Benjamin M. Brucker, MD

• Assistant Professor, Urology
• New York University

Branched serpentine vessels adjacent to keratin the presence of branched serpentine vessels adjacent to keratin is a strong clue to keratoacanthoma (7 pulse pressure reference range purchase plavix 75mg free shipping. Commonly keratoacanthomas are symmetrical lesions with a central keratin plug and vessels (linear blood pressure medication and hair loss purchase plavix 75 mg, looped arrhythmia ablation buy generic plavix line, serpentine heart attack 2013 purchase plavix 75 mg line, coiled or polymorphous) arranged in a radial pattern and with this morphology they are easily identified (2) blood pressure chart meaning 75mg plavix otc. The clue of branched serpentine vessels adjacent to keratin is particularly useful when the presentation is not typical heart attack restaurant order plavix toronto, but it is also often present in the more typical cases. There is an ongoing controversy among different schools of dermatopathologists whether keratoacanthomas are benign lesions or highly differentiated variants of squamous cell carcinoma (3). However, even the proponents of the concept that a keratoacanthoma is a benign neoplasm agree that lesions that appear as keratoacanthomas clinically or dermatoscopically should be excised to rule out squamous cell carcinoma. Ulceration may of course be caused by trauma to normal skin or benign lesions, but malignant neoplasms and especially basal cell carcinomas may ulcerate after trivial irritation. Adherent fiber may be found on basal cell carcinomas even when ulceration was not observed prior to dermatoscopy. As ulceration is often an important clue to malignancy, so is the presence of dermatoscopically observed adherent fiber (7. Top left: Adherent fabric fiber can easily be distinguished from intact hair on this ulcerated basal cell carcinoma. Top right: Adherent fiber lies over a focal ulcer on the surface of this basal cell carcinoma. Bottom left: Fabric fiber reveals the presence of ulceration which was not evident clinically on the surface of this squamous cell carcinoma. Bottom right: Focal ulceration on a nodular portion of a basal cell carcinoma is identified by a single adherent fabric fiber. The ulceration was not evident clinically and may have been missed dermatoscopically except for the adherent fiber. These 2 cases of tinea nigra were confirmed histopathologically when biopsied to exclude melanoma. Each of these keratoacanthomas has the typical morphology of a central keratin plug with vessels surrounding it in a radial pattern. Top left: Keratoacanthoma with polymorphous vessels (coiled and looped) including a focus of serpentine branched vessels just inferior to the central part of the keratin plug. Top right and bottom left and right: Keratoacanthomas with serpentine branched vessels adjacent to keratin. Circles, ovals, and distorted circles A pattern of circles on non-facial skin, not correlating to infundibulae and in conjunction with ovals and distorted circles is a strong clue to a seborrheic keratosis (7. The circles, ovals and distorted circles are produced by elongation and broadening of rete ridges due to acanthosis of the epidermis (7. Pigmentation of these structures is due to hyperpigmentation of basal keratinocytes. Double reticular lines Occasionally it is apparent on higher magnification that the individual "lines" forming a reticular pattern are actually double lines enclosing a hypopigmented space. The hypopigmented space between the pair of lines indicates that the rete ridges are not filled with pigment. If this pattern is found throughout a lesion it usually indicates a benign lesion. If, on the other hand, the rete ridges are broadened and filled with pigment (filled with neoplastic melanocytes) the hypopigmented space becomes pigmented and instead of double lines one sees thick reticular lines, which is a clue to melanoma. In this case the rete ridges are not filled with neoplastic melanocytes but with pigmented keratinocytes. Four dots in a square (four-dot clod) these structures were first described by Marghoob and Cowell (4) who called them "rosettes" (see also chapter 4). In the bottom lesion one can see the transformation of circles to parallel curved lines. If the rete ridges are thin and regular and the basal keratinocytes are hyperpigmented one sees reticular lines (like for example in solar lentigo and Clark nevi) and if the rete ridges are broadened by regular acanthosis (like in dermatofibroma) one sees small regular circles (top). If the rete ridges are broadened because of irregular acanthosis and the basal keratinocytes are hyperpigmented (like in some seborrheic keratoses) one sees distorted circles on dermatoscopy (bottom). At high magnification (bottom row) double reticular lines throughout the lesion are obvious. Left: With polarized light the 4-dots are seen very clearly on the pigmented portion of this actinic keratosis. Dermatoscopically (B, C) there are only thin gray circles on a brown structureless background. This is not the pattern of lichen-planus-like keratosis or pigmented actinic keratosis. Short white lines in an invasive melanoma arising in a pre-existing nevus (dermatoscopy on the right). In the appropriate context it is a clue to actinic keratosis or superficial squamous cell carcinoma but it is not as specific as initially thought. Gray circles versus gray dots on the face We consider that any dermatoscopic gray in head or neck lesions should be regarded as a clue to melanoma (5), with a differential diagnosis of lichen planus-like keratosis and pigmented actinic keratosis. When the gray is seen as thin gray circles, this is a far stronger clue to melanoma than gray dots, even when the dots are arranged as circles (7. They may be arranged in a reticular pattern or