Basic and Clinical Sciences (BCSE) 2025 – 400 Free Practice Questions to Pass the Exam

The contribution of increased fibrinogen due to inflammation to thrombotic effects in smokers is well-documented. Smoking has been shown to induce a chronic inflammatory state in the body, leading to elevated levels of fibrinogen, a key protein involved in blood clotting. Increased fibrinogen levels can enhance blood viscosity and promote the clotting process, thereby increasing the risk of thrombus formation.

Fibrinogen plays a crucial role in the coagulation cascade, as it is converted into fibrin during the process of clot formation. Elevated fibrinogen levels not only increase the likelihood of clot formation, but they can also contribute to the development of atherosclerosis due to endothelial damage and inflammatory processes triggered by smoking. This makes smokers more susceptible to cardiovascular events, including heart attacks and strokes, as a result of these thrombotic effects.

In contrast, options detailing increased hydration levels, renormalization of blood flow, and decreased platelet count do not encapsulate the well-established pathophysiological changes associated with smoking and thrombotic risk. Smoking typically leads to dehydration and does not normalize blood flow; rather, it can cause turbulence and stasis that are more conducive to thrombosis. Furthermore, smokers generally experience an increase, not a decrease