Tetracycline

Bertil Blok, MD, PhD

• Department of Urology
• Erasmus Medical Center Rotterdam, Netherlands

Vitiligo although radiation antibiotics nursing discount tetracycline 250 mg without a prescription, mechanical and immune facusually appears before the age of 20 years and is tors infection you get in hospital generic tetracycline 250 mg amex, and viruses have been implicated in the due to the absence of melanocytes and melanin in pathogenesis antibiotic groups buy tetracycline australia. Clinically do antibiotics for uti cause yeast infections buy 500 mg tetracycline, white asymptomatic Warty dyskeratoma appears usually in middlemacules varying in size from several millimeters to age antimicrobial light generic 500mg tetracycline visa, and men are more frequently affected than several centimeters in diameter appear antibiotics headache discount 250mg tetracycline with visa, which are women (ratio 2. The rarely affected, and only 20 oral dyskeratomas lesions are more frequently located on the dorsal were found in the literature in a review by me in aspect of the hands, the neck, periorificial regions 1985. Rarely, lesions may appear on the less nodular or papular elevation, with a small lips, whereas the oral mucosa usually remains central crater and smooth or papillomatous surunaffected (Fig. It is sessile with whitish or normal color and a diameter ranging from a few millimeters to 1 cm. Almost all intraoral lesions occur on keratinized areas (alveolar ridge, hard palate, gingiva) exposed to friction and mechanical irritation. Laboaratory test important to establish the diagnosis is the histopathologic examination. Hematologic Disorders Iron Deficiency Anemia Plummer-Vinson Syndrome Iron deficiency anemia represents an advanced Plummer-Vinson syndrome is characterized by a stage of iron deficiency. It may result from inadecombination of iron deficiency anemia, dysphagia, quate dietary iron intake, malabsorption, blood and, oral lesions, and it usually appears in middleloss, or rarely intravascular hemolysis with aged women. Iron deficiency anemia is wideto those seen in iron deficiency anemia, with a spread throughout the world and is more common characteristic smooth atrophic and red tongue among children, persons on a poor diet, and (Fig. The dysphagia is due to painful erosions and the clinical manifestations of chronic iron destrictures of the esophagus. Leukoplakia and oral ficiency anemia include fatigue, anorexia, and oropharyngeal squamous cell carcinoma may headache, lassitude, tachycardia, neurologic disdevelop. The oral manifestations include a burning sensation of the tongue, pallor of the oral Pernicious Anemia mucosa, and gradual atrophy of the filiform and Pernicious anemia is a megaloblastic anemia due fungiform papillae of the tongue. Progressively, to vitamin B12 deficiency, usually caused by a the dorsal surface of the tongue becomes smooth gastric mucosal defect that decreases intrinsic facand glistening (Fig. Other less frequent causes are total gastrecRarely, leukoplakia or superficial erosions may tomy, pancreatic dysfunction, parasitic diseases develop, and angular cheilitis and oral candidosis are common findings. Delayed wound healing and diseases of the ileum, all of which interfere with vitamin B12 absorption and antibodies against after surgical procedures may also be seen. The differential diagnosis includes pernicious Pernicious anemia affects either sex, usually anemia, geographic tongue, atrophic lichen after the 30th year of age. The clinical features planus, atrophic glossitis of tertiary syphilis, and include pallor, malaise, lassitude, weight loss, gasmalnutrition disorders. Laboratory tests helpful for the diagnosis include the oral manifestations are early and common. Before replacement therapy with iron tongue eventuates in a smooth, red, and shiny salts, it is imperative that all cases of iron defidorsal surface (Fig. The rest of the oral ciency anemia be thoroughly studied in order to mucosa may be pale, and superficial erosions may determine the exact cause. The differential diagnosis includes iron deficiency anemia, Plummer-Vinson syndrome, pellagra, and malnutrition disorders. Plummer-Vinson syndrome, redness and atrophy of tongue papillae associated with angular cheilitis. Hematologic Disorders Laboratory tests helpful in establishing the diagrecurrent ulcerations, bacterial infections, cannosis include blood count, hemoglobin determinadidosis and periodontal disease. The latter is very tion, vitamin B 12 serum level, the Schilling test, common and is characterized by severe gingival study of bone marrow aspirate, and elevated inflammation, tooth mobility, and extensive bone serum lactic dehydrogenase levels. The marginal and attached gingiva is fiery red and edematous, and usually the interdental Treatment consists of vitamin B, replacement. The differential diagnosis includes angranulocytosis, cyclic neutropenia, aplastic anemia, Thalassemias leukemia, acatalasia, hypophosphatasia, juvenile Thalassemias are a group of disorders that result diabetes mellitus, Papillon-Lefevre syndrome from an inherited abnormality of globin synthesis. Hematologic examination is the and yop) according to which globin chain or chains key to the diagnosis. Radiographic major, homozygous type) usually develops during examination of the oral cavity shows severe alveothe first few months of life and becomes progreslar bone loss. The course of the disease in childhood depends on whether or not the child is Treatment. The oral mucosa is pale; there is protrusion of the upper anterior teeth, open bite, and malocclusion (Fig. Glossodynia, loss of tongue Cyclic Neutropenia papillae, and swelling of parotid glands may occur. Cyclic neutropenia is a disorder of unknown cause characterized by a cyclic reduction in the number the diagnosis is based on specialized hematologic of circulating neutrophil leukocytes. The reduction in neutrophils occurs regularly at 3-week intervals and may last for I to 3 days. A recovery phase of 5 to 8 days follows when the Congenital Neutropenia number of neutrophils returns to normal. The disease is usually manifested in infancy or childCongenital neutropenia is also known as infantile genetic agranulocytosis. It is a rare disorder characterized by a complain of low-grade fever, malaise, headache, marked persistent decrease in circulating neutrophils, associated with severe life-threatening dysphagia, arthralgias, cervical adenitis, and skin infections. Painful oral ulcers covered by a whitish memthe exact cause is unknown although some patients have a probable autosomal recessive brane and surrounded by slight erythema are usugenetic defect. The size of ulcers varies from a few millimeters to 1 cm, and they may appear at defect in the granulocyte precursors is due to deficiency of a serum factor. Multiple bacterial infections characterize the Gingivitis is also a common finding of the disease. The differential diagnosis includes aphthous the most common infections involve the skin, ulcers, agranulocytosis, congenital neutropenia, lungs, middle ear, and urinary tract. Oral manifesacute leukemia, and primary and secondary tations are common and include persistent and syphilis. Hematologic Disorders Laboratory test helpful in establishing the diag12 to 24 hours, evidence of oral, pharyngeal, nosis is a repeated determination of neutrophils in respiratory, or gastrointestinal infections usually the peripheral blood. Oral mucosal lesions are an early sign and consist of necrotic ulcers covered by a gray-white Treatment is symptomatic. Corticosteroids and or dark "dirty" pseudomembranes without a red sometimes splenectomy may be helpful. The palate, gingiva, tongue, and tonsils Agranulocytosis are the most common sites of involvement. Severe necrotizing gingivitis with