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Ulcerated lesions

Cenital herpes simplex virus. Characterized by vesicular or ulcerative lesions. Diagnosis confirmed by virologic or serologic testing. Prodrome manifests as pain, burning, or itching at the site where lesions will develop. [Pg.724]

Acatalasemia is a rare hereditary deficiency of tissue catalase and is inherited as an autosomal recessive trait (03). This enzyme deficiency was discovered in 1948 by Takahara and Miyamoto (Tl). Two different types of acatalasemia can be distinguished clinically and biochemically. The severe form, Japanese-type acatalasemia, is characterized by nearly total loss of catalase activity in the red blood cells and is often associated with an ulcerating lesion of the oral cavity. The asymptomatic Swiss-type acatalasemia is characterized by residual catalase activity with aberrant biochemical properties. In four unrelated families with Japanese-type acatalasemia, a splicing mutation due to a G-to-A transition at the fifth nucleotide in intron 4 was elucidated (K20, W5). We have also determined a single base deletion resulting in the frameshift and premature translational termination in the Japanese patient (HI6). [Pg.35]

Basal cell carcinoma nodule with telangiectatic surface or ulcerated lesion with a pearly translucent border... [Pg.136]

Mucins are also thought to act in cooperation with trefoil proteins in the protection and repair of the epithelium (Kindon et al., 1995). Trefoil factors are expressed along the GI tract and increased levels are noted near sites of inflammation and ulcerative lesions (Babyatsky et al., 1996). Furthermore, it has been demonstrated that mouse intestinal trefoil factor may play a role in the alteration of the physicochemical nature of GC mucins during N. brasiliensis infection (Tomita et al., 1995). Perhaps in GI nematode parasite infection mucins are not aiding in the host s protective expulsion of the parasite, but rather are functioning in the repair of the damaged intestinal epithelium. [Pg.393]

Most primary infections are asymptomatic or minimally symptomatic Multiple painful pustular or ulcerative lesions on external genitalia developing over a period of 7-10 days lesions heal in 2-4 weeks (mean, 21 days)... [Pg.517]

Lichen planus is a condition of unknown aetiology presenting as small pruritic and shiny papules, which initially may appear purple in colour. It affects the limbs, wrists, trunk, genitalia and the mouth, in which case ulcerated lesions occur on the gingival tissue. Treatment for lichen planus involves the use of systemic antihistamines but sometimes corticosteroids are required. [Pg.39]

Gl lesions Potassium chloride tablets have caused stenotic or ulcerative lesions of the small bowel and death. These lesions are caused by a concentration of potassium ion in the region of a rapidly dissolving tablet, which injures the bowel wall and produces obstruction, hemorrhage, or perforation. The reported frequency of small bowel lesions is much less with wax matrix tablets and microencapsulated tablets than with enteric coated tablets. Immediately discontinue either type of tablet and consider the possibility of bowel obstruction or perforation if severe vomiting. [Pg.32]

Gl - Ulcerative lesions, diverticulitis or ulcerative colitis continuous tube drainage of the stomach or small intestine. [Pg.132]

Hemorrhagic tendency may be manifested by hematuria, skin petechiae, hemorrhage into or from a wound or ulcerating lesion, or petechial and purpuric hemorrhages throughout the body. [Pg.140]

Ulcerating lesions Topical treatment of ulcerating lesions of the oral cavity, such as recurrent aphthous stomatitis (canker sores). [Pg.1442]

Paromomycin - Use with caution in individuals with ulcerative lesions of the bowel to avoid renal toxicity through inadvertent absorption. [Pg.1653]

Clofazimine is given to treat sulfone-resistant leprosy or to patients who are intolerant to sulfones. It also exerts an antiinflammatory effect and prevents erythema nodosum leprosum, which can interrupt treatment with dapsone. This is a major advantage of clofazimine over other antileprosy drugs. Ulcerative lesions caused by Mycobacterium ulcerans respond well to clofazimine. It also has some activity against M. tuberculosis and can be used as last resort therapy for the treatment of MDR tuberculosis. [Pg.564]