perpendicular to each other but without crossing each other. Reticular white lines are seen in this dermatofibroma with both non-polarized (left) and polarized (right) dermatoscopy. Most white lines correspond to fibrosis or sclerosis in the dermis, some to hypergranulosis (for example the white lines seen in lichen planus), and some to a combination of both (8). In other situations, white lines are only seen when dermatoscopes with a polarizing light source are used (9). Polarizing specific white lines are seen as two groups of parallel lines, with the groups at right angles to each other (perpendicular white lines), and correspond to fibrosis in deeper parts of the dermis. In the short "Chaos and Clues" algorithm presented in chapter 5, any white lines seen either with polarizing or non-polarizing dermatoscopy are a clue to malignancy if they are whiter than normal skin. White lines are not highly specific, being seen commonly in melanomas (7) and Spitz nevi (10, 11) (7. White reticular lines rule out a basal cell carcinoma with a similar high degree of certainty as pigmented reticular lines (7. Angulated lines (polygons) Angulated lines (polygons) were first described as a clue to flat melanomas on non-facial, chronic sun-damaged skin by Keir (13) (7. These melanomas often mimic solar lentigo and may lack other, more conventional, melanoma clues. As defined by Keir, angulated lines (polygons) form multi-sided geometrical shapes which may be completely or incompletely enclosed. In a recent study by Jaimes and Keir (14) angulated lines were found in 44 % of flat melanomas on non-facial, chronic sun-damaged skin. Facial angulated lines have been termed rhomboids (15) or zig-zag pattern (16) by others. Angulated lines on facial skin can also be found in pigmented solar keratosis (5). White circles White circles are a clue to actinic keratosis and squamous cell carcinoma (including keratoacanthomas) (2) especially on, but not limited to the face (7. In flat pigmented lesions on the face which have evenly distributed gray dots (differential diagnosis: melanoma in situ, lichen planus-like keratosis, and pigmented actinic keratosis) the presence of white circles helps to make the diagnosis of pigmented actinic keratosis (5) (7. The clinical image on the left may be interpreted as pigmented basal cell carcinoma or as melanoma. Left: this invasive melanoma is asymmetric with clues to malignancy including gray dots and eccentric structureless areas. Right: this in-situ melanoma has some features suggestive of solar lentigo (curved lines, circles, scalloped border). Because this pigment can be in keratinocytes as well as melanocytes, no conclusion can be drawn about melanocytic status from this criterion alone (17) (7. While it is true that most lesions with reticular lines due to melanin pigment are melanocytic, there are frequent exceptions (see also chapter 2 for examples of non-melanocytic lesions with reticular lines). Reticular lines also occur in seborrheic keratoses, solar lentigines and dermatofibromas. Only the pathologist can see melanocytes and the pathologist must be the arbiter of melanocytic status. The differential diagnosis includes melanoma in situ, lichen planus-like keratosis, and pigmented actinic keratosis. The clue of white circles identifies these lesions as pigmented actinic keratosis. While in most cases this clue does correctly identify solar lentigines or flat seborrheic keratoses, this pattern may also be seen in melanoma. White dots and clods ("milia") indicate a seborrheic keratosis White dots and clods (milia) are produced by small intraepidermal accumulations of keratin. Although white dots and clods are most commonly found in seborrheic keratosis, they also occur in malignancies such as basal cell carcinoma and melanoma (7. Seborrheic keratosis should never be diagnosed on the basis of white dots and clods alone. This is a lesion with curved lines ("light-brown fingerprint like structures" in the metaphoric language) that could be easily discarded as a solar lentigo/flat seborrheic keratosis. This lesion could easily be mistaken for a seborrheic keratosis if it is not assessed in context. Clinically (left) this is a solitary lesion, whereas seborrheic keratoses usually are seen in large numbers. Dermatoscopically (right) there are no yellow or orange clods, the border is poorly demarcated, and the vessels are neither looped nor centered in hypopigmented clods. Therefore there is little support for a proposed diagnosis of seborrheic keratosis, even if white dots are the standout feature of this lesion. The presence of gray dots always raises the possibility of melanoma, and this was confirmed on histopathology (invasive < 1 mm). An unequivocal blue structureless area ("blue veil") is present on the dermatoscopic image, a finding not uncommon in acanthotic seborrheic keratosis. This seborrheic keratosis is chaotic, has reticular lines, and a few pseudopods at the periphery in the area indicated by the white rectangle. Whilst reticular lines are in synchrony with the diagnosis of a seborrheic keratosis, pseudopods are an unexpected finding. White dots ("milia") are not visible in this image taken with polarized dermatoscopy. Blue structureless area ("blue veil") indicates melanoma A blue structureless area is a good clue to differentiate a melanoma from a nevus. It is not a good clue to differentiate a melanoma from a seborrheic keratosis because acanthotic seborrheic keratoses frequently show a blue structureless area (7. Segmental pseudopods or segmental radial lines indicate a melanoma Although pseudopods are admittedly a very strong clue to melanoma they can be found in other lesions too. The absence of a parallel ridge pattern and the presence of a parallel furrow pattern in acral lesions does not exclude acral melanoma. This