821]    [Pg.1130]    [Pg.84]    [Pg.489]    [Pg.86]   
See also in sourсe #XX -- [ Pg.35 , Pg.351 ]

See also in sourсe #XX -- [ Pg.125 , Pg.132 ]




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