Page 250 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

column of blood increases the transmural
Nonatherosclerotic Peripheral pressure. The legs have deep and superficial
Vascular Diseases veins that are connected by perforating veins
(→ A, top right). Venous valves ensure ortho-
As in atherosclerosis (→ p. 236ff.), thrombo- grade flow against the force of gravity. The al-
embolism of other etiology can cause acute oc- ternating contraction and relaxation of the leg
clusion of arteries. The emboli usually origi- musculature and the movement of the joints
nate in the heart, for example, the left atrium are essential driving forces for venous return
(in atrial fibrillation; mitral stenosis, → p.194), via the deep veins (“joint–muscle pump”).
the left ventricle (dilated cardiomyopathy, When the leg muscles are relaxed, the valves
myocardial infarct), or from the cardiac valves in the perforating veins ensure blood flow
(endocarditis, mitral stenosis, valvar prosthe- from the surface to the deep veins and also
sis). Intracardiac shunts (→ p. 202) allow ve- prevent blood flowing in the opposite direc-
nous thrombi (see below) to pass into the arte-
tion when the muscles contract (→ A1).
Heart and Circulation depositions of immune complexes or by cell- (increased distensibility of the veins), work in
rial system (paradoxical emboli).
Often on the basis of a genetic predisposition
Several forms of vasculitis are initiated by
a standing or sitting position over many years
(lack of “pumping” effect) leads, depending on
mediated immune reactions in the arterial
age, to distension and a winding course of the
wall. In polyarteritis nodosa (affecting the small
superficial veins as well as to incompetence of
and medium-sized arteries)it is mostly thekid-
fro movement of the blood) in both the super-
sulting ischemia. In temporal or giant-cell arter-
ficial and the perforating veins (primary vari-
itis (large arteries, especially in the head re-
7 neys, heart, and liver that are affected by the re- the venous valves and flow reversal (to-and-
gion) facial pain and headaches, “claudication” cosis; → A2). Frequently they develop or get
of the muscles of mastication and, in some cir- worse during pregnancy or in obesity. In addi-
cumstances, blindness can occur. Takayasu ar- tion to cosmetic problems, a feeling of heavi-
teritis (large arteries in the thorax–neck region) ness, burning, pain, and edemas develop in
can lead to cerebral ischemia, angina pectoris, the legs. Inflammation (varicophlebitis) and its
or “claudication” in the arms (pulseless dis- spread to the deep veins can lead to chronic ve-
ease). Thromboangitis obliterans (Buerger’s dis- nous insufficiency (→ A5; for complications,
ease, affecting medium-sized and small arter- see below).
ies of thelimbs) occurs mostly in male smokers. If a thrombus forms in the deep veins of the
In addition to arterial occlusion and migrating legs (acute phlebothrombosis; → A3), the
superficial thrombophlebitis, Raynaud’s phe- valves of the perforating veins are torn and
nomenon occurs, painful vascular spasms (e.g., blood will drain via the superficial veins, caus-
precipitated by cold) with numbness in the fin- ing secondary varicosis. Causes of phlebo-
gers or toes that at first blanch (ischemia), then thrombosis are damaged veins, immobiliza-
become cyanotic (hypoxemia), and then turn tion (sitting during long journeys, confine-
pink again (reactive hyperemia). Raynaud’s ment to bed, paralysis), defective clotting inhi-
phenomenon also occurs in some connective bition, operations, trauma or (often undetect-
tissue diseases (scleroderma, systemic lupus ed) tumors. Contraceptive pills (ovulation in-
erythematodes, rheumatoid arthritis). The hibitors) increase the risk of phlebothrombo-
phenomenon may occur in younger women as sis. A very dangerous acute complication oc-
a primary disease, in the absence of any other curs when a thrombus is torn from its attach-
condition (Raynaud’s disease). ment, resulting in pulmonary embolism with
pulmonary infarction (→ A4). In the long term
chronic venous insufficiency develops (→ A5),
Venous Disease which through peripheral edema with protein
exudation and deposition (including pericapil-
Because of their thin walls with few muscles, lary fibrin cuff) in the skin, results in fibrosis,
240 the veins are prone to distension, especially in dermatosclerosis, tissue hypoxia, and ultimate-
the legs where the hydrostatic pressure of the ly in leg ulcers (→ A6).
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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