is melanoma because it is chaotic and there are clues to malignancy (eccentric structureless zone). A parallel furrows pattern indicates a benign acral lesion the absence of a parallel ridge pattern and the presence of a parallel furrow pattern in acral lesions does not exclude acral melanoma (18) (7. If there is chaos and a clue to melanoma then the lesion is suspicious for melanoma regardless of whether parallel lines are situated in the furrows or on the ridges. Serpentine branched vessels indicate a basal cell carcinoma While it is true that most basal cell carcinomas, especially when they are nodular, have serpentine branched vessels ("arborizing vessels"), it is not true that this arrangement of vessels is highly specific for basal cell carcinomas. Any tumor underneath the superficial vascular plexus may show serpentine branched vessels in dermatoscopy including other neoplasms (19), cysts (20), deposits, and inflammatory lesions (21) (7. Malignant neoplasms are chaotic Although most pigmented cutaneous malignant neoplasms are chaotic by dermatoscopy there are important exceptions: Small melanomas, nodular melanomas, and flat facial and acral melanomas are often symmetrical (7. Whilst in large and flat lesions chaos takes precedence over clues, clues are more important than chaos in small (5 mm and less) and nodular lesions. In these cases, information beyond dermatoscopy like the clinical context ("ugly duckling") or the history given by the patient ("changing lesion") may draw the attention of the examiner to the lesion. Serpentine branched vessels can be found in any tumor that is situated underneath the superficial vascular plexus, not only in basal cell carcinomas. Four examples are trichoepithelioma (top left), eccrine hidrocystoma (top right), pilar sheath acanthoma (bottom left), Merkel cell carcinoma (bottom right). Images courtesy of Nisa Akay, Jean-Yves Gourhant, Iris Zalaudek and Giuseppe Argenziano). The discrete gray circles (not dots arranged as circles) on dermatoscopy allow the diagnosis of melanoma in situ with confidence. Middle row: Melanomas that grow quickly may present as nodules and often lack chaos. The diagnosis of melanoma can be suspected because of white lines and a blue structureless area. Bottom row: Small melanoma (5 mm in diameter) that is not chaotic on dermatoscopy but has gray and blue clods in the center. On the clinical overview (top) this pigmented lesion is different than the other pigmented lesions in this area ("ugly duckling").

The encephalitic form (about 80% of the cases) produces the classic rabies manifestations of delirium alternating with periods of calm heart attack news cheap 75mg plavix mastercard, extremely painful laryngeal spasms on attempting drinking (hydrophobia) arteria brachialis cheap plavix, autonomic stimulation (hypersalivation) arrhythmia foods to eat 75 mg plavix, and seizures arrhythmia heart attack order generic plavix from india. Both forms progress relentlessly to coma arrhythmia games generic 75mg plavix, autonomic nervous system dysfunction pulse pressure quizlet 75 mg plavix otc, and death. Laboratory Findings Biting animals that appear well should be quarantined and observed for 10 days. A wild animal, if captured, should be sacrificed and the head shipped on ice to the nearest laboratory qualified to examine the brain for evidence of rabies virus. When the animal cannot be examined, raccoons, skunks, bats, and foxes should be presumed to be rabid. Pathologic specimens often demonstrate round or oval eosinophilic inclusion bodies (Negri bodies) in the cytoplasm of neuronal cells, but the finding is neither sensitive nor specific. If postexposure prophylaxis (discussed below) is given expediently, before clinical signs develop, it is nearly 100% successful in prevention of disease. Once the symptoms have appeared, death almost inevitably occurs after 7 days, usually from respiratory failure. Most deaths occur in persons with unrecognized disease who do not seek medical care or in individuals who do not receive postexposure prophylaxis. The very rare cases in which patients recover without intensive care are referred to as "abortive rabies. Symptoms and Signs While there is usually a history of animal bite, bat bites may not be recognized. The prodromal syndrome consists of pain at the site of the bite in association with fever, malaise, es kerrs oo k eb oo e//eb me Immunization of household dogs and cats and active immunization of persons with significant animal exposure (eg, veterinarians) are important. Animals that are frequent sources of infection to travelers are dogs, cats, and nonhuman primates. In some countries, the full spectrum of vaccines, from human diploid rabies to chromatographically purified rabies vaccine are available, whereas in others, the gamut is smaller. Neither the passive nor the active form of postexposure prophylaxis is associated with fetal abnormalities and thus pregnancy is not considered a contraindication to vaccination. The World Health Organization is embarking on a program to eliminate dog-transmitted human rabies by 2030. In some Western European countries, campaigns of oral vaccination of wild animals led to the elimination of rabies in wildlife. Local Treatment of Animal Bites and Scratches Thorough cleansing, debridement, and repeated flushing of wounds with soap and water are important. Any contact or suspect contact with a bat, skunk, or raccoon is usually deemed a sufficient indication to warrant prophylaxis. Postexposure treatment including both immune globulin and vaccination should be administered as promptly as possible when indicated. As much as possible of the full dose should be infiltrated around the wound, with any remaining injected intramuscularly at a site distant from the wound. Finger spaces can be safely injected