Summary
Highlights
Thrombosis requires endothelial injury, blood flow stasis, and hypercoagulability. A new thrombus shows alternating fibrin and platelet (light) and red blood cell (dark) layers, known as lines of Zahn, often with lipid deposition. An old thrombus involves organization with fibrosis and recanalization, forming new endothelial lining amidst remnants of the thrombus.
Necrotizing vasculitis, which can be infectious or non-infectious, involves inflammatory cells around blood vessels and fibrinoid necrosis. Non-infectious causes include circulating antibodies, while infectious causes include bacterial or fungal organisms. The presence of perivasculitis, where inflammatory cells surround the vessel, is also a characteristic.
Temporal arteritis primarily affects individuals aged 50 and above, causing symptoms like fever, fatigue, and weight loss. It can involve the temporal, vertebral, and ophthalmic arteries, potentially leading to blindness. Histologically, it presents with intimal thickening, a split-like lumen, and chronic granulomatous inflammation characterized by macrophages and T-cells, along with fragmentation of the elastic lamina.
Cystic medial necrosis typically affects the aorta and is often caused by hypertension. Hypertension leads to vasoconstriction of the vasa vasorum, causing medial ischemia. This results in the loss of smooth muscle cells and the deposition of amorphous material, specifically glycosaminoglycan, creating cystic spaces within the aortic media.
Aortic dissection is a medical emergency caused by an intimal tear in the aorta, allowing blood to accumulate between the intimal and medial layers. This can lead to hematoma formation or the creation of a 'double-barreled aorta' if another intimal tear forms. Susceptible groups include individuals aged 40-60 with hypertension and younger individuals with connective tissue diseases like Marfan syndrome, or it can be iatrogenic due to surgical manipulation.