The correct answer is D. This patient’s long airplane flight placed her at an increased risk of developing DVT. In addition, the patient has a positive Homans’ sign (calf pain on dorsi- flexion), which is seen in some patients with a DVT. Virchow’s triad refers to three factors that predispose a patient to developing a venous thrombosis: (1) local trauma to the vessel wall, (2) stasis, and (3) hypercoagulability. Throm- boxane A2 stimulates platelet aggregation and vasoconstriction and will be elevated at the site of a clot.
Answer A is incorrect. Leukotrienes (LT) C4, LTD4, and LTE4 are bronchoconstrictors that are believed to contribute to symptoms of asthma. 5-Lipoxygenase is the enzyme that converts arachidonic acid to 5-hydroperoxy-eicosatetraenoic acid, which is then used to produce leukotrienes.
Answer B is incorrect. Prostaglandin I2 (PGI2) is synthesized by vascular endothelium and smooth muscle. Its effects include inhibition of platelet aggregation, relaxation of smooth muscle, reduction of systemic and pulmonary vascular resistance by direct vasodilation, and natriuresis in kidney. Thus, PGI2 is not abundant locally at the site of a deep venous thrombosis because it does not promote platelet aggregation.
Answer C is incorrect. Renin is a circulating enzyme released mainly by the kidneys in response to low blood volume or low body NaCl content. Renin activates the renin-angiotensin system by cleaving angiotensinogen in the liver to produce angiotensin I. Angiotensin I is then further converted into angiotensin II in specialized lung, ultimately leading to constriction of blood vessels, an increase in ADH and aldosterone production, and stimulation of the hypothalamus to activate the thirst reflex, leading in turn to increased blood pressure.
Answer E is incorrect. Vascular endothelial growth factor (VEGF) is a substance made by cells that stimulates new blood vessel formation. The binding of VEGF turns on the receptors, which then generate signals inside the cell, ultimately leading to the growth of new blood vessels. Although this growth factor may be elevated at the site of the clot, it is not as abundant as thromboxane A2.