without development of a compartment syndrome. Two vaccines are licensed and available for use in humans in the United States: a human diploid cell vaccine and a purified chick embryo cell vaccine. The current vaccines may be given as four injections of 1 mL intramuscularly in the deltoid or, in small children, into the anterolateral thigh muscles on days 0, 3, 7, and 14 after exposure. An alternative vaccination strategy that takes only 1 week, with injections on days 0, 3, and 7 after exposure with a Vero cell vaccine is reportedly successful in achieving adequate neutralizing titers at days 14 and 28 in a study from Thailand. Allergic reactions to the vaccine are rare and include a report of sudden unilateral sensorineural hearing loss and immune thrombocytopenic purpura, although local reactions (pruritus, erythema, tenderness) occur in about 25% and mild systemic reactions (headaches, myalgias, nausea) in about 20% of recipients. The vaccine is commercially available or can be obtained through health departments. Preexposure Immunization Preexposure prophylaxis with three injections of human diploid cell vaccine intramuscularly (1 mL on days 0, 7, and 21 or 28) is recommended for persons at high risk for exposure: veterinarians (who should have rabies antibody titers checked every 2 years and be boosted with 1 mL intramuscularly); animal handlers; laboratory workers; Peace Corps workers; and travelers with stays over 1 month to remote areas in endemic countries in Africa, Asia, and Latin America. Immunosuppressive illnesses and agents including corticosteroids as well as antimalarials-in particular chloroquine-may diminish the antibody response. A single dose booster at 10 years after initial immunization increases the level of antibody titers. Unfortunately, data from travel services indicate that only a small proportion of travelers with anticipated lengthy stays in rabies-impacted areas receive the vaccine as recommended. Upper motor neuron lesion signs: exaggerated deep tendon reflexes, absent superficial reflexes, and spastic paralysis. Other recognized and reported arbovirus infections in 2014 include Jamestown Canyon virus (11 cases, 6 neuroinvasive), Powassan virus (8 cases, 7 neuroinvasive with 4 in Massachusetts), eastern equine encephalitis virus (8 cases, all requiring hospitalization, 3 neuroinvasive in New Hampshire, 2 died), and St. Eastern equine encephalitis is less common but was more often associated with deaths in children during 2003 to 2012. These arboviruses can also cause sporadic cases, neuroinvasive disease, and seasonal outbreaks. Pathogen-specific reservoirs (typically small mammals or birds) are responsible for maintaining the encephalitisproducing viruses in nature. For the eastern equine encephalitis virus, cotton rats and house sparrows serve as amplifying reservoirs. Birds are the main reservoir for West Nile virus and substantial avian mortality accompanies West Nile fever outbreaks (monitoring chickens is one mode of disease surveillance). The mosquito species associated with West Nile transmission is different in the Western vs Eastern United States (Culex tarsalis vs Culex pipiens) and consequently the terrain associated with highprevalence areas differs (open grasslands vs urban areas). Only dengue and Venezuelan equine encephalitis viruses produce viremias high enough to allow continued transmission to other mosquitoes and ticks between humans and vectors (mosquitoes of distinct species). Human-to-human transmission of the other arboviruses is usually related to blood (including granulocyte) transfusion or organ transplantation (although most infected donors give a history of clinically significant disease). Perinatal, transplacental, breastfeeding (rarely), laboratory, solid organ transplant, and possibly aerosol transmission of West Nile virus can also occur. Louis encephalitis and Powassan encephalitis occur among adults; western equine encephalitis, Venezuelan equine encephalitis, and La Crosse virus occurs primarily among children. West Nile fever, eastern equine encephalitis, and Jamestown Canyon virus are diseases of both children and adults. The mosquitoborne pathogens that routinely cause encephalitis include three togaviruses (causing Western, Eastern, and Venezuelan equine encephalitis), four flaviviruses (causing West Nile fever, St. Louis encephalitis, Japanese encephalitis, and Murray Valley encephalitis), and bunyaviruses (the California serogroup of viruses, including the La Crosse agent of California encephalitis). The tick-borne causes of encephalitis include the flavivirus of the Powassan encephalitis (northeastern United States and Canada), tick-borne encephalitis virus of Europe, and the Colorado tick fever reovirus. Tick-borne encephalitis virus, Colorado tick fever, and the arboviruses associated with viral hemorrhagic fever (including dengue) are discussed below, and only those viruses causing primarily encephalitis in the United States will be discussed here, although West Nile agent is being reported in many other areas, including Italy, Greece, Portugal, and Hungary as well as in Africa (Madagascar and South Africa), Canada, the Middle East, and West Asia. West Nile virus is the leading cause of domestically acquired arboviral disease in the United States. The total caseload in the United States (all but Alaska and Hawaii) from 1999 through 2015 includes 43,937 cases; of these, neuroinvasive disease was present in 20,265. In the United States, the highest incidence of neuroinvasive disease occurs in Nebraska, North and South Dakota, California, Louisiana, and Arizona, while the majority of cases occur in Texas, Arizona, and California. Outbreaks with West Nile infection tend to occur between mid-July and early September. Climatic factors, including elevated mean temperatures and