destruction of periodonAgranulocytosis is a serious disorder charactal tissues may occur (Figs. The oral terized by a severe reduction of neutrophils or lesions are frequently accompanied by increased complete absence of all granulocytes. It may be a salivation, painful mastication, and difficulty in primary process of unknown cause or secondary swallowing. Drug-induced agranulocytosis has a high mortality the differential diagnosis includes congenital rate. The important clinical conwhite blood counts in peripheral blood establish sequence of agranulocytosis is the risk of the diagnosis. The onset Treatment includes administration of antibiotics of agranulocytosis is sudden and is characterized and in selected cases white blood cell transfusions. Hematologic Disorders Aplastic Anemia the differential diagnosis includes aplastic anemia, leukemia, polycythemia vera, and agranAplastic anemia is a stem cell disorder characulocytosis. The onset of aplastic anemia is usually insidious, and nonspecific signs and symptoms, such as headache, fever, weakness, and fatigue, are early Myelodysplastic Syndrome manifestations. Slight pallor and a few petechiae on skin surfaces exposed to pressure are early Myelodysplastic syndrome includes a heterogediagnostic signs. Later, purpuric spots, which may nous group of refractory anemias often associated be spontaneous or related to trauma, may appear with thrombocytopenia, neutropenia, and/or anywhere. The exact cause of the syndrome is the oral manifestations are usually related to not clear although it may develop secondary to the degree of coexistent neutropenia and thromradiotherapy and chemotherapy and is more frebocytopenia. Necrotic ulcers similar to those seen in drome is classified into five groups depending on agranulocytosis may develop, particularly in areas hematologic disorders. The oral manifestations include persistent and recurthe differential diagnosis includes agranulocyrent ulceration (Fig. The differential diagnosis includes leukemia, agranulocytosis, cyclic neutropenia, congenital Laboratory tests helpful for diagnosis are examineutropenia, aplastic anemia, and thrombonation of bone marrow aspiration and biopsy in cytopenia. Thrombocytopenic Purpura Thrombocytopenic purpura is characterized by a decrease in platelets in the peripheral blood. The disease may be due to a primary failure of the bone marrow to generate platelets (for example, idiopathic thrombocytopenic purpura) or it may be secondary due to a myelotoxic agent (drugs, radiation, etc. Clinically, it is characterized by a purpuric rash on the skin and mucosae and a bleeding diathesis. In the oral mucosa, petechiae and ecchymoses usually occur, especially in the palate and buccal mucosa (Fig. Episodes of bleeding from the gastrointestinal and urinary tracts and epistaxis are likewise frequent findings. Idiopathic thrombocytopenic purpura, petechiae and ecchymoses of the buccal mucosa. Renal Diseases Uremic Stomatitis the differential diagnosis includes candidosis, stomatitis medicamentosa, allergic stomatitis, Uremia is a metabolic disorder due to accumulaagranulocytosis, and necrotizing ulcerative tion of nitrogenous waste products in the blood. Uremia may be the result of acute or chronic renal Laboratory tests to confirm the diagnosis include failure. Uremic stomatitis is a relatively rare disorurinalysis and blood urea level determination. The oral lesions improve after of uremic stomatitis are recognized: a) ulcerative hemodialysis and improvement of the underlying stomatitis characterized by painful superficial renal failure. Local treatment consists of improvulcers varying in size and covered by a ing oral hygiene and antimicrobial agents if necespseudomembrane (Fig. Xerostomia, uriniferous breath odor, unpleasant taste, hemorrhagic tendency and oral bleeding, and candidosis and other opportunistic infections (bacterial and viral) may also be seen (Fig. Uremic stomatitis, ulcerations covered by a necrotic pseudomembrane on the buccal mucosa. Metabolic Diseases the most common presenting symptoms are faAmyloidosis tigue, weakness, weight loss, edema, dyspnea, Amyloidosis is a rare metabolic disorder charachoarseness, bleeding, pain, carpal tunnel synterized by the extracellular deposition of a fibrildrome, etc. Deposition in sufficient amounts in vital tissues the most common cutaneous lesions are purpura, and organs can induce symptoms and signs or even petechiae, papules, nodules, and rarely bullous death. The oral mucosa is based on clinical, histochemical, and immunologic involved early in the course of the disease, and the criteria; primary, secondary, senile, familial. The tongue is characteristically affecting mainly men, usually older than the age of enlarged, firm, and indurated with red-yellowish 50 years. The gingiva is systemic amyloidosis are associated with multiple usually clinically normal. In this form of the disease amyloid lesions is a typical feature of oral amyloidosis. The infiltrates predominantly the gastrointestinal prognosis is unfavorable, with a mean survival tract, joints, skeletal muscles, heart, nervous sysperiod of about 2 years from the onset of symptem, skin, oral mucosa, and rarely other organs. Metabolic Diseases Secondary amyloidosis (amyloid A proteinreduced mobility of the tongue. Oral paraplegia and other chronic neurologic diseases, infections and ulcers may also be seen. Hoarseondary amyloidosis infiltrates predominantly the ness is the most characteristic symptom present kidneys, spleen, liver, adrenals, and rarely other from infancy or early childhood and is due to organs. The oral mucosa and the skin are rarely incomplete closure of the vocal cords because of involved. Histopathologic examination of biopsy specimens is necessary to establish the Treatment. Ascorbic acid, colchicine, steroids, melphalan, and dimethyl sulfoxide have Treatment is supportive. Lipoid Proteinosis Lipoid proteinosis, or hyalinosis cutis et mucosae, or Urbach-Wiethe disease, is a rare hereditary metabolic disorder transmitted as an autosomal recessive trait. The disease primarily affects the skin, oral mucosa, larynx, and rarely other organs. It is characterized by the deposition of an amorphous hyaline-like material (glycoprotein) in the mucous membranes and skin. Clinically, the early skin changes are characterized by the presence of papules, nodules, and pustules (Fig. These acnelike scars, although more evident on the face, are also seen on other skin regions. Verrucous hyperkeratotic lesions in areas exposed to pressure or trauma may also occur. The face, eyelid margin, pressure, and exposed areas are the most frequently affected sites. In young patients the oral changes consist of induration of the lip mucosa and the posterior part of the tongue. By the second decade, granular lesions appear on the lip and papular lesions on the palate and tongue. Metabolic Diseases Glycogen Storage Disease Type 1 b Xanthomas the glycogen storage diseases are a group of Xanthomas are papules, nodules, or plaques of genetic disorders involving the metabolic pathyellowish color that are due to lipid deposits in the ways of glycogen. The major lipid stored is usurare severe autosomal recessive metabolic disease ally cholesterol ester, although in some cases tricaused by a defect in the microsomal translocase glycerides are primarily present. The clinical features of classified into several forms and frequently reprethe disease are hypoglycemia, hyperlipidemia, sent the hallmark of particular syndromes. The hepatomegaly, delayed physical development, clinical importance of xanthomas is the fact that bleeding diathesis, short stature, hepatic their presence implies an underlying disease. Oral of the extremities, and in areas of friction and manifestations are frequent and include rapidly repeated minor trauma.

