Eicosanoids
Start with the big picture
Arachidonic acid released from membrane phospholipids is metabolized through COX-1/2 to prostaglandins, prostacyclin, and thromboxane, or through 5-LOX to leukotrienes and lipoxins. These mediators signal locally through G protein-coupled receptors and are rapidly degraded. Their differing effects help explain clinical uses across several systems: prostacyclin analogs in pulmonary hypertension, prostaglandins in obstetric care, and prostaglandin analogs in glaucoma. The pathway also informs antiplatelet use of low-dose aspirin and leukotriene-targeted asthma treatments. Understanding the balance between mediator effects, pathway enzymes, and drug actions provides a framework for connecting eicosanoid biology with therapeutic applications and adverse effects.
What you'll learn
- Trace arachidonic acid metabolism through COX and 5-LOX pathways.
- Compare COX-1 and COX-2 roles described in the source.
- Relate major prostanoids and leukotrienes to their physiological effects.
- Identify clinical applications of medicines that modulate eicosanoid pathways.
- Recognize selected adverse effects and risks associated with these medicines.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