rainfall, correlate with increased West Nile infection. La Crosse virus was the second most commonly reported cause of arboviral disease in 2014 with 76 reported cases of neuroinvasive disease and the highest incidence s errs ook e ook e/eb e/eb /t. Symptoms include fever, malaise, sore throat, headache, gastrointestinal upset, lethargy, and stupor progressing to coma. Using blood donor surveys, it is estimated that only about 26% of infections are symptomatic (women and the highly viremic are more symptomatic). Acute flaccid (poliomyelitis-like) paralysis is seen in 10% of West Nile virus neuroinvasive disease and less commonly with the other arboviruses. Other signs include tremors, seizures, cranial nerve palsies, and pathologic reflexes. The disease manifestations associated with West Nile virus infection are strongly age-dependent: the acute febrile syndrome and mild neurologic symptoms (but on occasion meningitis) are more common in the young, aseptic meningitis and poliomyelitis-like syndromes are seen in middle-aged persons, and frank encephalopathy is seen more often in older adults. All forms of disease tend to be severe in immunocompromised persons in whom neuroinvasive manifestations and associated high mortality are more apt to develop. Host genetic variation in the interferon response pathway is associated with both risk for symptomatic West Nile virus infection and West Nile virus disease progression. A chronic syndrome consisting of myalgias, arthralgias, and difficulty with concentration and memory is reported in over half the symptomatic cases. Retinopathy occurs in 24% of patients with a history of West Nile virus infection with increased risk in those with encephalitis. Documentation of a fourfold increase in acute/convalescent IgG titers is confirmatory for all arboviruses. Antibodies to arboviruses persist for life, and the presence of IgG in the absence of a rising titer of IgM may indicate past exposure rather than acute infection. Serologic tests are available commercially and through local and state health departments. Cross-reactivity exists among the different flaviviruses, so a plaque reduction assay may be needed to definitively distinguish between West Nile fever, St. Such measures include reduction of intracranial pressure (mannitol) and monitoring of intraventricular pressure. In 2014, one of the largest prospective clinical investigations of West Nile virus neuroinvasive disease in the United States revealed that 7 (12%) of 55 patients died. Otherwise, age older than 50 years is an important risk factor for severe disease and death. Other risk factors for mortality include black race, chronic kidney disease, hepatitis C virus infection, and immunosuppression. Recovery of persons with severe neurologic compromise may take months; in a cohort of 157 persons infected with West Nile virus, 40% continued to experience symptoms related to their infection up to 8 years later. Sequelae of West Nile virus infection include a poliomyelitis-like syndrome, cognitive complaints, movement disorders, epilepsy, and depression; and they may become apparent late in the course of what appears to be a successful recovery. New neurologic abnormalities are noted up to 11 years after acute illness, including gait abnormalities, hearing loss, abnormal reflexes, and muscle weakness. The long-term prognosis is generally better for Western equine than for Eastern equine or St. Mosquito avoidance (repellents, protective clothing, and insecticide spraying) is effective prevention. Since 2003, all blood donations in the United States are screened with nucleic acid amplification tests for West Nile virus. Laboratory precautions are indicated for handling all these pathogens, in particular the West Nile virus. West Nile virus retinopathy and associations with long term neurological and neurocognitive sequelae. West Nile virus and other nationally notifiable arboviral diseases-United States, 2014. Long-term neurological outcomes in West Nile virus-infected patients: an observational study. Most cases occur in the summer and late fall, although in tropical and subtropical areas transmission occurs throughout the year. The virus is transmitted by mosquitoes, especially Culex tritaeniorhynchus, but also other Culex species and Armigeres subalbatus. Wading birds and pigs more commonly sustain the infection as reservoirs in nature, since the viremia in humans is transient and not usually high enough to sustain transmission. The 1% of patients in whom disease develops report sudden-onset headaches, nausea and vomiting, followed by mental status changes, parkinsonian movement disorders, and in a smaller percentage, seizures, typically in children. Louis encephalitis and West Nile encephalitis, although epidemiologic data readily distinguishes these infections in most instances. Definitive diagnosis requires fourfold increase in virusspecific IgG confirmed by plaque reduction neutralization assay. It is the most common cause of encephalitis in East Asia with over 68,000 estimated annual cases. It is geographically contained to East Asia but the area of distribution includes 24 countries, extending from Pakistan to Japan and from es kerrs oo k eb oo e//eb me Four effective types of vaccine against Japanese encephalitis are available. It is usually a consequence of exposure to infected ticks during outdoor activities in forested areas, although unpasteurized milk from viremic livestock (goats, sheep, cows) is also a recognized mode of transmission. Surges in cases over the last 20 years are thought to be a consequence of agricultural policies that alter land cover, host prevalence, climatic factors, and human behavior (including pesticide usage and travel to endemic areas). The maximum altitude for occurrence of cases has increased to about 5000 feet (1500 meters).

