Test on Flap Pathophysiology and Pharmacology

Question 1: Histamine released by mast cells is identified as a primary factor causing damage to vascular walls during the reperfusion phase of ischemia-reperfusion injury.

A. Ano

B. Ne

Explanation: The study materials state that superoxide radicals (O2•) produced by platelets, neutrophils, and endothelial cells are responsible for damaging vascular walls during reperfusion. Histamine is mentioned as changing membrane permeability and resulting in edema formation during surgical trauma, not as a primary cause of vascular wall damage specifically during reperfusion.

Question 2: According to the study materials, which of the following substances are described as contributing to vasoconstriction and promoting intravascular platelet aggregation in the context of flap surgery?

A. Norepinephrine released by sympathetic nerve endings

B. Thromboxane A2 released by platelets

C. Endothelin-1 released by traumatized vascular endothelial cells

D. Histamine released by mast cells

Explanation: The study materials state that traumatized sympathetic nerve endings release norepinephrine (NE), causing vasoconstriction and platelet aggregation. It also mentions that thromboxane A2 (TXA2) released by platelets and endothelin-1 (ET-1) released by traumatized vascular endothelial cells can cause vasoconstriction and intravascular platelet aggregation. Histamine, however, is noted to change membrane permeability, resulting in edema formation, rather than directly causing vasoconstriction and platelet aggregation in this context.

Question 3: The infarct-protective effect of remote preischemic conditioning in pig skeletal muscle is biphasic.

A. Ano

B. Ne

Explanation: Moses et al. demonstrated that the infarct-protective effect of remote preischemic conditioning in pig skeletal muscle is biphasic, with an early phase waning within 6 hours and a late phase reappearing within 24 hours and lasting up to 72 hours.

Question 4: Which of the following observations presents an argument against the universal and critical role of neutrophils in the pathogenesis of ischemia–reperfusion injury?

A. Activated neutrophils produce superoxide (O2•) via NADPH oxidase, leading to tissue damage.

B. Myeloperoxidase (MPO) in neutrophils catalyzes the conversion of H2O2 to hypochlorous acid (HOCl), a potent cytotoxic agent.

C. Ischemia–reperfusion injury could be induced in neutrophil-free systems such as cultured animal cardiomyocytes.

D. Neutrophil depletion significantly reduced necrosis in pig latissimus dorsi muscle flaps subjected to ischemia and reperfusion.

Explanation: The study materials state that 'ischemia–reperfusion injury could be induced in neutrophil-free systems such as in cultured animal cardiomyocytes and human atrial strips and in isolated perfused animal hearts,' which challenges the idea that neutrophils are always essential for this type of injury. The other options describe mechanisms or findings that support the role of neutrophils in ischemia-reperfusion injury.

Question 5: Does increasing the width of a pedicle flap directly convert a random-pattern skin flap into an arterialized skin flap to augment its viability?

A. Ano

B. Ne

Explanation: Increasing the width of pedicle flaps adds additional vessels of the same type and perfusion pressure, which does not increase the length of flap viability. The conversion of a random-pattern skin flap to an arterialized skin flap for augmented viability is achieved by incorporating a direct artery or a larger perforator.