Page 248 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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modify by oxidation of those LDLs that have en- An aneurysm is a circumscribed bulging of
tered the endothelium (→ C7). Oxidized LDLs an arterial vessel due to congenital or acquired
damage the endothelium and there induce wall changes. It takes on the following forms:
the expression of adhesion molecules which ! True aneurysm (→ B, left) with extension to
allow vessel musculature to proliferate. Oxida- all three wall layers (intima, media, and adven-
tion also results in altered binding of LDLs. titia). In 90–95% of cases it is caused by ath-
They can no longer be recognized by ApoB 100 erosclerosis with hypertension. Frequently the
receptors (→ p. 246ff.), but rather by so-called abdominal aorta is affected. In rare cases it
scavenger receptors that are contained in large may be congenital or caused by trauma, cystic
amounts within the macrophages. Conse- medial necrosis (Marfan’s, Ehlers–Danlos, or
quently, these now phagocytize large amounts Gsell–Erdheim syndrome), or infection (syphi-
of LDLs and are transformed into sedentary lis, mycosis in immune-deficient patients).
foam cells (→ C9). Lipoprotein(a) can be oxi- ! False aneurysm (pseudoaneurism), consist-
ing of a perivascular hematoma over a tear in
dized and phagocytized in a similar fashion.
Heart and Circulation cytes and thrombocytes trigger the migration sel lumen. It is caused by trauma or infection
Simultaneously, chemotactic factors of mono-
the intima and media, connected with the ves-
(accident, operation, arterial catheterization).
of smooth muscle cells from the media into the
! Dissecting aneurysm (→ B, middle), usually
intima (→ C6). Here they are stimulated to
in the ascending aorta in which, after perfora-
proliferate by PDGF and other growth-promot-
ing factors (from macrophages, thrombocytes,
tion of the intima, blood under high (arterial)
degenerative) media so that intima and adven-
themselves). They, too, are transformed into
foam cells by uptake of oxidized LDLs
titia become separated along an advancing
7 damaged endothelium, and the muscle cells pressure “burrows” a path within the (usually
(→ C10). They form an extracellular matrix length of wall.
(collagen, elastin, proteoglycans) that also ! Arteriovenous aneurysm occurs when an an-
contributes to atheroma formation. eurysm ruptures into a vein, producing an ar-
The consequences of plaque deposition teriovenous fistula.
(→ B) are narrowing of the lumen that can lead One of the catastrophic complications of an
to ischemia. Coronary heart disease (→ aneurysm is rupture. If it occurs in a large ves-
p. 218ff.) as well as chronic occlusive arterial sel, hemorrhagic shock will dominate the clini-
disease of the limbs with painful ischemia on cal picture (→ p. 230ff.). Rupture of an intra-
exercise (intermittent claudication) are exam- cranial artery (often the anterior communi-
ples of this. Other consequences of plaque for- cating artery) together with subarachnoid
mation are stiffening of the vessel wall (calcifi- bleeding is an acute risk to cerebral function.
cation), thrombus formation that obstructs the Rupture of an aneurism near the heart (espe-
residual lumen and can cause peripheral em- cially a dissecting aneurism) can cause acute
boli (e.g., cerebral infarction, stroke) as well as pericardial tamponade (→ p. 228) and, if the
bleeding into the plaques (additional narrow- aortic root is involved, aortic regurgitation
ing by the haematoma) and the vessel wall. (→ p. 200). Other complications are thrombosis
Thus weakened, the wall may be stretched in the aneurism, occlusion at the orgin of an ar-
(aneurysm; see below) and even rupture, with tery as well as emboli to distal vessels (ische-
dangerous bleeding into the surrounding tis- mia or infarction, respectively; → B, right).
sues, for example, from the aorta (see below)
or cerebral vessels (massive intracerebral
bleeding, stroke; → p. 360).

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