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It is true for the rare Merkel cell carcinoma pulse pressure 43 generic plavix 75 mg otc, and cutaneous metastases regardless of the origin of the primary malignancy heart attack sam tsui chrissy costanza of atc purchase discount plavix on line. In the absence of a confident specific benign diagnosis hypertension kidney infection trusted plavix 75 mg, non-pigmented nodules with branched serpentine vessels should be submitted for histopathology pulse pressure 19 order plavix 75mg mastercard. Eccrine poroma is characterized by a combination of coiled heart attack quotes cheap 75mg plavix mastercard, serpentine and branched vessels arrhythmia electrophysiology cheap plavix online master card. Top left: Keratoacanthoma with central keratin plug (with blood spots) and radial vessels. Top right: Basal cell carcinoma with radial vessels and serpentine branched vessels. The radial vessels in this basal cell carcinoma are unusual and due to ulceration. Bottom left: Polymorphous vessels without a specific arrangement in a poorly differentiated squamous cell carcinoma (note ulceration and adherent fibers). Bottom right: Polymorphous vessels without a specific arrangement in a melanoma (invasion thickness: > 1 mm). When a melanoma occurs as a non-pigmented nodule, the vessels are usually polymorphous and randomly arranged (6. According to Menzies (43), vessels in amelanotic nodular melanoma are often arranged in the center of the lesion. Helical vessels are not common, but when seen are quite specific for melanoma, usually primary but sometimes metastatic (6. Pink or red clods, and white lines also should be viewed with caution when seen in conjunction with vessels as dots or lines. Summary In summary, the investigator is confronted with the limits of dermatoscopy when trying to assess non-pigmented lesions. Because diagnostic uncertainty is greater for non-pigmented lesions than in pigmented ones, histopathology will be required more often to establish an accurate diagnosis. Importantly, the investigator must recognize this greater uncertainty, and avoid making decisions that exceed the limitations of the method. A Merkel cell carcinoma presenting as non-pigmented ulcerated nodule with serpentine branched vessels on dermatoscopy (right). Any non-pigmented lesion that is ulcerated or has white clues (white lines in any lesion and in raised lesions, keratin, white circles or white structureless areas) should be biopsied or excised to rule out malignancy. If ulceration and white clues are absent one should try to make a specific diagnosis based on other clues. If a specific benign diagnosis cannot be made with confidence the lesion should be biopsied or excised to rule out malignancy. The top case shows the typical specific arrangement of linear vessels in the center of the clods. Bottom: A nodular lesion that primarily shows vessels as dots on dermatoscopy, but also other types of vessels which do not follow any special arrangement. The hemorrhagic crust due to ulceration (seen as a single black clod) is a clue to malignancy in the absence of trauma. Top: A flat lesion with white lines on dermatoscopy requires histology to rule out malignancy. Middle: A nodule with white lines on dermatoscopy requires histology to rule out malignancy. Bottom: A nodule without specific clues except remnants of brown pigmentation in the periphery. Top: A flat lesion with a raised center without any specific clues and short linear vessels in the raised center. It depends on how confident one can diagnose a congenital nevus here to decide if this lesion should be excised or not. The physician who took care of this patient was confident enough to leave this lesion. Middle: A non-pigmented nodule that is ulcerated on dermatoscopy should be excised or biopsied to rule out malignancy. Because a confident benign diagnosis is not possible it is advisable to remove the lesion to rule out malignancy. Histopathologic diagnosis: Fibroepithelioma of Pinkus (a variant of basal cell carcinoma). Top: An ulcerated nodule with a yellow serum crust on dermatoscopy should be excised or biopsied to rule out malignancy. Bottom: A non-pigmented nodule with coiled and looped vessels but no specific clues. Because a confident benign diagnosis is not possible it is advisable to remove the lesions to rule out malignancy. Differences between polarized light dermoscopy and immersion contact dermoscopy for the evaluation of skin lesions. Structural correlations between dermoscopic and histopathological features of juvenile xanthogranuloma. The clinical and dermoscopic features of invasive cutaneous squamous cell carcinoma depend on the histopathological grade of differentiation. Prediction without Pigment: a decision algorithm for non-pigmented skin malignancy. They usually point towards a diagnosis, but very few clues are specific for a particular diagnosis in all contexts. Studies which state that a particular clue has a given sensitivity and specificity should be interpreted with caution as there is always a selection bias (usually admitted) in the choice of included lesions, the series may not be large, and all too often the clue is only evaluated in a limited context, most commonly of distinguishing nevus from melanoma. Branched fine lines in flat acral lesions Brown or gray branched fine lines sprinkled with dots in a flat acral lesion is a very distinctive pattern. As tinea nigra commonly occurs on the feet where surgery is technically difficult, the diagnosis is best confirmed by a successful trial of treatment with topical antifungal cream. This leads to resolution of the lesion within 3 weeks and avoids a biopsy to exclude melanoma. Negative pigment network and shiny white streaks: a dermoscopic-pathological correlation study. Clinical and dermoscopic features of atypical Spitz tumors: A multicenter, retrospective, case-control study. Dermoscopic clues to differentiate facial lentigo maligna from pigmented actinic keratosis. By keeping a few basic principles in mind, the number of biopsies can be reduced without increasing the risk of missing a melanoma. In principle, melanomas may occur anywhere in the nail unit, but in practice almost all originate in the nail matrix. Nail matrix pigmented neoplasms create longitudinal pigmentation of the nail plate, known as longitudinal melanonychia. Melanomas that do not arise in the nail matrix but in the nail bed do not produce longitudinal melanonychia. Initially the nail changes produced by nail bed melanoma may be mistaken for "nail dystrophy" or "onychomycosis" and