By F. Jesper. Transylvania University.

However cheap 52.5mg nicotinell mastercard, the effect of soluble metals on periprosthetic cells is a complex function of cell type purchase 17.5mg nicotinell with mastercard, composition purchase 52.5 mg nicotinell amex, and concentration of metal generic 52.5mg nicotinell visa. In vitro investigation has determined the stimulatory effect of some metals (e 35mg nicotinell free shipping. This differential impact of metal ions on some cell types and not others (particularly fibroblasts and osteoblasts) may potentially explain how fibrous membranes so readily form around implants initially placed in intimate contact with bone (i. Adverse local and remote tissue responses purportedly associated with particulate debris may be due in part to specific soluble metals resulting from implant degradation. High concentrations of metals negatively impact all types of cells at some level [39–50]. For certain cell types, such as human osteoblasts, these effects have been somewhat character- ized. One of the main functions of osteoblasts (if not the main function) is to produce organic bone matrix, 90% of which is type I collagen. Type I collagen is comprised of three helical chains. The third chain, 2[I], is similar in structure yet genetically distinct from 1[I]. Metal particles and ions have been found to decrease gene expression of procollagen 1[I] before decreases could be observed in other more osteo- blast-specific markers of bone deposition, such as gene expression of osteocalcin, osteonectin, and alkaline phosphatase [51–53]. Other metal-induced effects on osteoblasts have been noted, such as the production of cytokines which recruit, prime, and activate inflammatory cells. In- terleukin-6 is secreted by osteblasts in response to Al, Fe, Mn, Na, Ni, and V chloride solutions (more toxic metals). The concentrations of metal ions associated with toxic osteoblast responses can be detected within some ranges of metal concentrations reported to exist in periprosthetic tissue (Table 4). Comparison of the effects of metal ions on osteoblasts to the effects of particles previously reported [54 demonstrates the potential of specific metal ions released from implants or particulate implant debris to play a clinical role in the pathogenesis of osteolysis. This contention is supported by past investigations where metal ions such as Al, V, and Ti have been shown to inhibit apatite formation in vitro by binding and blocking potential crystal growth sites. This poisoning of crystal growth sites by metal ions may thus act to interfere with normal in vivo osteoid mineralization and remodeling process of bone [55,56]. Important to the assessment of metal-induced osteolysis is the role of other peri-implant cells such as fibroblasts, osteoclasts, macrophages, and lymphocytes, which, after exposure to metal ions, may affect osteoblast function through paracrine mediators. Although osteoclast activity has been reportedly impaired by exposure to metal ions at sublethal concentrations, these effects may be overridden by metal-induced autocrine and paracrine induction of IL-6, which can act to directly stimulate osteoclast activity. Thus, further study using mixed cell populations is required to more comprehensively assess released implant metal effects within the peri-implant milieu. Particulate Debris Corrosion Histological sections of the tissues surrounding stainless steel internal fixation devices generally show encapsulation by a fibrous membrane with little or no inflammation over most of the 82 Hallab et al. At screw–plate junctions, however, the membranes often contain macrophages, foreign body giant cells, and a variable number of lymphocytes in association with two types of corrosion products: iron containing granules and microplates of relatively larger particles of a chromium compound(s). Chromium microplates are of variable morphology and are found within the tissues as closely packed, platelike particle aggregates ranging in size from 0. They are often found free within acellular collagen or within frankly necrotic tissue. Several multinucleated foreign body giant cells are usually present within or bordering collections of these particles. In hematoxylin and eosin preparations, the majority of microplates are yellow or apple-green. Many microplates, however, stain darkly with hematoxylin and these microplates also react strongly to staining for iron. Electron microprobe energy dispersive x-ray analyses indicate that microplates are a chromium compound containing iron and a substantial amount of phosphorus. Iron granules are often seen surrounding chromium microplates, but the granules are found alone as well. Iron granules are yellow-brown, mainly spherical, and 0. They are predominantly intracellular, most often in macrophages, but may also be found in fibrocytes. X-ray diffraction indicates that the granules consist of a mixture of two or more of the iron oxides, Fe2O3 and Fe2O3, and the hydrated iron oxides Fe2O3 H2O and Fe2O3 H2O. Particles of the chromium–phosphate hydrate–rich material can be found at the bearing surface of the UHMWPE acetabular liners, suggesting they may participate in articular surface three-body wear resulting in an increased production of polyethylene debris.