The oral mucosal lesions are almost always pres25) antibiotic blue capsule tetracycline 500 mg with mastercard, hyperhidrosis antibiotics for staph buy generic tetracycline 500 mg online, dermal and mucosal bullae antimicrobial bath rug order tetracycline 500mg on-line, ent as thick and white or grayish-white areas that blepharitis (Fig antibiotic resistance evolution buy tetracycline with american express. These lesions appear at birth or shortly thererent blisters that rupture antibiotics for dogs with skin infections purchase tetracycline 500mg, leaving a raw ulcerated after 100 oz antimicrobial replacement reservoir buy tetracycline 250 mg otc. The differential diagnosis should include leukoAtrophy of the oral mucosa is the result of repeated episodes. Finally, leukoplakia and squaplakia, lichen planus, white sponge nevus, dyskeratosis congenita, hereditary benign intramous cell carcinoma may occur (Fig. Laboratory tests somewhat helpful for diagnosis are the blood cell examination and low serum gamma globulin levels. Dyskeratosis congenita, leukoplakia and verrucous carcinoma of the dorsal surface of the tongue. Hypohidrotic Ectodermal Dysplasia Focal Palmoplantar and Oral Mucosa Hyperkeratosis Syndrome Hypohidrotic ectodermal dysplasia is characterized by dysplastic changes of tissues of ectoderFocal palmoplantar and oral mucosa hypermal origin and is usually inherited as an X-linked keratosis syndrome is inherited as an autosomal recessive trait, therefore affecting primarily dominant trait. The clinical hallmarks are characteristic keratosis palmoplantaris and attached gingival facies with frontal bossing, large lips and ears, and hyperkeratosis and by many other names. Marked hyperkeratosis of the the characteristics finding in the oral cavity is attached gingiva is a constant finding (Fig. When teeth However, other areas bearing mechanical are present, they are hypoplastic and often have a pressure or friction, such as the palate, alveolar conical shape. In some cases xerostomia may mucosa, lateral border of the tongue, retromolar occur as a result of salivary gland hypoplasia. The pad mucosa, and the buccal mucosa along the disease usually presents during the first year of occlusal line may manifest hyperkeratosis, prelife, with a fever of unknown cause along with the senting clinically as leukoplakia. The hyperretarded eruption or absence of the deciduous keratosis appears early in childhood or at the time teeth. The severity of the hyperkeratotic lesions increases with age and varies among the differential diagnosis includes idiopathic patients, even in the same family. Rarely, oligodontia, Papillon-Lefevre syndrome, chondroectodermal dysplasia, cleidocranial dysplasia, hyperhidrosis, hyperkeratosis, and thickening of the nails may be observed. The differential diagnosis should include pachyLaboratory tests useful in establishing the diagonychia congenita, dyskeratosis congenita, Papilnosis are dental radiographs and the demonstralon-Lefevre syndrome, and oral leukoplakia and tion of hypohidrosis or anhidrosis. No reliably successful treatment exists, but aromatic retinoids may occasionally be as early as possible. Focal palmoplantar and oral mucosa hyperkeratosis syndrome, hyperkeratosis of the palm. Focal palmoplantar and oral mucosa hyperkeratosis syndrome, hyperkeratosis of the soles. Papillon-Lefevre Syndrome agranulocytosis, Chediak-Higashi syndrome, leukemia, and diabetes mellitus. Eruption of the deciduous teeth proretinoids may help in the treatment of skin lesions. The severe periodontitis and oral hygiene instruction are to be recomresults in premature loss of all the deciduous teeth mended. The inflammatory response subsides at this stage and the gingiva resumes its normal appearance. The periodontitis again develops with the eruption of the permanent teeth and results in their loss by the age of 14. The oral mucosa appears normal even during the phase of active periodontal breakdown. The skin lesions usually appear between the second and fourth year of life and consist of welldemarcated, reddened and scaly hyperkeratosis of the palms and soles. Similar scaly red plaques may be seen on the dorsum of the fingers and toes, over the tibial tuberosity, and other areas of the skin. The differential diagnosis should include juvenile periodontitis, histiocytosis X, acatalasia, hypophosphatasia, hypohidrotic ectodermal dysphasia, focal palmoplantar and oral mucosa hyperkeratosis syndrome, other disorders that are associated with palmoplantar hyperkeratosis, congenital neutropenia, cyclic neutropenia, 3. Focal palmoplantar and oral mucosa hyperkeratosis syndrome, hyperkeratosis of the attached gingiva. Papillon-Lefevre syndrome, premature loss of deciduous teeth in a 6-year-old patient. Benign acanthosis nigricans, hypertrophy and elongation of the filiform papillae of the tongue. The benign variety is subdivided into: (1) genetic type that is manifested during childhood Dyskeratosis Follicularis or early adolescence and rarely affects the oral cavity; (2) acanthosis nigricans that occurs as Dyskeratosis follicularis, or Darier-White disease, part of other syndromes, such as Prader-Willi, is an uncommon disorder inherited as an autoCrouzon, and Bloom syndromes, insulin-resistant somal dominant trait. The scalp, forehead, chest and back, 25 to 60 years of age and involves the skin only. Malignant acanthosis nigricans is an acquired Clinically, multiple skin papules that occasionform that is associated with a malignancy. They are brownish-red in color and are involves the oral mucosa in about 10 to 15% of the covered by a yellowish to tan scaly crust. The tongue and lips are very often involved, trophic and ulcerated lesions may also occur. The oral mucosa is affected in 20 the filiform papillae, resulting in a shaggy appearto 40% of the cases, but the severity of oral lesions ance of the tongue (Fig. The lips may be is independent of the activity of the disease in the enlarged and covered by papillomatous growths, skin. The skin is thick the typical oral lesions are small whitish conwith small velvety papillary lesions, tags (Fig. The most common sites of and become hypertrophic, assuming a cobblestone involvement are the axillae, neck, groins, appearance (Fig. Dyskeratosis follicularis, multiple whitish confluent papules on the gingiva and alveolar mucosa. Genetic Diseases the differential diagnosis includes acanthosis nitopathologic, biochemical, ultrastructural, and gricans, papillary hyperplasia of the palate, warty genetic criteria the disorder falls into three major dyskeratoma, and familial benign pemphigus. In the oral mucosa a few bullae may rarely occur, Familial Benign Pemphigus leaving erosions that heal without scarring (Fig. Familial benign pemphigus, or Hailey-Hailey disIn the atrophic subgroup belong junctional ease, is a rare skin disease inherited as an autoepidermolysis bullosa, which is also called epidersomal dominant trait. Clinically, it is characterized molysis bullosa letalis, and generalized atrophic by a reccurent group of small flaccid vesicles arisbenign epidermolysis bullosa. The skin lesions are usually consist of generalized bullae formation, which localized, with a tendency to spread peripherally, heal without scarring. The although the center heals with pigmentation or oral mucosa shows bullae, severe ulcerations, and exhibits granular vegetations. The disease appears most frequently lesions in the generalized atrophic benign type. The oral lesions conIn the dystrophic subgroup belong dominant sist of groups of small vesicles that rupture easily, dystrophic epidermolysis bullosa and recessive leaving denuded localized areas covered with dystrophic epidermolysis bullosa. Clinically, bullae occur in to third decade and has a good prognosis, areas of friction, which rupture leaving ulcers and although the clinical course is characterized by scarring after the acute eruption. The tongue remissions and exacerbations and shows little tenbecomes depapillated and scarred (Fig. Finally, leukoand cicatricial pemphigoid and transient acanplakia, and squamous cell carcinomas may tholytic dermatosis. Histopathologic examination Generalized skin bullae leaving ulcerations that supports the clinical diagnosis. The lesions antifungal or antibacterial ointments or creams are more often found on the hands, feet, knees, are of value in cases with secondary infection of and elbows. Systemic steroids are used only in Dystrophy and loss of the nails are common severe cases. Epidermolysis Bullosa the differential diagnosis should include pemphiEpidermolysis bullosa is a group of inherited disgus, bullous pemphigoid, linear IgA disease, bulorders characterized by bullae formation on the lous erythema multiforme, dermatitis herpetiforskin and mucous membranes spontaneously or mis, cicatricial pemphigoid of childhood, and bulafter mechanical friction. Histopathologic examination is the differential diagnosis should include multiple important to establish the final diagnosis of differmucosal neuromas, multiple endocrine neoplasia ent groups of epidermolysis bullosa. Histopathologic examination of steroids, vitamin E, phenytoin, and retinoids have oral and skin neurofibromas is helpful in establishbeen used in severe cases. Treatment is supportive and presents many problems for the dermatologist, surgeon, Neurofibromatosis and endocrinologist. The cardinal features of the disease are the cafe-au-lait