fibrinoid necrosis

In most forms, it is accompanied by destruction of the vessel wall, often seen as fibrinoid necrosis.

They are pathognomic foci of fibrinoid necrosis found in many sites, most often the myocardium.

These oral manifestations are caused by the typical necrotizing microvasculitis with fibrinoid necrosis.

Fibrinoid necrosis is a special form of necrosis usually seen in immune reactions involving blood vessels.

Fibrinoid necrosis is a special form of necrosis usually caused by immune-mediated vascular damage.

Fibrinoid necrosis of the Glomeruli (as a result of malignant hypertension)

In malignant hypertension these hyperplastic changes are often accompanied by fibrinoid necrosis of the arterial intima and media.

Fibrinoid necrosis of vessel wall (amorphous eosinophilic vessel wall).

Endothelial injury can occur as a consequence of severe elevations in blood pressure, with fibrinoid necrosis of the arterioles following.

Fibrinoid necrosis also occurs in the walls of arterioles in malignant hypertension (blood pressure greater than 200/130 mmHg).

Further aggregation of immune complex-related processes induce a local fibrinoid necrosis with ischemia-aggravating thrombosis in the tissue vessel walls.

Although they are usually indicative of fibrinoid necrosis associated with malignant hypertension, Siegrist streaks also occur in patients with temporal arteritis.

Involvement of the endocardium typically results in fibrinoid necrosis and verrucae formation along the lines of closure of the left-sided heart valves.

Histological examination of nodules shows that they consist of a shell of fibrous tissue surrounding a center of fibrinoid necrosis.

During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue.

Interlobular and afferent arterioles show fibrinoid necrosis and intimal hyperplasia and are often occluded by thrombi.

Fisher considered this small-vessel disease to be the result of hypertension, induced in the acute stage by fibrinoid necrosis that would lead to occlusion and hence lacunar stroke.

Histopathological changes are that of a chronic granulomatous disorder, characterized by fibrinoid necrosis, infiltration by polymorphonuclear cells, lymphocytes, plasma cells and macrophages.

As observed under methods of histopathology, acute necrotizing vasculitis within the affected tissues is observed concomitant to neutrophilic infiltration, along with notable eosinophilic deposition (fibrinoid necrosis).

The nodule has a central area of fibrinoid necrosis that may be fissured and which corresponds to the fibrin-rich necrotic material found in and around an affected synovial space.

The response is characterized by an inflammatory infiltrate of mostly macrophages and natural killer cells (with small numbers of T cells), intravascular thrombosis, and fibrinoid necrosis of vessel walls.

The renal lesion associated with malignant hypertension consists of fibrinoid necrosis of the afferent arterioles, sometimes extending into the glomerulus, and may result in focal necrosis of the glomerular tuft.

Fibrinoid necrosis is a form of necrosis, or tissue death, in which there is accumulation of amorphous, basic, proteinaceous material in the tissue matrix with a staining pattern reminiscent of fibrin.

(The term Histiocyte can also simply refer to a cell from monocyte origin outside the blood system, such as in a tissue (as in rheumatoid arthritis as palisading histiocytes surrounding fibrinoid necrosis of rheumatoid nodules).

Several authorities have stated that malignant hypertension (implying the presence of arterial fibrinoid necrosis and usually a diastolic blood pressure <140 mm Hg with retinal changes such as haemorrhages, exudates and papilloedema) is rare in diabetics and that generally the degree of hypertension tends not to be severe (Drury, 1983).