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PH-CV19

Vasculitis

How inflammation of the vessel wall narrows, blocks, weakens or tears vessels, and why the size of vessel affected decides whether it causes blindness, absent pulses, infarcts, aneurysms, purpura or glomerulonephritis.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Describe how the walls of large, medium and small vessels differ, and why vessel size shapes what vasculitis does.
  • Explain the three main routes of wall injury (immune complexes, ANCA-activated neutrophils, and T cells with macrophages) and relate them to fibrinoid necrosis, leukocytoclasis and granulomas.
  • Relate giant cell arteritis and Takayasu arteritis to granulomatous inflammation that narrows the aorta’s branches.
  • Compare polyarteritis nodosa, Kawasaki disease and the ANCA-associated and immune-complex small-vessel vasculitides by vessel, antibody and organs affected.
  • Use the Chapel Hill classification, ANCA patterns, biopsy and imaging to tell the vasculitides apart, and explain how the main treatments act on the mechanism.

What it is

Vasculitis is inflammation of the wall of blood vessels. The inflamed wall can narrow or block, weaken into an aneurysm or leak, so the tissue it supplies is starved of blood or bleeds. Primary vasculitides have no known cause and are named, in the 2012 Chapel Hill consensus, mainly by the size of vessel they affect; secondary vasculitis follows an infection, a drug, a cancer or another inflammatory disease such as lupus.

5 types to tell apart
Large-vessel vasculitis
The aorta and its major branches: giant cell arteritis (over 50) and Takayasu arteritis (young adults, mostly women). Granulomatous inflammation narrows the branches.
Medium-vessel vasculitis
The main visceral arteries and their first branches: polyarteritis nodosa and Kawasaki disease. Necrotising inflammation causes aneurysms, thrombosis and infarcts.
Small-vessel vasculitis: ANCA-associated
Granulomatosis with polyangiitis, microscopic polyangiitis and eosinophilic granulomatosis with polyangiitis. Neutrophils activated by ANCA injure capillaries and venules, leaving few immune deposits (pauci-immune).
Small-vessel vasculitis: immune complex
IgA vasculitis, cryoglobulinaemic vasculitis, anti-GBM disease and hypocomplementaemic urticarial vasculitis: immune complexes deposit in or form within the walls of capillaries and venules.
Secondary vasculitis
Vasculitis with a probable cause or a parent disease: hepatitis B in some polyarteritis nodosa, hepatitis C in most cryoglobulinaemic vasculitis, drugs, cancers, lupus and rheumatoid arthritis.

US spelling: leucocytes → leukocytes.

Normal function

Vessels of every size, built on one wall plan

Every artery has three coats. The lines the intima; the media of smooth muscle and elastin gives strength and tone; the outer adventitia of connective tissue carries the vessel’s own small blood vessels, the , which feed the outer part of a thick arterial wall. A fenestrated sheet of elastin, the , separates intima from media.

The wall changes with size. Large (elastic) arteries such as the aorta have a thick media of that absorb each heartbeat. Medium (muscular) arteries, such as the coronary, renal, mesenteric and temporal arteries, have a that sets how much blood each organ receives. Small vessels (arterioles, capillaries and venules) have one or two layers of or none; leucocytes leave the blood mainly through the postcapillary venules.

Healthy endothelium keeps blood flowing: it resists clotting, controls what crosses the wall and lets leucocytes stick only when local signals call them. Because each size of vessel supplies tissue differently, an injured large artery starves a whole limb, eye or brain territory, an injured medium artery infarcts a patch of an organ, and injured small vessels leak blood into the skin, lungs or glomeruli.

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