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ICD-9 chapters; Chapter Block Title I 001–139: Infectious and Parasitic Diseases II 140–239: Neoplasms III 240–279: Endocrine, Nutritional and Metabolic Diseases, and Immunity Disorders IV 280–289: Diseases of the Blood and Blood-forming Organs V 290–319: Mental Disorders VI 320–389: Diseases of the Nervous System and Sense Organs ...
IgA vasculitis (HSP), previously known as Henoch–Schönlein purpura, is a disease of the skin, mucous membranes, and sometimes other organs that most commonly affects children. In the skin, the disease causes palpable purpura (small, raised areas of bleeding underneath the skin), often with joint pain and abdominal pain .
The definite diagnosis of vasculitis is established after a biopsy of involved organ or tissue, such as skin, sinuses, lung, nerve, brain, and kidney. The biopsy elucidates the pattern of blood vessel inflammation. Some types of vasculitis display leukocytoclasis, which is vascular damage caused by nuclear debris from infiltrating neutrophils. [37]
Necrotizing vasculitis, also called systemic necrotizing vasculitis, [1] is a general term for the inflammation of veins and arteries that develops into necrosis and narrows the vessels. [ 2 ] Tumors , medications, allergic reactions , and infectious organisms are some of the recognized triggers for these conditions, even though the precise ...
It is an autoimmune disease and a form of vasculitis that affects small- and medium-size vessels in many organs but most commonly affects the upper respiratory tract, lungs and kidneys. [6] The signs and symptoms of GPA are highly varied and reflect which organs are supplied by the affected blood vessels.
The signs and symptoms of microscopic polyangiitis may resemble those of granulomatosis with polyangiitis (GPA) (another form of small-vessel vasculitis) but typically lacks the significant upper respiratory tract involvement (e.g., sinusitis) frequently seen in people affected by GPA. [citation needed]
Systemic venous angiitis or vasculitis is an inflammatory disease of the blood vessels walls, secondary to autoimmune diseases. It is essentially a T helper cell driven reaction, recruited by dendritic cells. The vascular impact can affect the blood circulation in the veins and thus give rise to the syndrome of Hughes-Stovin.
C1q is an integral component within the complement pathway – a complicated cascade of protein interactions, culminating in an immune response against a broad variety of pathogens. The anti-C1q antibodies found in patients with hypocomplementemic urticarial vasculitis activate C1q, which instigates activation of the entire complement pathway.