Monckeberg's sclerosis(redirected from Mönckeberg's sclerosis)
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Related to Mönckeberg's sclerosis: Mönckeberg's arteriosclerosis
an induration or hardening, especially of a part from inflammation, or in disease of the interstitial substance. The term is used chiefly for such a hardening of the nervous system due to hyperplasia of the connective tissue or for hardening of the blood vessels. Called also induration. adj., adj sclerot´ic.
amyotrophic lateral sclerosis see amyotrophic lateral sclerosis.
arteriolar sclerosis arteriolosclerosis.
disseminated sclerosis multiple sclerosis.
familial centrolobar sclerosis a progressive familial form of leukoencephalopathy marked by nystagmus, ataxia, tremor, parkinsonian facies, dysarthria, and mental deterioration.
focal glomerular sclerosis focal segmental glomerulosclerosis.
glomerular sclerosis glomerulosclerosis.
hippocampal sclerosis loss of neurons in the region of the hippocampus, with gliosis; sometimes seen in epilepsy.
lateral sclerosis a form seated in the lateral columns of the spinal cord. It may be primary, with spastic paraplegia, rigidity of the limbs, and increase of the tendon reflexes but no sensory disturbances, or secondary to myelitis, with paraplegia and sensory disturbance.
medial calcific sclerosis (Mönckeberg's sclerosis) Mönckeberg's arteriosclerosis.
multiple sclerosis see multiple sclerosis.
systemic sclerosis systemic scleroderma.
tuberous sclerosis a congenital heredofamilial disease, transmitted as an autosomal dominant trait, characterized principally by the presence of hamartomas of the brain (tubers), retina (phakomas), and viscera, mental retardation, seizures, and adenoma sebaceum, and often associated with other skin lesions.
Monckeberg's sclerosisAn age-related degenerative disorder of the muscle coat of medium-sized arteries with severe hardening from CALCIFICATION. The condition causes some rise in systolic blood pressure but is otherwise unimportant. (Johann George Monckeberg, 1877–1925, German physician).
MÖnckeberg's sclerosis; Moenckeberg's sclerosis; medial arterial calcification; MAC calcification of tunica media of small and medium-sized arteries, visible on radiograph
MAC of larger arteries is associated with peripheral vascular disease and old age
MAC of small arteries (e.g. intermetatarsal arteries) is strongly associated with distal sensory neuropathy and diabetes mellitus (see Table 1)
|Vascular||Accelerated formation of atherosclerosis, especially affecting distal (lower-limb) arteries|
Abnormal vascular endothelium and associated changes of the microvasculature
Medial arterial sclerosis; MÖnckeberg's sclerosis of the intermetatarsal arteries
|Altered blood components||Abnormal erythrocytes cause tissue ischaemia (erythrocytes do not adopt normal flow characteristics in small vessels; oxygen dissociation is reduced)|
Abnormal white blood cells predispose to poor healing and susceptibility to infection (white blood cells show less effective phagocytosis, release fewer growth factors and reduced destruction of microorganisms)
|Neurological||Abnormal peripheral (motor, sensory and autonomic) nerve conduction, with reduced perception of and reaction to potentially damaging stimuli; autonomic dysfunction predisposes to dryness of the skin, heel fissures, abnormalities of skin blood flow and Charcot joint formation (neuroarthropathy)|
|Increased susceptibility to infection||Owing to the combined effects of neurological and vascular complications, and altered blood components (see above)|
|Impaired vision||Diabetic retinopathy and cataract formation reduce the patient's ability to examine the feet and react promptly to potential problems at an early stage|
|Renal disease||Renal dysfunction predisposes to peripheral oedema|
Correlation of renal disease and median arterial calcification (MÖnckeberg's sclerosis)
Risk of digital gangrene in renal transplant patients
|Non-enzymatic glycation of protein||Affects all body proteins, causing ‘stiffness’ of globular and structural proteins, with:|
• Joint immobility, especially of the subtalar joint
• Loss of normal resilience of epidermal keratin
• Contracture of the fascial structures (formation of the diabetic ‘claw-foot’, with increased loading under the metatarsal heads)
• Impaired wound healing, with chronic underlying fibrosis and ischaemia of long-standing chronic wounds (ulcers) and reduced tissue viability