spots and the skin neurofibromas. The skin neurofibromas are multiple and may be either cutaneous or subcutaneous (Fig. The oral cavity is uncommonly affected but may exhibit multiple or, rarely, isolated nodular neurofibromas, which vary in size (Fig. Epidermolysis bullosa, recessive dystrophic, scarring, dystrophy and loss of the fingernails. The angiomatous lesions may sometimes be Chondroectodermal dysplasia, or Ellis-van Creexcised surgically, cauterized, or treated with the veld syndrome, is inherited as an autosomal recescryoprobe. The main characteristics are bilateral polydactyly, chondrodysplasia of long bones, involvement of ectodermal tissues (hair, nails, Peutz-Jeghers Syndrome teeth), and, rarely, congenital heart disease. The most constant oral finding is fusion of the Peutz-Jeghers syndrome is transmitted as an autoupper or lower lip to the gingiva, resulting in the somal dominant disorder with a high degree of disappearance of the mucolabial fold or multiple penetrance, characterized by intestinal polyposis fibrous bands (Fig. The manconical teeth with enamel hypoplasia are also ifestations, which may be apparent at any age, present. About 50% of tal syndrome, acrofacial dysostosis of Weyers, the patients have numerous dark spots on the other forms of chondrodystrophies. Pigmented spots 1 to 10 mm in diameter are always found in the oral mucosa, particularly on the lower lip and the buccal mucosa, but rarely on the upper lip, the tongue, the palate, and the gingiva (Fig. Oral pigmentation constitutes the most important diagnostic finding and appears Hereditary Hemorrhagic in the form of oval, round, or irregular brown or Telangiectasia black spots or patches. Radiologic evaluation of the gasand small vessels, the disease usually develops trointestinal tract is helpful in establishing the during adolescence and affects both sexes. These lesions have a bright red, purple, or violet color and disappear on pressure with a glass slide. The oral mucosa is frequently involved with multiple lesions on the lip and the dorsum of the tongue (Fig. Hemorrhage from oral lesions is frequent after minimal mechanical damage, such as tooth brushing. Epistaxis and gastrointestinal bleeding are early, common, and occasionally serious complications. Chondroectodermal dysplasia, disappearance of the mucolabial sulcus and multiple fibrous bands. It is not clear whether it represents an mainly of the colon, multiple osteomas, other inherited disorder or a dysplasia. The skin lesions are epidermal and sebaple enchondromas, principally in the small bones ceous cysts, subcutaneous fibromas and other fiof the hands and feet, although any bone of carbrous tissue disorders, and rarely increased skin tilaginous origin may be affected; multiple hemanpigmentation. Multiple osteomas are a common giomas localized on the skin, mucosae, and visfinding usually located at the facial bones and the cera; phleboliths; and pigmented skin macules. Oral manifestations include multiple the oral mucosa is rarely affected and the oral osteomas of the jaws (Fig. The and impacted teeth, odontomas, and rarely benign tongue is the most frequent site of hemangiomas, fibrous soft tissue tumors (Fig. The oral but the buccal mucosa, lips, soft palate, and other lesions are innocent but intestinal polyps have a oral regions can also be involved (Fig. Surgical excision of the enchondromas and hemangiomas may be attempted if they are symptomatic. Genetic Diseases Tuberous Sclerosis the differential diagnosis of oral lesions should include multiple fibromas, multiple condylomata Tuberous sclerosis, or Bourneville-Pringle synacuminata, focal epithelial hyperplasia, and drome, is transmitted as an autosomal dominant neurofibromatosis. Histophatologic examination of icap, paraventricular calcifications, multiple small skin and oral mucosa lesions and skull radiographs gliomas, mucocutaneous manifestations, skeletal are helpful in the diagnosis. Characteristic lesions occur on the face, principally along the nasolabial fold and cheeks. These are numerous small nodules, red to pink in color, which are actually angiofibromas, although the prevailing term is "adenoma sebaceum" (Fig. Other cutaneous changes are white macules (maple leaf or ash leaf), cafe-au-lait spots, skin tags, and multiple periungual fibromas (Fig. The gingiva or other parts of the oral mucosa may exhibit confluent nodules a few millimeters to less than 1 cm in diameter, which are of whitish or normal color (Fig. Tuberous sclerosis, confluent whitish nodules on the gingiva and the alveolar mucosa. Sturge-Weber Syndrome Klippel-Trenaunay-Weber Syndrome Sturge-Weber syndrome is a sporadic congenital dysplasia. It is characKlippel-Trenaunay-Weber syndrome, or angioterized by hemangiomas of the face and oral osteohypertrophy, is a rare dysplastic vascular mucosa, and of the leptomeninges, calcification of disorder. It is characterized by multiple facial the brain, ocular disorders, epilepsy, and mild hemangiomas (Fig. It is unilateral, vascular cutaneous lesions, ocular disorders has a bright red or purple color, and is confined (scleral pigmentation, cataract, glaucoma, and iris roughly to the area supplied by the trigeminal heterochromia) (Fig. Clinically, the are unilateral, rarely cross the midline, and may oral hemangiomas are usually located on the soft involve the upper gingiva, buccal mucosa, lips, and hard palates and gingiva, which may be and tongue (Fig. Premature tooth eruption and red or purple color and a usually flat but may also bony overgrowth may produce malocclusion. Care must be taken during tooth extractions because hemorTreatment is supportive. When the classic signs and symptoms are present, the diagnosis of Sturge-Weber syndrome is apparent. The differential diagnosis includes large disseminated hemangiomas and the Klippel-Trenaunay-Weber syndrome. Laboratory tests helpful in diagnosis and management are angiography, electroencephalography, skull radiographs, and computed tomography.

Aggravating and Relieving Features Cold antibiotic joint replacement dental cheap generic tetracycline uk, poor sleep antibiotics make acne worse before better purchase tetracycline 500mg fast delivery, anxiety antimicrobial keyboard and mouse generic 500 mg tetracycline mastercard, humidity zinc vs antibiotics for acne discount 250mg tetracycline overnight delivery, weather change antimicrobial toilet seat purchase tetracycline 500 mg with amex, fatigue antibiotic resistant bacteria in dogs discount tetracycline line, and mental stress intensify symptoms in 6070%. Symptoms are typically made worse or brought on by prolonged or vigorous work activity. Signs Tender points, widely and symmetrically distributed, are the characteristic sign of the syndrome. Relief Relief may be provided by reassurance and explanation about the nature of the syndrome and possible mechanisms of pain: anxiety may thus be reduced, expensive and hazardous investigations and treatments limited, and use of medication reduced. Low dose amitriptyline, cyclobenzaprine, and aerobic exercise have been shown, in placebo controlled double blind studies, to improve symptoms. Blood flow during exercise is reduced, and decreased oxygen uptake in muscles has been noted. Two studies have found increased levels of substance P in the cerebrospinal fluid of patients. In general, these findings, some of which may be secondary phenomena, have been insufficient to explain the major signs and symptoms of the syndrome. It also is noted frequently following trauma, and has been known to Page 46 develop after apparent viral illness. Thus the syndrome may be the final common pathway, perhaps as hyperalgesia, for a number of causative factors. Trauma or degenerative changes in the cervical or lumbar regions might precipitate the syndrome. An association with previous major depression in patients and families has suggested a genetic factor. Classification Criteria for Primary and Concomitant Fibromyalgia (from Wolfe et al. History of Widespread Pain Definition Pain is considered widespread when all of the following are present: pain in the left side of the body, pain in the right side of the body, pain above the waist and below the waist. In addition, axial skeletal pain (cervical spine or anterior chest or thoracic spine or low back) must be present. In this definition, shoulder and buttock pain is considered as pain for each involved side. Pain in 11 of 18 Tender Point Sites on Digital Palpation Definition Pain, on digital palpation, must be present in at least 11 of the following 18 tender point sites: Occiput: bilateral, at the suboccipital muscle insertions. Low Cervical: bilateral, at the anterior aspects of the intertransverse spaces at C5-C7. Supraspinatus: bilateral, at origins above the scapula spine near the medial border. Second Rib: bilateral, at the second costochondral junctions, just lateral to the junctions on upper surfaces. Gluteal: bilateral, in upper outer quadrants of buttocks in anterior fold of muscle. For classification purposes, patients will be said to have fibromyalgia if both criteria are satisfied. The presence of a second clinical disorder does not exclude the diagnosis of fibromyalgia. