Bruising: Signs of symptoms, causes
Bruising may occur in Cushing's syndrome, uremia syndrome, platelet dysfunction, adhesion to the vessel wall, anemia, and other factors such as cephalosporins and aspirin.
Because of a very small injury, they do not normally cause bruising.
Figure. Mechanism of bruising in renal failure
The loss of subcutaneous connective tissue due to the catabolic effect of glucocorticoids exposes the underlying blood vessels, which can rupture. The mechanism is similar to that of stretch marks.
This mechanism is complex and unclear. Hyperemia changes the function of platelets, leading to the ineffective function of platelet activation, aggregation, and adhesion to the endothelium.
The key factors that cause blood clotting disorders are shown in the picture.
Abnormal secretion of agglutination factors, an imbalance between platelet aggregation-stimulating agonists and platelet aggregation inhibitors, too high concentration of parathyroid hormone inhibits platelet aggregation, and decreased thromboxane A2 all contribute to inhibition of platelet aggregation or decrease in platelet activity.
Adhere to the circuit wall
Several factors contribute to a decrease in the adhesion of platelets to the vessel walls. Normally, platelets have a number of proteins that help to bind platelets together and with the walls of the vessels - forming blood clots, preventing bleeding. Urea-derived toxins reduce glycoprotein GP 1b and disrupt the function of certain receptors (αIIb β3), which are essential for vascular adhesion and normal interaction between vWF and fibrinogen, thereby inhibiting clot formation. In addition, an increase in a number of other factors that inhibit blood clotting, such as NO and PGI2, is also seen in patients with uremia. Increased levels of these inhibitors can also create incomplete blood clots, which in turn can cause blood bruises.
Red blood cells are indispensable factors in platelet activation and forming blood clots. In normal amounts, they 'push' platelets towards the lumen endothelial cells and increase ADP, increasing platelet activation. Patients with uremia often have anemia, so these normal processes are reduced or lost, resulting in prolonged bleeding time. Some studies suggest that this is the main reason for the prolonged bleeding time.
Drugs, including cephalosporins and aspirin, affect platelet function.