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Plaque ulceration

Vascular imaging allows determination of supply vessel occlusions, the presence of clots and wall abnormalities, such as atherosclerotic plaques and possible plaque ulceration, and, if they exist, to assess their effect on blood flow. [Pg.465]

As a result of the hyperglycemia, hyperinsulinemia, dyslipi-demia, and hypercoagulability associated with diabetes, diabetic patients are at particularly high risk for complications of atherosclerosis, Diabetes accelerates the natural course of the atherosclerotic process, precipitating more diffuse disease (4,5), increased rates of plaque ulceration and thrombosis (6), and a doubling of the five-year mortality rate when compared with nondiabetic CAD patients. [Pg.473]

Eliasziw M, Streifler JY, Fox AJC for the North American Symptomatic Carotid Endarterectomy Trial (1994). Significance of plaque ulceration in symptomatic patients with high-grade carotid stenosis. Stroke 25 304-308... [Pg.169]

Irregular/ulcerated plaque 2.03 (1.31-3.14) 0.0015 Irregular/plaque ulcerated 2.0 2.0... [Pg.182]

Data on the prognostic significance of carotid plaque qualitative parameters in neurologically asymptomatic patients are either lacking (plaque ulceration) or conflicting (plaque echogenecity). Some studies have shown that echolucent carotid plaques are associated with a two- to fivefold increased risk for stroke. However, the clinical utility of these observations for triaging patients to carotid revascularization awaits prospective confirmation (33). [Pg.169]

Bromides have sedative and anticonvulsant properties. At high levels they replace chlorides in nerve transport mechanisms, stabilising the membrane and impairing nerve transmission. Bromide salt is an effective antiepileptic and sedative in small doses and was once a common ingredient of many medicines. Intoxication by bromides (bromism) is reported at serum levels as low as 400 mg/1, with 1500 mg/1 considered to be toxic. The most common manifestations of bromism are psychiatric and dermatologic (bromoderma). Patients present with weakness, slurred speech, emotional instability, agitation, hallucinations, seizures and coma. Bromoderma occurs in approximately 35% of cases and is characterised by acneiform eruptions or, less commonly, granulomatous plaques, ulcers or bullae, usually on the face and trunk. [Pg.463]

Wood, S.,et ah, Erythrosine is a potential photosensitizer for the photodynamic therapy of oral plaque biofihns, J. Antimicrob. Chemother., 57, 680, 2006. Hurlstone, D.P., et ah. Indigo carmine-assisted high-magnification chromoscopic colonoscopy for the detection and characterisation of intraepithelial neoplasia in ulcerative colitis a prospective evaluation. Endoscopy, 37,1186, 2005. [Pg.616]

Endoscopy revealing whitish plaques with progression to superficial ulceration of the esophageal mucosa... [Pg.1204]

Degree of plaque disruption (i.e., erosion, ulcer) Cholesterol, Lp(a)... [Pg.219]

Neovascularization in artherosclerotic lesions may be regulated by VEGF, as this factor is over-expressed by different cells in the plaque tissue [40-42]. The increased serum levels of VEGF that correlate with disease activity in patients with Crohn s disease and ulcerative colitis, indicate a role for this cytokine in promoting inflammation. Most likely, increased vascn-lar permeability and/or wound healing via its pro-angiogenic activity are the basis for this effect [43]. [Pg.177]

Nickel itch is a dermatitis resulting from sensitization to nickel the first symptom is usually pruritis, which occurs up to 7 days before skin eruption appears. The primary skin eruption is erythematous, or follicular it may be followed by superficial discrete ulcers that discharge and become crusted or by eczema. The eruptions may spread to areas related to the activity of the primary site such as the elbow flexure, eyelids, or sides of the neck and face. In the chronic stages, pigmented or depigmented plaques may be formed. Nickel sensitivity, once acquired, is apparently not lost of 100 patients with positive patch tests to nickel, all reacted to the metal when retested 10 years later. ... [Pg.509]

Unlabeled uses For possible treatment of plaque psoriasis, ulcerative colitis, psoriatic arthritis, psoriasis, and juvenile arthritis. [Pg.2016]

Atherosclerosis mainly affects large- and mediumsized arteries. Extracranial manifestations at the carotid bifurcation statistically dominate the intracranial arteries. Besides typical manifestations at the carotid siphon or the vertebrobasilar junction, atherosclerosis is occasionally also found in peripheral intracranial vessel segments. Typical sequelae of atherosclerosis are stenosing plaque formations, ulcerations, dilatations or the evolution of fusiform aneurysms, which can be accompanied by extensive formation of thrombus. [Pg.87]