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia: report of the Multicenter Criteria Committee. Note: Specific Myofascial Pain Syndromes Synonyms: fibrositis (syndrome), myalgia, muscular rheumatism, nonarticular rheumatism. Specific myofascial syndromes may occur in any voluntary muscle with referred pain, local and referred tenderness, and a tense shortened muscle. Passive stretch or strong voluntary contraction in the shortened position of the muscle is painful. Satellite tender points may develop within the area of pain reference of the initial trigger point. Diagnosis depends upon the demonstration of a trigger point (tender point) and reproduction of the pain by maneuvers which place stress upon proximal structures or nerve roots. This suggests that the syndrome is an epiphenomenon secondary to proximal pathology such as nerve root irritation. Others may be coded as required according to individual muscles that are identified as being a site of trouble. Rheumatoid Arthritis (I-10) Definition Aching, burning joint pain due to systemic inflammatory disease affecting all synovial joints, muscle, ligaments, and tendons in accordance with diagnostic criteria below. Main Features Diffuse aching, burning pain in joints, usually moderately severe; usually intermittent with exacerbations and remissions. Diagnostic criteria of the American Rheumatism Association describe and further define the illness. They are as follows: (1) morning stiffness, (2) pain on motion or tenderness at one joint or more, (3) swelling of one joint, (4) swelling of at least one other joint, and (5) symmetrical joint swelling. Further criteria include: (6) subcutaneous nodules, (7) typical radiographic changes, (8) positive test for rheumatoid factor in the serum, (9) a poor response in the mucin clot test in the synovial fluid, (10) synovial histopathology consistent with rheumatoid arthritis, and (11) characteristic nodule pathology. Definite rheumatoid arthritis may be diagnosed on five criteria, and probable rheumatoid arthritis on three criteria. Signs Tenderness, swelling, loss of range of motion of joints, ligaments, tendons. Relief Usually good relief of pain and stiffness can be obtained with nonsteroidal anti-inflammatory drugs, but some patients require therapy with gold or other agents. Morning stiffness in and around joints lasting at least one hour before maximal improvement. Simultaneous soft tissue swelling or fluid in at least three joint areas observed by a physician. Positive serum rheumatoid factor, demonstrable by any method for which any result has been positive in less than 5% of normal control subjects. Radiographic changes typical of rheumatoid arthritis on posterior-anterior hand and wrist radiographs; this must include erosions or unequivocal bony decalcification which is periarticular. A patient fulfilling four of these seven criteria can be said to have rheumatoid arthritis. Differential Diagnosis Systemic lupus erythematosus, palindromic rheumatism, mixed connective tissue disease, psoriatic arthropathy, calcium pyrophosphate deposition disease, seronegative spondyloarthropathies, hemochromatosis (rarely). The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Site Joints most commonly involved are distal and proximal interphalangeal joints of the hands, the carpometacarpal thumb joint, the knees, the hips, and cervical and lumbar spines. Main Features There is deep, aching pain which may be severe as the disease progresses. The pain is felt at the joint or joints involved but may be referred to adjacent muscle groups. The pain tends to become more continuous as the severity of the process increases. Stiffness occurs after protracted periods of inactivity and in the morning but lasts less than half an hour as a rule. Radiological evidence of osteoarthritis occurs in 80% of individuals over 55 years of age. There is a greater prevalence relatively in men under the age of 45 compared with women, and in women over the age of 45 compared with men. Signs Clinically, joint line tenderness may be found and crepitus on active or passive joint motion; noninflammatory effusions are common. Later stage disease is accompanied by gross deformity, bonyhypertrophy, contracture. X-ray evidence of joint space narrowing, sclerosis, cysts, and osteophytes may occur. Usual Course Initially there is pain with use and minimal X-ray and clinical findings. Later pain becomes more prolonged as the disease progresses and nocturnal pain occurs. Relief Some have relief with nonsteroidal anti-inflammatory agents or with non-narcotic analgesics. Physical Disability Progressive limitation of ambulation occurs in large weight-bearing joints. Diagnostic Criteria No official diagnostic criteria exist for osteoarthritis, although criteria have been proposed for osteoarthritis of the knee joint. Noninflammatory arthritis of one or several diarthrodial joints, occurring in the absence of any known predisposing cause, with loss of cartilage and/or bony sclerosis (or osteophyte formation) demonstrable by X-rays. Differential Diagnosis Calcium pyrophosphate deposition disease; presence of congenital traumatic, inflammatory, endocrinological, or metabolic disease to which the osteoarthritis may be secondary. Main Features the disorder occurs clinically in about 1 in 1000 adults, more often in the elderly, but radiology shows the presence of the disease in 5% of adults at the time of death. There are four major clinical presentations: (1) pseudogout: acute redness, heat, swelling, and severe pain which is aching, sharp, or throbbing in one or a few joints; the attacks last from 2 days to several weeks, with freedom from pain between attacks; (2) pseudorheumatoid arthritis: marked by deep aching and swelling in multiple joints, with attacks lasting weeks to months; (3) pseudo-osteoarthritis: see the description of osteoarthritic features; and (4) pseudarthritis with acute attacks: the pain being the same as in osteoarthritis but with superimposed acute painful swollen joints. X-rays show calcification in the cartilage of the wrists, knees, and symphysis pubis. Relief Acute attacks respond well to nonsteroidal antiinflammatory drugs, with or without local corticosteroid injections. A definite diagnosis can be made if 1 above is present, or if 2 and 3 are present. Calcium pyrophosphate crystal deposition disease: pseudogout articular chondrocalcinosis. Gout (I-13) Definition Paroxysmal attacks of aching, sharp, or throbbing pain, usually severe and due to inflammation of a joint caused by monosodium urate crystals. Site First metatarso-phalangeal joints, midtarsal joints, ankles, knees, wrists, fingers, or elbows. Main Features More common in men in the fourth to sixth decades of life and in postmenopausal women. Acute severe paroxysmal attacks of pain occur with redness, heat, swelling, and tenderness, usually in one joint. The patient is often unable to accept the weight of bedclothes on the joint and unable to bear weight on the affected joint. Associated Symptoms In the acute phase, patients may be febrile and have leukocytosis. Signs Redness, heat, and tender swelling of the joint, which may be extremely painful to move. Usual Course Initially the disorder is monoarticular; in 50% of patients the first metatarso-phalangeal joint is involved in the great toe. Attacks may become polyarticular and recur at shorter intervals and may eventually resolve incompletely leaving chronic, progressive crippling arthritis. Relief Responds well to nonsteroidal anti-inflammatory agents, intravenous colchine, and local steroid injections. Complications Renal calculi, tophaceous deposits, and chronic arthritis with joint damage. Demonstration of intracellular sodium urate monohydrate crystals in synovial fluid leukocytes by polarizing microscopy or other acceptable methods of identifying crystals. Demonstration of sodium urate monohydrate crystals in an aspirate or biopsy of a tophus by methods similar to those in 1. In the absence of specific crystal identification, a history of monoarticular arthritis followed by an asymptomatic intercritical period, rapid resolution of synovitis following Colchicine administration, and the presence of hyperuricemia. Differential Diagnosis Calcium pyrophosphate deposition disease, infection, palindromic rheumatism. Hemophilic Arthropathy (I-14) Definition Bouts of acute, constant, nagging, burning, bursting, and incapacitating pain or chronic, aching, nagging, gnawing, and grating pain occurring in patients with congenital blood coagulation factor deficiencies and secondary to hemarthrosis. As the first joints become progressively affected, other remaining articular and muscle areas are involved with changes of disuse atrophy or progressive hemorrhagic episodes. Main Features Prevalence: hemophilic joint hemorrhages occur in severely and moderately affected male hemophiliacs. Acute hemarthrosis occurs most commonly in the juvenile in association with minor trauma. In the adult, spontaneous hemorrhages and pain occur in association also with minor or severe trauma. Characteristically the acute pain is associated with such hemarthrosis, which is relieved by replacement therapy and rest of the affected limb. A reactive synovitis results from repeated hemarthroses, which may be simply spontaneous small recurrent hemorrhages. The pain associated with them is extremely difficult to treat because of the underlying inflammatory reaction. Time Course: the acute pain is marked by fullness and stiffness and constant nagging, burning, or bursting qualities. It is incapacitating and will cause severe pain for at least a week depending upon the degree of intra-capsular swelling and pressure.

