Hemostasis is a vital process that stops the bleeding from an injured blood vessel.
It involves an enzyme-catalyzed cascade called blood coagulation, which leads to stable blood clot formation.
When a clot blocks blood flow in vessels, it is called thrombosis.
Thrombotic diseases, such as myocardial infarction, stroke, and deep vein thrombosis, can be life-threatening.
Such conditions are treated by anticoagulants like unfractionated heparin or UFH.
UFH binds the endogenous anticoagulant, antithrombin, and enhances its inhibition of coagulation proteases to prevent blood clotting.
UFH is usually administered intravenously for rapid onset of action but needs close monitoring due to its variable pharmacokinetics.
Low-molecular-weight heparins or LMWHs, like enoxaparin and dalteparin, are smaller fragments of UFH that have the same efficacy as UFH.
&#160;LMWHs are given subcutaneously and have greater bioavailability than UFH. Monitoring is not mandatory for LMWHs, making them the preferred choice for anticoagulation therapy.

anticoagulant drugs: low-molecular-weight heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the blood, which may be inherited as thrombophilia.
Arterial and venous thrombi have distinct structures and characteristics. Arterial thrombi mainly consist of platelets within a fibrin mesh and are often associated with atherosclerosis. They can cause tissue ischemia or cell death. Venous thrombi have a small white head and a large jelly-like red tail. Thrombi can break off and circulate in the bloodstream as emboli, potentially causing severe complications when they lodge in vital organs such as the lungs or brain.
The coagulation process involves a complex enzyme cascade that converts liquid blood into a gel-like clot. This cascade is tightly regulated by inhibitors such as antithrombin III to prevent excessive clotting. The vascular endothelium also plays an active role in limiting thrombus extension. The intrinsic or &#39;contact&#39; pathway and the tissue factor pathway contribute to fibrin formation during coagulation. Thrombin, a key enzyme, plays multiple roles in the process, including fibrinogen cleavage, platelet aggregation, and modulation of smooth muscle contraction.
The endothelium has a dual role in promoting and limiting thrombosis. It produces substances such as prostaglandin I2 and nitric oxide, which inhibit platelet function and promote vasodilation. The endothelium also synthesizes tissue plasminogen activator and expresses thrombomodulin, which activates protein C&#8212;an anticoagulant that inactivates factors Va and VIIa. Genetic mutations, such as the factor V Leiden mutation, can lead to inherited thrombophilia by causing resistance to activated protein C.
Thrombotic and thromboembolic diseases have significant consequences, including myocardial infarction, stroke, deep vein thrombosis, and pulmonary embolism. Antiplatelet and fibrinolytic drugs are commonly used to treat platelet-rich &#39;white&#39; thrombi. At the same time, injectable anticoagulants (heparins and thrombin inhibitors) and oral anticoagulants (warfarin and related compounds) are utilized for &#39;red&#39; thrombi. Heparin, both unfractionated and low-molecular-weight preparations, is a potent anticoagulant that inhibits coagulation by activating antithrombin III. Low-molecular-weight heparins (LMWHs) are often preferred due to their more predictable effects, longer half-life, and lower incidence of certain side effects.

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, ...

anticoagulant-drugs-low-molecular-weight-heparins

Nanyang Technological University

Education

JoVE Core

Pharmacology

Unit 1

Cardiovascular Drugs: Anticoagulants and Antianginal Agents

KEY TERMS AND CONCEPTS

anticoagulant drugs: vitamin k antagonists and direct oral anticoagulants

anticoagulant-drugs-vitamin-k-antagonists-direct-oral

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K ...

antiplatelet drugs: prostaglandin synthesis, p2y12 and glycoprotein iib/iiia inhibitors

antiplatelet-drugs-prostaglandin-synthesis-p2y12-glycoprotein-iibiiia

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood ...

lipid-lowering drugs: statins and miscellaneous agents

lipid-lowering-drugs-statins-and-miscellaneous-agents

Lipid-Lowering Drugs: Statins and Miscellaneous Agents

Hyperlipidemia, a medical condition often referred to as high cholesterol, is characterized by abnormally elevated levels of lipids in the bloodstream. ...

ischemic heart disease: overview

Ischemic Heart Disease: Overview

Ischemic heart disease occurs when the heart&#39;s blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from ...

antianginal drugs: nitrates and &#946;-blockers

Antianginal Drugs: Nitrates and &#946;-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris &#8212; a condition marked by chest pain owing to diminished blood flow to the heart.
...

antianginal drugs: calcium channel blockers and ranolazine

antianginal-drugs-calcium-channel-blockers-and-ranolazine

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers ...

key terms and concepts

486 Views. Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of th...

Video: Anticoagulant Drugs: Low-Molecular-Weight Heparins

JoVE Core Pharmacology provides engaging animations that explain fundamental concepts, including drug effects, classification, and pharmacokinetics. Scientist-in-action videos illustrate real-world research conducted in today's laboratories.

11.1 : Anticoagulant Drugs: Low-Molecular-Weight Heparins

11.2 : Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

11.3 : Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

11.4 : Lipid-Lowering Drugs: Statins and Miscellaneous Agents

11.5 : Ischemic Heart Disease: Overview

11.6 : Antianginal Drugs: Nitrates and β-Blockers

11.7 : Antianginal Drugs: Calcium Channel Blockers and Ranolazine