Fig. 5.13a,b. Detailed depiction of a rather complex carotid stenosis with several sharp plaques and an ulceration (arrow) on CE-MRA (b) to an extent matching DSA (a)... [Pg.88]

Atheromatous plaques are typically slow growing or quiescent for long periods but may suddenly develop fissures or ulcers (Fig. 6.5). Activated plaques trigger platelet aggregation. [Pg.58]

Fig. 6.6. Digitally subtracted arterial arigiogram showirig an ulcerated plaque at the carotid bifurcation, with contrast seen within the plaque (arrow). Fig. 6.6. Digitally subtracted arterial arigiogram showirig an ulcerated plaque at the carotid bifurcation, with contrast seen within the plaque (arrow).
However, without formal risk models, clinicians are often inaccurate in assessment of risk in their patients (Grover et al. 1995). Moreover, the absolute risk of a poor outcome for patients with multiple specific characteristics cannot simply be derived arithmetically from data on the effect of each individual characteristic such as age or severity of illness that is, one cannot simply multiply risk ratios for these characteristics together as if they were independent. Even if one could, it would still be rather complicated. In a patient with symptomatic carotid stenosis, for example, what would the risk of stroke without endarterectomy be in a 78-year-old (high risk) female (lower risk) with 80% stenosis who presented within two days (high risk) of an ocular ischemic event (low risk) and was found to have an ulcerated carotid plaque (high risk) ... [Pg.180]

The same agents as in systemic mucormycosis may lead to a subcutaneous, localized variant of mucormycosis, presenting with plaques, pustules, abscesses, ulcerations and finally skin necrosis. [Pg.150]

Histoplasma capsulatum var. duboisii causes African histoplasmosis, skin manifestations being the prominent sign in this variant. Three patterns may be differentiated clinically superficial (ulcerating papules or nodules, infiltrated plaques, target phenomenon ), subcutaneous granulomas (first hot and tender, then cold, rupture) and osteomyelitic lesions, the latter often demanding surgical procedures combined with amphotericin B and ketoconazole. [Pg.153]

Mucous plaque keratitis can be treated with 10% acetylcysteine but also resolves without treatment. Keeping the eye moist with artificial tears may be helpful. Exposiue keratitis and neruotropic keratitis are best treated with artificial tears, lid taping at bedtime, and, if necessary, tarsorrhaphy. Therapeutic contact lenses should not be used because of the risk of developing infectious ulcers in an eye with decreased sensitivity. [Pg.533]

EpitheUal macroerosion Plaques Pannus/ neovascularization Keratitis Shield ulcer Scarring High... [Pg.557]

Injection-site reactions are common after subcutaneous injection of interferon beta-lb, and are more frequent than with any other available interferons. In a multicenter placebo-controUed trial, 65% of patients receiving interferon beta-lb had reactions at the injection site compared with 6% in the placebo group (2). In contrast, only 5% of those who received interferon beta-la had injection site reactions (3). The clinical features of injection site reactions to interferon beta-lb mostly consist of benign inflammatory reactions, but they can sometimes be more severe, with sclerotic dermal plaques, painful erythematous nodules, and deep cutaneous ulcers with skin necrosis (SEDA-21,... [Pg.1834]

Severely ulcerated psoriatic plaques and acute extensive exfoliative dermatitis occurred in a 37-year-old man who had taken methotrexate for 5 years for psoriasis (74). [Pg.2282]

Wessels JA+, Arthritis Rheum 54(4), 1087 Ulceration of psoriatic plaques... [Pg.370]


See other pages where Plaque ulceration is mentioned: [Pg.60]    [Pg.171]    [Pg.313]    [Pg.152]    [Pg.75]    [Pg.60]    [Pg.171]    [Pg.313]    [Pg.152]    [Pg.75]    [Pg.143]    [Pg.73]    [Pg.1225]    [Pg.202]    [Pg.254]    [Pg.250]    [Pg.263]    [Pg.5]    [Pg.1422]    [Pg.161]    [Pg.164]    [Pg.290]    [Pg.315]    [Pg.323]    [Pg.155]    [Pg.5187]    [Pg.470]    [Pg.535]    [Pg.565]    [Pg.134]   
See also in sourсe #XX -- [ Pg.87 ]




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