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Question:

A 64-year-old man is brought to the emergency department due to severe chest pain, diaphoresis, and shortness of breath.  Symptoms began suddenly on awakening and have worsened over the past 2 hours.  Blood pressure is 150/90 mm Hg and pulse is 102/min.  Physical examination reveals an S4.  ECG shows ST-segment depression and T-wave inversion in the lateral leads.  Coronary angiography reveals a ruptured atherosclerotic plaque, with a thrombus in the left circumflex artery that causes near-total occlusion.  Normal endothelial cells surrounding the lesion have released large amounts of a chemical substance that help decrease thrombus propagation by inhibiting platelet aggregation.  Which of the following substances was most likely secreted by these endothelial cells?

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Explanation:

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The formation of a platelet plug (primary hemostasis) is essential for preventing bleeding after damage to vascular endothelium; it occurs in 3 steps:

  • Platelet adhesion takes place via von Willebrand factor acting as a connector that binds platelets to underlying collagen
  • Platelets become activated and secrete multiple substances, including adenosine diphosphate, ionized calcium, and fibrinogen, from their alpha and delta (dense) granules.
  • Thromboxane A2 (Choice F) is released and acts as a vasoconstrictor and potent stimulator of platelet aggregation.  Adenosine diphosphate also stimulates platelet aggregation.

Balance is required as excessive platelet plug formation can lead to a pathologic thrombus that restricts blood flow (eg, myocardial infarction).  To oppose the functions of thromboxane A2, the endothelium secretes prostacyclin (prostaglandin I2), which is derived from arachidonic acid and synthesized from prostaglandin H2 by prostacyclin synthase.  Once secreted, prostacyclin acts locally to inhibit platelet aggregation and adhesion to the vascular endothelium and to cause vasodilation.  Nitric oxide aids in these functions as well.  Atherosclerosis can impair the ability of endothelial cells to synthesize prostacyclin and nitric oxide, creating localized predisposition to excessive platelet thrombus formation.

A synthetic prostacyclin, epoprostenol, is used in the treatment of pulmonary hypertension, peripheral vascular disease, and Raynaud syndrome.

(Choice A)  Hageman factor (factor XII) is synthesized by the liver and is activated by exposed collagen following damage to endothelial cells.  It participates in secondary hemostasis by activating the intrinsic clotting pathway; it also activates fibrinolysis.

(Choice B)  Kallikrein converts kininogen into bradykinin.  It also may play a role in triggering the fibrinolytic pathway, but it does not inhibit platelet aggregation.

(Choice D)  Protein C is a vitamin K–dependent factor synthesized by the liver.  It regulates the coagulation cascade by inactivating factors Va and VIIIa.

(Choice E)  Serotonin has a wide range of functions, including mediation of mood (in the central nervous system) and gastrointestinal motility.  It is also released from the delta granules of activated platelets and facilitates localized vasoconstriction.

Educational objective:
Prostacyclin (prostaglandin I2) is synthesized from prostaglandin H2 by prostacyclin synthase in vascular endothelial cells.  Once secreted, it inhibits platelet aggregation and causes vasodilation to oppose the functions of thromboxane A2 and help maintain vascular homeostasis.