| Class | Parenteral anticoagulant |
|---|---|
| Chemistry |
Glycosaminoglycan |
| Routes of administration |
IV ands subcut |
| Absorption |
Minimal oral bioavailability (~ 1%) |
| Solubility |
pKa -2.0 to -4.0, excellent solubility in water |
| Distribution |
Highly protein-bound, mainy to lipoproteins (LDL) |
| Metabolism |
Sequestered into reticuloendothelial cells and degraded gradually into inactive and renally cleared metabolites. |
| Elimination |
Biphasic (saturable) metabolism: with low doses, a rapid saturable clearance (by reticuloendothelial tissues), which becomes slower with high doses when this system is saturated. Monitored by APTT, which incorporates an assessment of thrombin activity |
| Time course of action |
Half-life of 25 units per Kg = 30 minutes |
| Target receptor |
Antithrombin III |
| Mechanism of action |
By binding to antithrombin III and causing the active site to undergo a conformational change, heparin increases its availability to its normal ligands, including factor Xa and thrombin. The result is an increase in the activity of antithrombin, which manifests in the form of the anticoagulant effect |
| Clinical effects |
Anticoagulation, bleeding, the possibility of HITS. |
| Literature reference |
TGA PI document |
| CICM details of understanding | Level 1 |
| Mentioned around Deranged Physiology |
Unfractionated and low molecular weight heparin; related to Heparin-Induced Thrombocytopenia, Heparin resistance and Reversal agents for anticoagulants from the Second Part Exam. |
| Related SAQs |
Question 20 from the first paper of 2024 (heparin vs. enoxaparin) Question 20 from the second paper of 2018 (heparin vs. enoxaparin) Question 5 from the second paper of 2017 (heparin vs. enoxaparin) Question 4 from the second paper of 2011 (heparin vs. hirudin) Question 8(p.2) from the second paper of 2009 (heparin vs. enoxaparin) Question 2 from the first paper of 2008 (heparin vs. enoxaparin) |