The flagellate leishmania is transmitted to humans by the bite of the female sandfly of the genus Phlebotomus. Three principal diseases result from infection with Leishmania spp. L. donovani causes visceral leishmaniasis (kala-azar) L. tropica and L. major produce cutaneous leishmaniasis, and L. braziliensis causes South American mucocutaneous leishmaniasis. In visceral leishmaniasis, the protozoan parasitizes the reticuloendothelial cells, and this results in an enlargement of the lymph nodes, liver, and spleen the spleen can become massive. Cutaneous leishmaniasis remains localized to the site of inoculation, where it forms a raised disfiguring ulcerative lesion. South American leishmaniasis is variable in its presentation. It is characterized by ulceration of the mucous membranes of the nose, mouth, and pharynx some disfiguring skin involvement also is possible. [Pg.607]

Potassium salts Anticholinergic drugs decrease GI transit, increase local exposure to potassium, thereby causing ulcerative lesions... [Pg.20]

The diagnosis of cutaneous anthrax, likewise, is initially difficult. A history of skin contact with anthrax spores or potentially anthrax-contaminated animal products is helpful. In early stages, the skin lesion is very nonspecific, hut the later presence of a painless black eschar accompanied hy severe localized edema is essentially pathognomonic for the diagnosis. Other causes of painful lymphadenopathy such as staph, strep, plague, and tularemia may mimic cutaneous anthrax. Cutaneous anthrax lesions can also resemble the necrotic ulcerated lesions due to brown recluse spider bite. [Pg.407]

This ester-type anesthetic is poorly absorbed. Because it contains benzocaine, which has a low water solubility, it is prepared in a base containing petrolatum and sodium carboxymethylcellulose. Eugenol is included for its antiseptic and anodyne properties. Hydroxy-quinoline sulfate is a preservative. This ointment can be directly applied to abraded or ulcerated lesions with minimal systemic effects. It is sometimes used to temporarily relieve denture sores and painful lesions. [Pg.901]

Oral effects of aldesleukin include xerostomia with reversible salivary gland hypofunction, a burning sensation in the mouth, taste disorders, mucosal atrophy, mucositis, glossitis, and ulcerative lesions (70,71). [Pg.63]

Ulcerative lesions of the vagina can occur in patients taking penicillamine, as a manifestation of pemphigus or cicatricial pemphigoid, or following impaired collagen synthesis (SED-8, 533) (315). [Pg.2741]

A 77-year-old man developed three ulcerated lesions on his tongue because he had difficulty in swallowing salsalate tablets. He was taught how to swallow tablets and instructed to take them with water to avoid prolonged contact of salsalate with the tongue. Three weeks later, his lesions had healed and no new ones had appeared (2). [Pg.3103]

Keratitis and keratoconjunctivitis in association with equine herpes virus (EHV) respiratory disease has been recorded in foals. In adult horses, putative viral superficial keratitis, unassociated with systemic disease, is commonly seen in practice in the UK and may occur sporadically in the USA and mainland Europe. No specific virus has been isolated consistently from affected eyes and the suspected viral etiology is based largely upon the response to topical antiviral treatment. The disease is characterized by acute ocular pain and focal epitheliopathy. Two specific forms of the disease are encountered. Type 1 is characterized by epithelial fissuring, which occasionally results in dendritic or, rarely, frankly ulcerative lesions. Type 2 is characterized by shallow pimctate ulceration. [Pg.233]

Treatment is symptomatic and supportive for wound care (similar to loxoscelism) and hematologic complications. Surgical graft repair for severe ulcerative lesions may be warranted. [Pg.142]

Rats that received phenylmercuric acetate in their drinking water for 2 years showed decreases in hemoglobin, hematocrit, and red blood cell counts at a dose of 4.2 mg Hg/kg/day (Solecki et al. 1991). The anemia observed in this study may have been secondary to blood loss associated with the ulcerative lesions in the large intestine seen at this dose (see Gastrointestinal Effects above). No treatment-related changes were observed in hematological parameters measured in rats (strain not specified) exposed via the diet for 2 years to 0.1 mg Hg/kg/day as methylmercuric chloride (Verschuuren et al. 1976). [Pg.132]


See other pages where Ulcerated lesions is mentioned: [Pg.188]    [Pg.136]    [Pg.1170]    [Pg.267]    [Pg.285]    [Pg.158]    [Pg.759]    [Pg.766]    [Pg.188]    [Pg.301]    [Pg.499]    [Pg.270]    [Pg.442]    [Pg.681]    [Pg.1356]    [Pg.2465]    [Pg.2467]    [Pg.1986]    [Pg.194]    [Pg.62]   
See also in sourсe #XX -- [ Pg.901 ]




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Gastrointestinal ulcerative lesions

Lesion

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