Uncommon occurrences of air embolism: description of cases and review of the literature antibiotic resistance game generic tetracycline 250 mg with visa. Systemic air embolism causing acute stroke and myocardial infarction after percutaneous transthoracic lung biopsy a case report antibiotics pharmacology purchase tetracycline 250mg mastercard. Cerebral arterial gas embolism following diagnostic bronchoscopy: delayed treatment with hyperbaric oxygen antibiotic resistance oxford purchase tetracycline overnight. Delayed hyperbaric oxygen therapy for air emboli after open heart surgery: case report and review of a success story antimicrobial cleaning cartridge 6 pack generic tetracycline 500mg fast delivery. Closon M antibiotics for acne weight gain tetracycline 250 mg discount, Vivier E buy antibiotics for sinus infection cheap tetracycline 500 mg mastercard, Breynaert C, Duperret S, Branche P, Coulon A, De La Roche E, Delafosse B. Air embolism during an aircraft fight in a passenger with a pulmonary cyst: a favorable outcome with hyperbaric therapy. Simulated microgravity produces attenuated barorefex-mediated pressor, chronotropic, and inotropic responses in mice. Massive ischemic stroke due to pulmonary barotrauma and cerebral artery air embolism during commercial air travel. Retrograde blood fow in the brachial and axillary arteries during routine radial arterial catheter fushing. Non-dysbaric arterial gas embolism associated with chronic necrotizing pneumonia, bullae and coughing: a case report. Coronary air embolism: incidence, severity, and suggested approaches to treatment. Cerebrovascular accident during endoscopy consider cerebral air embolism, a rapidly reversible event with hyperbaric oxygen therapy. Two cases of cerebral air embolism that occurred during esophageal ballooning and endoscopic retrograde cholangiopancreatography. Near-fatal systemic oxygen embolism due to wound irrigation with hydrogen peroxide. Gas embolism produced by hydrogen peroxide irrigation of an anal fstula during anesthesia. Acute cerebral gas embolism from hydrogen peroxide ingestion successfully treated with hyperbaric oxygen. Venous oxygen embolism produced by injection of hydrogen peroxide into an enterocutaneous fstula. Massive air embolism during interventional laser therapy of the liver: successful resuscitation without chest compression. Hyperbaric oxygen treatment of cerebral air embolism from orogenital sex during pregnancy. Fatal air embolism occurring during consensual intercourse in a non-pregnant female. Fatal cerebral air embolus complicating multimodality treatment of esophageal cancer. Coronary air embolism associated with atrioesophageal fstula after ablation of atrial fbrillation. Esophageal injury and atrioesophageal fstula caused by ablation for atrial fbrillation. Delayed presentation of cerebral air embolism from a left atrial-esophageal fstula: a case report and review of the literature. Fatal carbon dioxide embolism complicating attempted laparoscopic cholecystectomy-case report and literature review. Pulmonary interstitial edema after probable carbon dioxide embolism during laparoscopy. Gas embolism during laparoscopy: a report of seven cases in patients with previous abdominal surgical history. Fatal gas embolism during transurethral incision of the bladder neck under spinal anesthesia. Carbon dioxide embolism diagnosed by transesophageal echocardiography during endoscopic vein harvesting for coronary artery bypass grafting. Probable gas embolism during operative hysteroscopy caused by products of combustion. Precordial Doppler diagnosis of haemodynamically compromising air embolism during caesarean section. Fatal air embolism in an adolescent with Duchenne muscular dystrophy during Harrington instrumentation. Intraoperative visible bubbling of air may be the frst sign of venous air embolism during posterior surgery for scoliosis. Pulmonary edema as a radiologic manifestation of venous air embolism secondary to dental implant surgery. Cerebral gas embolism resulting from inhalation of pressurized helium [published erratum appears in Ann Emerg Med 1996 Nov;28(5):588]. Reversal of visual loss with hyperbaric oxygen treatment in a patient with Susac Syndrome. Correlation of electro-retinographic changes with visual prognosis in central retinal artery occlusion. Hyperbaric oxygen and acetazolamide improve visual acuity in patients with cystoid macular edema by diferent mechanisms. Ocular massage in a case of central retinal artery occlusion the successful treatment of a hitherto undescribed type of embolism. Minimally invasive therapy for clinically complete central retinal artery occlusion-results and meta-analysis of literature. Efect of hyperbaric oxygenation on microcirculation: Use in therapy of retinal vascular disorders. Care of sudden blindness: a case report of acute central retinal artery occlusion reversed with hyperbaric oxygen therapy (abstract). Observations on therapeutic results in 80 cases of central serous retinopathy treated with hyperbaric oxygenation. Presented at the 5th Chinese conference on hyperbaric medicine, Fuzhow, China; 1986 Sept 26-29. Multiple occlusive retinal arteritis in both eyes of a patient with rheumatoid arthritis. Hyperbaric oxygenation combined with nifedipine treatment for recent-onset retinal artery occlusion. Hyperbaric oxygen treatment in vascular insufciency of the retina and optic nerve. Proceedings of the second international congress on clinical and applied hyperbaric medicine. Hyperbaric oxygenation following stellate ganglion block in patients with retinal artery occlusion. Recovery from blindness through hyperbaric oxygen in a case of thrombosis on the central retinal artery. High pressure oxygen therapy in ocular diseases: With special reference to the efect of concomitantly used stellate ganglion block. Branch artery occlusion: A complication of iron-defciency anemia in a young adult with a rectal carcinoid. Swaby K, Valderrama O, Schifman J (2005) Treatment of Disc Edema and Retinal Artery Occlusion With Hbo During the Tird Trimester of Pregnancy. Inoue, O; Kajiya, S; Yachimori, (2009) Treatment Of Central Retinal Artery Occlusion(Crao) And Branch Retinal Artery Occlusion (Brao) By Hyperbaric Oxygen Terapy(Hbo) 107 Eyes Over 20 Years. Treatment of a patient with acute central retinal artery occlusion with hyperbaric oxygen therapy. Early hyperbaric oxygen treatment for nonarteritic central retinal artery obstruction. American College of Cardiology; American Heart Association: American College of Cardiology/American Heart Association clinical practice guidelines: Part I. Masters T, Westgard B, Hendrikson S (2015) Central Retinal Artery Occulsion Treated with Hyperbaric Oxygen: A Retrospective Review. Desola J, Papoutsidakis E, Martos P (2015) Hyperbaric oxygenation in the treatment of Central Retinal Artery Occlusions: An analysis of 214 cases following a prospective protocol. Lu C, Wang J, Zhou D (2015) Central retinal artery occlusion associated with persistent truncus arteriosus and single atrium: a case report. Tang P, Engel K, and Parke D (2016) Early Onset of Ocular Neovascularization After Hyperbaric Oxygen Terapy in a Patient with Central Retinal Artery Occlusion. Management of Central Retinal Artery Occlusion following successful Hyperbaric Oxygen Terapy: A Case Report. A Rare Complication after Septoplasty: Visual Loss due to Right Retinal Artery Spasm. Comparison of Hyperbaric Oxygen versus Iloprost Treatment in an Experimental Rat Central Retinal Artery Occlusion Model. Cardiovascular Risk Factors in Central Retinal Artery Occlusion: Results of a Prospective Standardized Medical Exam. Rethinking the Standard of Care for Patients with Central Retinal Artery Occlusion. Chapter 2B: Arterial Insufficiencies: Hyperbaric Oxygen Therapy for Selected Problem Wounds Enoch T. Regulation of wound-healing angiogenesis-efect of oxygen gradients and inspired oxygen concentration. A comparison of the efects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Regulation of wound healing and fbrosis by hypoxia and hypoxia-inducible factor-1. Macrophage-derived growth factors in wound healing: regulation of growth factor production by the oxygen microenvironment. Efect of oxygen supply on wound healing and formation of experimental granulation tissue. Angiogenesis and vasculogenesis: inducing the growth of new blood vessels and wound healing by stimulation of bone marrow-derived progenitor cell mobilization and homing. Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. Paper presented at: Fourth International Congress on Hyperbaric Medicine 1970; Tokyo. Regeneration of the skin epithelium in healing wounds under noral conditions and at reduced baroetric pressure. Efect of long-term hypoxia on protein synthesis in granuloma and in some organs in rats. Factors infuencing the outcome of lowerextremity diabetic ulcers treated with hyperbaric oxygen therapy. The predictive value of transcutaneous oxygen tension measurement in diabetic lower extremity ulcers treated with hyperbaric oxygen therapy: a retrospective analysis of 1,144 patients. Transcutaneous oximetry in clinical practice: consensus statements from an expert panel based on evidence. Relationship between ulcer healing after hyperbaric oxygen therapy and transcutaneous oximetry, toe blood pressure and ankle-brachial index in patients with diabetes and chronic foot ulcers. A clinical practice guideline for the use of hyperbaric oxygen therapy in the treatment of diabetic foot ulcers. Use of in-chamber transcutaneous oxygen measurement to determine optimal treatment pressure in patients undergoing hyperbaric oxygen therapy. A prospective randomized double-blinded controlled trial evaluating indocyanine green fuorescence angiography on reducing wound complications in complex abdominal wall reconstruction. Intraoperative indocyanine green fuorescence angiography to predict wound complications in complex ventral hernia repair. Efectiveness of intraoperative indocyanine-green fuorescence angiography during inguinal lymph node dissection for skin cancer to prevent postoperative wound dehiscence. The use of indocyanine green angiography to prevent wound complications in ventral hernia repair with open components separation technique. Indocyanine green fuorescence monitoring of perineal wound contamination in abdominoperineal resection: a preliminary report. Use of indocyanine green fuorescent angiography in a hyperbaric patient with soft tissue radiation necrosis: a case report. Visulization of angiogenesis and vasculogenesis in a late tissue radiation injury of the chest wall treated with adjuvant hyperbaric oxygen therapy using fuorescence angiography. The use of indocyanine green fuorescence angiography to assess perfusion of chronic wounds undergoing hyperbaric oxygen therapy. Efect of hyperbaric oxygen treatment on oxygen tension and vascular capacity in irradiated skin and mucosa. Hyperbaric oxygen attenuates apoptosis and decreases infammation in an ischemic wound model. Hyperbaric oxygen selectively induces angiopoietin-2 in human umbilical vein endothelial cells. Hyperbaric oxygen therapy mediates increased nitric oxide production associated with wound healing: a preliminary study. Hyperbaric oxygen induces a cytoprotective and angiogenic response in human microvascular endothelial cells. Hyperglycemia regulates hypoxia-inducible factor1alpha protein stability and function. Hyperbaric oxygen induces basic fbroblast growth factor and hepatocyte growth factor expression, and enhances blood perfusion and muscle regeneration in mouse ischemic hind limbs. Paper presented at: Sixth International Congress on Hyperbaric Medicine 1979; Aberdeen, Scotland. Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer.

Perform a focused physical examination for the causes of benign intracranial hypertension (pseudotumour cerebri) infection after sex buy cheap tetracycline 500mg on line. Take a directed history and perform a focused physical examination for myotonia dystrophia infection root canal buy 500mg tetracycline with visa. Take a directed history and perform a focused physical examination for limb girdle dystrophy 60 virus 404 error buy generic tetracycline 250 mg. Perform a focused physical examination to determine if a lesion affects functions of the dominant cerebral hemisphere antimicrobial wound spray purchase tetracycline pills in toronto. Perform a focused physical examination to determine the location of lesions causing sensory loss antimicrobial ointment neosporin buy tetracycline 250 mg amex. Perform a focused physical examination for meningitis (the numbers in prackets represent valves for sensivity) 80 antibiotic not working cheap tetracycline online mastercard. Perform a directed physical examination of the pulmonary system for tracheal deviation 3. Perform a directed physical examination of the pulmonary system for consolidation, collapse, effusion, or fibrosis. Perform a focused physical examination to distinguish between the major causes of dullness at a lung base. Take a focused history and perform a directed physical examination for chronic bronchitis. Take a directed history and perform a focused physical examination for fibrosing alveolitis. Perform a focused physical examination of the joints of the upper and lower body and from the abnormal articular findings, give the most likely diagnosis. Take a directed history for the common side effects of nonsteroidal anti-inflammatory drugs. Take a directed history and a focused physical examination for features differentiating diseases affecting the elbow. Perform a focused physical examination for diseases that may have positive rheumatoid factor. Perform a focused physical examination to distinguish between papilladema vs papillitis. Perform a focused physical examination for the causes of the Argyll Robertson pupil. Take a directed history and perform a focused physical examination for a lesion at the cerebellopontine angle. Take a directed history and perform a focused physical examination to determine the causes of dysarthria (disorder of articulation). Perform a focused physical examination to distinguish between an intramedullary from an extramedullary cord lesion. Perform a focused physical examination to localize a spinal cord lesion to a specific lumbar or sacral nerve root level 30. Perform a focused physical examination for the causes and site of spinal cord compression 33. Take a directed history and perform a focused physical examination for tabes dorsalis. Perform a focused physical examination of the sensory dermatomes of the peripheral nervous system, and give their signature zones. Perform a focused physical examination for the cause of a carcinomatous neuropathy. Perform a focused physical examination for Charcot-Marie-Tooth disease (features of hereditary motor and sensory neuropathy). Perform a focused neurological examination to determine the location of an arterial cerebral occlusion. Take a directed history to detect disease of the frontal, parietal or temporal lobe, or the motor cortex. R Thomson 8 Introduction the language of neurology Agnosia o Failure to recognize, whether visual, auditory or tactile; Related to receptive dysphagia. The Medical Society, Faculty of Medicine, University of Toronto 2005, page 156-159. Cranial nerves Remember: You need to establish where the lesion is, and what the likely lesion is. R Thomson 14 Vagal o Motor to soft palate, larynx and pharynx (from nucleus ambigus) o Sensory and motor for heart, respiratory passengers and abdominal viscera (from dorsal nucleus) Spinal accessory o Motor to sterno mastoid and trapezius o Accessory fibres to vagus Hypoglossal Motor to tongue and hyoid bone depressors Source: Burton J. R Thomson 15 V (Trigeminal) o Sensory Pain, temperature and light touch for same side of face, cornea, sinuses, nasal mucosa, teeth, tympanic membrane, anterior 2/3 of tonguefi The Medical Society, Faculty of Medicine, University of Toronto 2005, pages 157-158. Central scotoma Left homonymous hemianopia with macular sparing Adapted from: Talley N. A1: o the pupil react to light but not to accommodation o Seen in parkinsonism caused by encephalitis lethargic Q2: What causes miosisfi A2: o Old age o Pilocarpine (treatment for glaucoma) Q3: What non-neurological conditions cause an eccentric pupilfi R Thomson 25 Argyll Robertson pupil (distinguish) Pontine lesion Narcotics o Sympathetic Horner syndrome o Drugs Pilocarpine eye drops Adapted from: Baliga R. R Thomson 26 Benzene Tobacco o Metabolic Diabetes mellitus B12 deficiency Intestinal or uterine haemorrhage o Demyelinating disease eg. Papilladema Papillitis Optic disc o Swollen without venous o Optic disc swollen