Anticoagulants: Warfarin
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Anticoagulants: Warfarin
Prerequisite basic sciences
Prerequisite basic sciences
Prerequisite basic sciences
Prerequisite basic sciences
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Anticoagulants: Warfarin
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Anticoagulants: Warfarin
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2016
Anticoagulant drugs p. 420
warfarin as p. 444
Bleeding
warfarin p. 444
Extrinsic pathway p. 206
warfarin and p. 444
Fresh frozen plasma p. 436
warfarin reversal p. 726
for warfarin toxicity p. 249
Heparin p. 443
warfarin vs p. 444
Hypercoagulability p. 696
warfarin adverse effect p. 444
Necrosis p. 207
warfarin p. 444
Prothrombin
warfarin effect on p. 444
Spontaneous abortion
warfarin p. 638
Stroke p. 529
warfarin for p. 444
Teratogens p. 638
warfarin as p. 444
Vitamin K
warfarin reversal p. 726
for warfarin toxicity p. 249, 444
Warfarin p. 444
adverse effects of p. 435
coagulation cascade p. 420
cytochrome P-448 and p. 253
for DVT p. 697
griseofulvin and p. 197
heparin vs p. 444
PT measurement p. 433
reversal of p. 726
teratogenicity p. 638
therapeutic index of p. 235
toxicity treatment p. 249, 436
vitamin K antagonist p. 69
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Transcript
Anticoagulant medications are used to prevent blood clots from forming. These medications work by interfering with the normal function of plasma proteins called coagulation factors, which take part in secondary hemostasis. But let’s focus specifically on the anticoagulant warfarin, which works by preventing the synthesis of coagulation factors II, VII, IX and X, and anticoagulation proteins C and S. Now, to understand the regulation of clot formation we first need to talk briefly about hemostasis-- in which hemo refers to the blood, and stasis means to halt or stop. Hemostasis is divided into two phases: primary and secondary hemostasis.
Primary hemostasis involves the formation of a platelet plug around the site of an injured blood vessel, and secondary hemostasis reinforces the platelet plug with the creation of a protein mesh called fibrin. To get to fibrin, a set of coagulation factors each of which or enzymes need to be activated. These enzymes are activated via a process called proteolysis- which is where a portion of the protein is clipped off. In total, there are twelve coagulation factors numbered factors I-XII, but there’s no factor VI. Most of these factors are produced by liver cells, and it turns out that producing coagulation factors II, VII, IX, and X requires an enzyme that uses vitamin K.
Now, when vitamin K is absorbed from the digestive tract and travels to the liver, it’s in its dietary form and it’s called vitamin K quinone. An enzyme, called quinone reductase, takes electrons from NADPH, and donates them to vitamin K quinone, converting it into the reduced form which is called vitamin K hydroquinone. Then, vitamin K hydroquinone acts as a cofactor by donating its electrons to an enzyme called gamma glutamyl carboxylase, which converts the non-functional forms of coagulation factors II, VII, IX, and X into their functional forms. Gamma glutamyl carboxylase adds a carboxyl group, which is a chemical group made up of one carbon, and two oxygens, onto the end of glutamic acid residues on the proteins.
Sources
- "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
- "Rang and Dale's Pharmacology" Elsevier (2019)
- "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
- "Overview of hemostasis" J.C. Aster, H. Bunn (Eds.), Pathophysiology of Blood Disorders, 2e. McGraw-Hill. (2016)
- "Nomograms" D. Nicoll, C. Mark Lu, S.J. McPhee (2017)
- "Ischemic Stroke: Risk Stratification, Warfarin Teatment and Outcome Measure" J Atr Fibrillation (2015)
- "Critical Issues and Recent Advances in Anticoagulant Therapy: A Review" Neurology India (2019)
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