Pathogenesis Used infrequently as an adjunct treatment for chronic alcoholism discount nicotinell 52.5mg with mastercard. Occurs after several months of therapy on standard doses nicotinell 35 mg on-line. Diagnosis Mild slowing of motor NCV discount 17.5mg nicotinell fast delivery, diminished sensory amplitudes cheap nicotinell 52.5 mg otc, distal denervation best nicotinell 52.5mg. References Frisoni GB, Di Monda V (1989) Disulfiram neuropathy: a review (1971–1988) and report of a case. Alcohol Alcohol 24: 429–437 Mokri B, Ohnishi A, Dyck PJ (1981) Disulfiram neuropathy. Neurology 31: 730–735 315 Polyneuropathy and chemotherapy Toxic neuropathies caused by chemotherapy are usually dose-dependent, and have a potential reversibility after termination of the drug treatment. Little is known about the influence of preexisting polyneuropathies in the development of a chemotherapeutically induced neuropathy (except vincristine given in patients with hereditary sensorimotor neuropathy), and the toxicity of only a few drug combinations have been described. This is of importance as chemo- therapy is not always used as a single agent therapy, but patients often receive drug combinations or second line therapy. Additionally also biological agents such as antibodies, interferons, cytokines and vaccines are used in cancer therapy and also have a risk of inducing polyneuropathies. Clinical distribution: Most neuropathies caused by chemotherapeutic agents are symmetric and length dependent, with a stocking glove distribution of sensory loss. Sensory symptoms and distal weakness ( lower extremities) occur. The development of distal sensory symptoms (numbness or paresthesias) can be used as a possible sign of neurotoxicity. Overview of the most frequently used chemotherapeutic agents causing poly- neuropathy Cisplatinum and • Cumulative dose approximately: Frequent derivatives 400 mg • Sensory neuro(neurono)pathy, with dysfunction of large fibers, ataxia • Persistence despite discontinuation (“coasting effect”). Combination Paclitaxel) involved with cisplatinum increases toxicity Vinca alkaloids Sensorimotor polyneuropathy, all fibers Frequent (vincristine and involved. Distal paresthesias (as initial derivatives) sign), areflexia, foot drop. Rarely: cranial nerves, or autonomic symptoms VM-26 and VP-16 Mild sensorimotor polyneuropathy Rare 316 Vinca alkaloids Genetic testing NCV/EMG Laboratory Imaging Biopsy + Symptoms Paresthesias on fingers and toes, sensory loss for pin prick and light touch. Clinical syndrome/ Dose dependent mixed sensorimotor polyneuropathy. Pathogenesis Vinca alkaloids bind to microtubules and interfere with their assembly. Structur- al changes account for abnormal axoplasmic transport and are related to axonal degeneration. Diagnosis Electrophysiology: axonal damage with an EMG that shows neurogenic changes. Differential diagnosis Paraneoplastic neuropathy, other chemotherapeutic agents. Prognosis Potentially reversible, sensory symptoms improve within some months. Rapid onset, often with burning pain, with rare weakness. While cisplatin and carboplatin have a similar spectrum of dose dependent Clinical syndrome/ neuropathy, oxaliplatin has two types of toxicity. Patients experience dysesthesias and paresthesias, aggravated by cold. The symptoms recur after each chemotherapy cycle with oxaliplatin. Additional symptoms also include eye and jaw pain, leg cramps, and voice changes. The chronic toxicity is a dose dependent polyneuropathy, resembling cis platinum neuropathy. Proximal and distal weakness and sensory loss, ataxia.

On examination buy discount nicotinell 35mg, you note a large erythematous 17.5 mg nicotinell mastercard, scaly patch on the trunk generic 17.5mg nicotinell with amex. The lesion on the upper thigh is a thicker plaque that is deeper red in color buy generic nicotinell 52.5mg. Skin biopsy reveals atypical lymphoid cells in the epider- mis that have hyperconvoluted (cerebriform) nuclei buy nicotinell 52.5mg with mastercard. There is also a bandlike lymphocytic infiltrate in the upper dermis. A diagnosis of mycosis fungoides is made on the basis of the histologic report. Which of the following clinical and therapeutic statements is NOT characteristic of this disorder? The rash is caused by a cutaneous lymphoma that is most commonly of B cell origin B. The condition can be associated with generalized erythroderma and circulating atypical lymphocytes with cerebriform nuclei C. Early-stage disease that is confined to patches or plaques in the skin is primarily treated with topical therapy involving steroids or chemotherapeutic agents D. Ulcerations from the cutaneous lesions should be monitored closely and treated aggressively because sepsis originating from these lesions is a common cause of death in these patients E. Patients with visceral involvement have a poor prognosis; the median survival is 2. The vast majority of these are T cell in origin and are known as cutaneous T cell lymphomas (CTCLs). Mycosis fungoides is the name commonly applied to this condition, although there are other variants. Five percent of patients with CTCL present with Sézary syndrome and have generalized erythroderma and circulating atypi- cal T cells (Sézary cells); this condition represents the leukemic variant of CTCL. CTCL can be difficult to diagnose, given its indolent course and the fact that its appearance is simi- lar to those of other benign inflammatory conditions of the skin, including psoriasis, eczema, contact dermatitis, and drug reactions. The lesions typically appear in a bathing trunk distribution. Staging of the disease is based on the surface area of skin involved with patches or plaques and the involvement of lymph nodes, visceral organs, and blood. Early- stage disease is primarily treated with topical therapy (such as corticosteroids, nitrogen mustard, or carmustine) and radiation of the lesions. Advanced disease is associated with a poor prognosis. The most serious complications of CTCL are infections: sepsis from ulcer- ated cutaneous tumors is a common cause of death in these patients. A 56-year-old white man presents to your office for evaluation of bumps on his upper back and chest. His wife reports that he has had them for years, but they seem to be increasing in number. Examination reveals several sharply circumscribed papules measuring from 2 mm to 2 cm in diameter on the patient’s upper back and chest. The lesions are light brown and have a stuck-on appearance. Dermatosis papulosa nigra 2 DERMATOLOGY 27 Key Concept/Objective: To be able to recognize seborrheic keratosis and to be familiar with the differential diagnosis of lesions with a similar appearance This patient’s lesions are consistent with seborrheic keratosis (seborrheic wart). Seborrheic keratosis is a very common epithelial tumor that tends to occur on the upper trunks of light-skinned adults. The color can range from dirty yellow to dark brown, and their size varies from 1 mm to several cm. They may be rough or smooth but often have a waxy surface. Dermatosis papulosa nigra is similar to seborrheic keratosis but tends to occur in dark-skinned individuals (this patient is white) and is usually localized on the face. In addition, dermatosis papulosa nigra tends to pres- ent at an earlier age than does seborrheic keratosis.

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