ANTICOAGULANTES: TIPOS, MECANISMOS, USOS CLÍNICOS Y RIESGOS VILLAMEDIC 2026

Anticoagulants are essential medications in internal medicine, cardiology, emergency medicine, and primary care because they prevent the formation and progression of blood clots that can cause venous thrombosis, pulmonary embolism, stroke, and acute myocardial infarction. In this video, we systematically review what anticoagulation is, how the different groups of anticoagulants work, and how to use them safely in clinical practice for students, interns, residents, and on-call physicians. We begin by defining anticoagulation as a pharmacological measure aimed at preventing the growth of an existing blood clot and the occurrence of new thromboembolic events in conditions such as deep vein thrombosis, pulmonary embolism, atrial fibrillation, and valvular heart disease. I explain in simple terms the difference between anticoagulants and thrombolytics, the purpose of each, and the concepts of primary and secondary prevention of thrombotic events. In the section on classification and mechanisms of action, we differentiate between: Parenteral anticoagulants Unfractionated heparin and low molecular weight heparins: these act by potentiating antithrombin, inhibiting thrombin and factor Xa, with a rapid onset and short half-life, making them ideal for prophylaxis and acute treatment of thromboembolic disease. Classic oral anticoagulants (vitamin K antagonists) Warfarin and acenocoumarol: these block the recycling of vitamin K in the liver and prevent the synthesis of factors II, VII, IX, X, and proteins C and S, requiring close monitoring via INR. Direct oral anticoagulants (DOACs) Direct thrombin inhibitors (dabigatran) and factor Xa inhibitors (rivaroxaban, apixaban, edoxaban), with more predictable pharmacokinetics, fewer interactions, and no need for INR monitoring in most patients. In the clinical section, we address the most frequent indications for anticoagulant therapy: Non-valvular atrial fibrillation, where anticoagulation significantly reduces the risk of stroke and systemic embolism, using scores such as CHADS2 and CHA2DS2-VASc to determine who should be anticoagulated. Venous thromboembolism (deep vein thrombosis and pulmonary embolism), for both prophylaxis and treatment, in both high-risk medical and surgical patients. Valvular heart disease and prosthetic heart valves, especially with vitamin K antagonists in mechanical prostheses or situations of high thrombotic risk. We analyze practical management and monitoring: How to adjust vitamin K antagonist doses according to INR and what therapeutic ranges are typical in different clinical scenarios. What to consider when choosing between heparins and DOACs (renal function, age, comorbidities, adherence, bleeding risk, prosthetic heart valves, etc.). Key aspects of periprocedural and in-surgical management: when to discontinue, when to restart, and how to reduce the risk of both bleeding and thrombosis. In the section on safety and adverse effects, I explain that the main complication of anticoagulant therapy is hemorrhage, which can present as mucosal, gastrointestinal, urinary, intracranial, or other types of bleeding. You will see warning signs that the patient and physician should recognize (black or red stools, red urine, persistent gingival bleeding, severe headache, sudden neurological deficit) and how to act in the event of suspected severe bleeding. We also review drug and dietary interactions, especially with vitamin K antagonists, where other medications, supplements, and foods rich in vitamin K can increase or decrease the effect of the anticoagulant. I discuss patient education strategies: always take the medication at the same time, do not modify the dose on your own, inform the doctor of all medications and herbal remedies you use, and attend regular follow-up appointments as prescribed. Finally, we discuss prevention and monitoring of anticoagulated patients: how to stratify bleeding risk (HAS-BLED and other clinical factors), choose the most appropriate anticoagulant based on the patient's profile, and define the treatment duration in each context (AF, DVT/PE, acute coronary syndrome, valvular heart disease). I also explain when it is reasonable to de-escalate, change medication, or discontinue anticoagulation, always considering the balance between thrombotic and bleeding risk. #anticoagulants #anticoagulation #heparin #warfarin #acenocoumarol #DOACs #dabigatran #rivaroxaban #apixaban #venousthromboembolism #atrialfibrillation #stroke #pulmonaryembolism #INR #HASBLED #pharmacology #internalmedicine #emergencymedicine #familymedicine #anticoagulatedpatient #patientsafety #healtheducation #medicineinspanish #Mediesfera