pulsation Visual acuity o Normal (early) o Poor Blind spot o Large o Large central scotoma Visual fields ofperipheral constriction o Onset usually sudden and o Usually slow onset of bilateral unilateral o Colour vision normal o Eye movementno pain o Painful Adapted from: Baliga R. Useful background: Cervical sympathetic pathway to the eye Mid brain (superior colliculus) Tectospinal tract C8, T1 and 2 ventral roots Cervical sympathetic trunk Internal carotid and cavernous nerve plexus Ophthalmic division of the trigeminal nerve Source: Burton J. Perform a focused physical examination to determine the cause of unequal pupils (anisocoria). R Thomson 29 Useful background: Useful terms Odds that a given symptom or sign is present in a person without the targeted disorder. R Thomson 32 o Lyme disease Degenerative o Multiple sclerosis o Syringobulbia Adapted from: Baliga R. Perform a focused physical examination of the patient with a large pupil which reacts slowly to light and accommodation (Holmes-Adie syndrome). At baseline, there is anisocoria with the right pupil larger than the left (first row). After instillation of dilute pilocarpine eye drops (fourth row), the pupil constricts markedly. R Thomson 34 Useful background: the relative afferent papillary defect (Marcus Gunn Pupil) Room Licat symmetric Swinging Flashlight Normal eye illuminated pupils constrict Abnormal eye illuminated pupils dilate Marcus Gunn pupil this shows a patient with an abnormal right optic nerve. R Thomson 35 Secondary to ocular disease o Glaucoma o Opthalmitis o Trauma (contusion cataract) Metabolic o Diabetes mellitus o Hypoparathyroidism (lamellar cataract) o Corticosteroid therapy Miscellaneous causes o Atopic eczema Heat and irradiation Adapted from: Burton J. Q: What is the neurological changes associated with hyperparathyroidism A: Cataracts Papilloedema Basal ganglia defects Benign intracranial hypertension Source: Burton J. R Thomson 37 Useful background: Cardinal positions of gaze Adapted from: Filate W. Useful background: Common causes of third nerve palsy Infection o Encephalitis o Basal meningitis o Carcinoma at the base of the skull Infiltration o Parasellar neoplasms o Meningioma at the wing of sphenoid o Tumors, collagen, vascular disorder, syphilis. R Thomson 41 Useful background: Causes of a red and painful eye Disease Distribution of Corneal Pupil Vision Iris Discharge redness surface Bacterial o Peripheral Normal o Normal o Normal o Normal o Mucoconjunctconjunctiva o Reactive puralent tivitis o Bilateral (central sparing) Acute iritis o Around Dull o Irregular o fi/ o Normal o Watery cornea shape blurred o Unilateral o Miotic o Photoo Slowly phobia reactive Acute o Around Dull o Oval o fi/ o Corneal o Watery closure cornea partially blurred edema glaucoma o Unilateral dilated o Nonreactive Corneal o Around Dull o Normal o o Defect o Watery/ ulcer/ cornea Fluoo Reactive shadow mucoabrasion o Unilateral rescein purulent dye stains ulcer Irregul ar light reflex Disease Distribution of Corneal Pupil Vision Iris Discharge redness surface Subo Localised Normal conjunctival hemorrhage hemorrhage o No posterior limit Conjunctival o Localised Normal hemorrhage hemorrhage o Posterior limit present Adapted from: Talley N. A: o Facial and trigeminal nerves o Corticospinal tract o Median longitudinal fasciculus o Parapontine reticular formation o Temporal bone Source: Baliga R. Useful background: Ramsay-Hunt Syndrome (herpes zoster of geniculate ganglion) Pain in ear and mastoid region Facial paresis or spasm Deafness, dizziness or hyperacusis Vesicles on auricle or anterior fauces Ipsilateral taste loss in anterior two-thirds tongue Source: Burton J. A1: oThe nervus intermedius of Wrisberg oTaste sensation from the anterio two thirds of the tongue oProbably, cutaneous impulse from the anterio wall of the external auditory canal. R Thomson 51 Useful background: Causes of multiple cranial nerve palsies inherited o Arnold Chiari malformation Infection o Guillain Barre syndrome (spares sensory nerves) o Tuberculosis o Sarcoidosis infiltration o Nasopharyngeal carcinoma o Hematological malignancy, o Brainstem tumor (eg in the cerebellopontine angle) have similar signs Vascular o Brainstem vascular disease causing crossed sensory or motor paralysis. R Thomson 52 Causes o Infection Local meningeal involvement Syphilis Tuberculosis o Infiltration Acoustic neuroma. Medical Society, Faculty of Medicine, University of Toronto, 2005, pages 153 to 154 and 157 to 158. The Medical Society, Faculty of Medicine, University of Toronto, 2005, page 162; Baliga R. Perform a focused physical examination to determine the site of defect and the causes of dysarthria (disorder of articulation). Perform a focused physical examination for posterior inferior cerebellar artery thrombosis. Take a directed history and perform a focused physical examination for the jugular foramen syndrome. Nystagmus and vertigo Useful background: Nystagmus Definition o A series of involuntary, rythamic oscillation of one or both eyes. R Thomson 59 Peripheral lesions o Severe vertigo + nausea/vomiting in acute phase o Lying still, fixing eyes on bright objects helps symptoms Central lesions Fast Findings with a right sided side lesion looking to the left Slow drifting phase Vestibular nystagmus Central (vestibular Peripheral nuclei) (labyrinth or vestibular nerve) Vertigo Rare Yes Auditory symptoms No Yes Lying still, fixing eyes on No Yes bright objects helpful Adapted from: Davey P. R Thomson 61 Headache and facial pain Useful background: Mechanisms of headache production Muscle o Skeletal muscle contraction. Useful background: History taking for headache Likely many aspects of history taking, a combination of pretest probability estimation, a system of inquiry, and thoughtful reiteration and probing work best. Two of the following are present: unilateral pain, pulsing or throbbing quality to pain, moderateto-severe intensity preventing daily activities, or pain provoked by routine physical activity iv. One of the following is present: nausea, vomiting, photophobia, phonophobia, or osmophobia v. R Thomson 65 and flushing of the forehead lasting minutes to hours, in bouts lasting several weeks, and coming a few times a year. The Medical Society, Faculty of Medicine, University of Toronto, 2005, page 172; Jugovic P. Take a directed history and perform a focused physical examination to distinguish between pseudobalbar and bulbar palsy. R Thomson 71 o Chronic Alcoholic cerebellar degeneration Hypothyroidism Hydrocephalus Chronic infection (panencephalitis, rubella, prion disease) Vitamin E deficiency Paraneoplastic syndrome Alcoholic cerebellar degeneration o An ataxia that affects the trunk and gait (upper body ataxia and dysarthria are less frequent). A:o Roussy-Levy disease: hereditary spinocerebellar degeneration with atrophy of lower limb muscles and loss of deep tendon reflexes. Q: Name the three parts of the cerebellum, and perform a focused physical examination to distinguish which part is causing the ataxia. A:o Paleocerebellum Gait ataxia (inability to do tandem walking): anterior lobe o Aerchicerebellum Truncal ataxia (drunken gait, titubation): flocculonodular or posterior lobe o Neocerebellum Limb ataxia, especially upper limbs and hyponia: lateral lobes Source: Baliga R. Perform a focused physical examination to distinguish between sensory ataxia and cerebellar ataxia. Clinical Cerebellar ataxia Sensory ataxia Site of lesion o Cerebellum Posterior column or peripheral nerves Deep tendon o Unchanged or Lost or diminished reflexes pendular Deep sensation o Normal Decreased or lost Sphincter o None Decreased when disturbances posterior column involved, causing overflow incontenence Source: Baliga R. A1: o Cerebellar signs on the side opposite the third nerve palsy (which is produced by damage to the nucleus itself or to the nerve fascicle). R Thomson 75 Spinal cord and nerve roots Useful background: Spinal cord Transverse section Gracilis Cuneatus Crossed pyramidal Post. Useful background: Spinal cord disorders Paraplegia or quadriplegia due to complete transverse lesions Effect depends on level. The Medical Society, Faculty of Medicine, University of th Toronto, 2005 Filate W. The Medical Society, Faculty of Medicine, University of Toronto, 2005,page 175; Talley N.

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