thus remain unrecognized. Anatomy of the nail In order to understand nail pigmentation, one must understand the anatomy of the nail organ. Its lateral margins are surrounded by the lateral nail fold while its proximal end is spanned by the proximal nail fold. The narrow cornified portion of proximal nail fold which glides on 1 to 2 mm of the nail plate is known as the cuticle. The nail matrix itself lies below the lunula, the white arc at the proximal end of the nail plate (8. Dermatoscopy of nail pigmentation Dermatoscopy of the nail plate requires a high viscosity ("stiff") contact fluid like ultrasound gel. Thinner fluids like paraffin oil and alcohol do not stay in place due to the highly irregular contour of the nail organ. In longitudinal melanonychia, these parallel lines extend continuously from the lunula to the free end of the nail plate. Longitudinal melanonychia usually occupies just a part, and less frequently the entire width, of the nail plate. It is attributable to the increased production of melanin in the nail matrix, which may or may not be caused by a proliferation of melanocytes. Gray pigmentation of lines is usually attributable to an increase of melanin, but it is not associated with proliferation of melanocytes in the nail matrix. The most common causes of gray parallel lines are lentigines (melanotic macules) of the nail matrix, ethnic hyperpigmentation, drug induced hyperpigmentation, hyperpigmentation during pregnancy, and traumatic or inflammatory hyperpigmentation (4). Top row, left: Regularly arranged brown parallel lines in a nevus of the nail matrix. Top row, right: Light-brown parallel lines arranged regularly (the lines are equally spaced) in a nevus of the nail matrix. Melanocytic lesions originate in the nail matrix, further proximally below the lunula. The fact that the lesion is broader in its proximal portion than in its distal portion is a sign of rapid growth. Middle row, right: Gray parallel lines due to manipulation ("onychotillomania") in a finger nail. Bottom row, left: Brown and gray parallel lines due to chronic friction trauma of the nail of the big toe. Bottom row, right: In situ melanoma of the nail matrix with light-brown lines arranged unevenly (the distance between the lines varies). Friction induced pigmentation of the toe can sometimes show a mix of brown and gray lines and then it is difficult to differentiate this condition from melanocytic lesions (8. The brown lines caused by trauma are created by a mixture of hemorrhage and post-inflammatory hyperpigmentation. Gray parallel lines are seen in many inflammatory conditions; for instance, onychomycosis (dermatophytes and even Candida albicans may produce melanin), lichen planus and (more rarely) psoriasis. Brown or black parallel lines are usually caused by proliferation of melanocytes in the nail matrix. In cases of nevus, the lines are (approximately) the same color and width, equally spaced, and arranged in a strictly parallel manner (8. In cases of melanoma, however, they are "chaotic", which means that they vary in color and width, the distance between the lines varies (8. Note that there are blood spots, which show that a single criterion can be misleading if the context is ignored. This is a pattern of a melanoma and the unusual finding of blood spots should not alter your diagnosis. The Hutchinson sign and the micro-Hutchinson sign must not be confused with the pseudo-Hutchinson sign (8. The pseudo-Hutchinson sign occurs when pigmentation of the nail plate is visible through the cuticle. Melanoma in the nail matrix usually is found on the big toe, thumb or index finger; other digits are rarely affected. While clinically (left) pigmentation is subtle, dermatoscopy on the right clearly shows pigmentation of the cuticle (micro-Hutchinson sign), a clue to melanoma. Pigmentation of the nail plate visible through the cuticle is termed Pseudo-Hutchinson sign. The clinical image is top left, the other images show a chronologic sequence of dermatoscopic images. At the first visit (top right) the pigmentation is broader in the proximal nail plate than in the distal nail plate, which indicates that the lesion is still growing. One year later (bottom left) the pigmentation in the proximal and distal nail plate have the same width, which indicates that the lesion stopped growing. The exceptional reports of melanoma of the nail matrix in prepubescent children are most probably congenital nevi that have been misdiagnosed as melanomas. Congenital nevi of the nail matrix (which may not be visible at birth) commonly show clues to melanoma including signs of growth. In growing lesions the pigmentation is broader in the proximal part of the nail plate and smaller in the distal part (8. While this feature would be regarded as a clue to malignancy in adults one should not be too concerned if it occurs in children. Usually this sign of growth will disappear if the lesion is monitored for some months. Therefore, even if clues to malignancy are present, biopsy of the nail matrix in prepubertal children should be performed very rarely, and only after careful consideration.

Bacteria Trichomycosis palmellina is probably the only bacterial infection whose diagnosis is facilitated even slightly by dermatoscopy blood pressure goals cheap plavix 75 mg line. This disease is caused by Corynebacterium tenuis and is seen on dermatoscopy as a yellow hypertension journal articles cheap plavix generic, black or red structureless area that surrounds the axillary hair (29) hypertension treatment guidelines 2013 buy generic plavix from india. The mite lives in burrows in the stratum corneum and causes skin lesions and a sometimes intractable itch blood pressure chart 17 year olds discount plavix 75 mg with mastercard. To make the diagnosis without dermatoscopy the mite prehypertension need medication purchase plavix master card, which is barely visible with the unaided eye low vs diamond heart attack cheap plavix 75mg, has to be located microscopically in skin scrapings. However, the mite is easily demonstrated on dermatoscopy with no need for skin scrapings (8. On dermatoscopy one sees a curved or serpentine line, which corresponds to the burrow (8. The dermatoscopic appearance on the right shows the typical thin branched gray lines of tinea nigra. On the clinical close-up (bottom left) one can see non-specific erythematous papules. At the end of the line the mite is seen as a small, dark triangle (anterior portion of the parasite). Occasionally mite excrement is seen as black dots within the thick curved line (38). Lice (pediculosis capitis/phthiriasis pubis) can also be diagnosed in vivo with the dermatoscope. If they are empty (after the nymphs have hatched) there will be transparent clods with a flat end. These should be distinguished from debris of hair gel or dandruff, which will be seen as polygonal clods with white dots and lines (39). A rather rare disease in high latitudes is caused by the sand flea Tunga penetrans. On dermatoscopy one finds a round, black or red structureless area with a central black clod or a dot (8. Dermoscopy provides useful information for the management of melanonychia striata. Nail matrix biopsy of longitudinal melanonychia: diagnostic algorithm including the matrix shave biopsy. Surgical Pearl: Dermoscopy of the free edge of the nail to determine the level of nail plate pigmentation and the location of its probable origin in the proximal or distal nail matrix. Dermoscopic patterns of acral melanocytic nevi: their variations, changes, and significance. Anatomical and histopathological correlates of the dermoscopic patterns seen in melanocytic nevi on the sole: a retrospective study. Dermoscopic patterns of benign volar melanocytic lesions in patients with atypical mole syndrome. The furrow ink test: a clue for the dermoscopic diagnosis of acral melanoma vs nevus. Early acral melanoma in situ: correlation between the parallel ridge pattern on dermoscopy and microscopic features. A comparison of dermoscopic features among lentigo senilis/initial seborrheic keratosis, seborrheic keratosis, lentigo maligna and lentigo maligna melanoma on the face. Reflectance confocal microscopy correlates of dermoscopic patterns of facial lesions help to discriminate lentigo maligna from pigmented nonmelanocytic macules. The impact of in vivo reflectance confocal microscopy on the diagnostic accuracy of lentigo maligna and equivocal pigmented and nonpigmented macules of the face. Dermoscopy of pigmented lesions of the vulva: a retrospective morphological study. Recurrent melanocytic nevi and melanomas in dermoscopy: results of a multicenter study of the International Dermoscopy Society. Dermatoscopy of unpigmented lesions of the skin: a new classification of vessel morphology based on pattern analysis. Collision of basal cell carcinoma with seborrhoeic keratosis: a dermoscopic aid to histopathology Cutaneous collision tumour (melanocytic naevus, basal cell carcinoma, seborrhoeic keratosis): a clinical, dermoscopic and pathological case report. A dermatoscopically diagnosed collision tumour: malignant melanoma arising within a seborrhoeic keratosis. Dermatoscopy aids in the diagnosis of the solitary red scaly patch or plaque-features distinguishing superficial basal cell carcinoma, intraepidermal carcinoma, and psoriasis. Dermoscopy of molluscum contagiosum: a useful tool for clinical diagnosis in adulthood. Differential diagnosis of plantar wart from corn, callus and healed wart with the aid of dermoscopy. However, in the earliest stages many melanomas lack the dermatoscopic criteria to allow diagnosis (1). Indeed, it seems likely that all melanomas go through a stage without any morphologic features to suggest the true diagnosis (2). Melanomas which can be identified by the naked eye are usually larger than one centimeter in size and have usually been present for several years. As critics of dermatoscopy remark, in these advanced cases one does not require dermatoscopy at all. For smaller and earlier lesions however, naked eye examination does not perform so well, but the majority of these smaller melanomas are still easily diagnosed with the dermatoscope. There is one clue that is present in every malignancy, even when all others are lacking: change over time. Digital dermatoscopic monitoring is comparison of serial dermatoscopic images to detect change over time, enabling the diagnosis of inconspicuous melanomas. Monitoring can also be used to reduce the number of biopsies of pigmented lesions with equivocal clues to malignancy. The disadvantage of this clue is that, unlike clues based on morphology, at least two sequential observations are needed. In other words, monitoring only works if a given lesion is imaged at an initial consultation, and the patient returns for subsequent examinations. In practical terms, it also requires sequential images of sufficient quality to detect change. Monitoring is most useful for high risk individuals with a very large number of nevi. Over their lifetimes many of these patients are subjected to large numbers of biopsies. Sometimes this is unavoidable, but far too often it is an indiscriminate process, of no benefit to the patient. The monitoring strategies outlined below greatly reduce the number of biopsies needed, without increasing the risk of missing a melanoma. Initially melanomas are small and inconspicuous and lack any characteristic clues. It takes some time for melanomas to develop their typical clinical characteristics, such as asymmetry, variegate colors, and irregular borders. Different diagnostic methods are required at different stages in this development. An increasing number of so-called digital dermatoscopes are being offered on the market. The basic principle of digital dermatoscopes is simple: instead of the operator looking through the instrument to see the image, a hand-held dermatoscope is attached to a digital video camera. The camera is connected to a monitor that displays the dermatoscopic image in real time, and also to a computer to allow capture and storage of images from the camera (9. Dedicated software permits efficient administration of the saved images, which makes comparing images obtained at different points in time much easier. The image quality of these digital dermatoscopes has lagged behind that of images captured by attaching a camera to a conventional hand-held dermatoscope, but the development of high resolution digital imaging systems is seeing this gap narrowing. A frequently underestimated advantage of digital dermatoscopy is patient participation in the examination. When using a conventional dermatoscope the patient cannot see the lesion being examined. During digital dermatoscopy the patient and the doctor can view the image on the monitor simultaneously. On the top and on the bottom left are two MoleMax systems (Derma Medical Systems, Vienna, Austria) on the bottom right is a Fotofinder (Fotofinder Systems GmbH, Bad Birnbach, Germany). While monitoring is conceptually very simple, there are issues around which lesions should be monitored. As nevi also change over time, there are also issues regarding what changes indicate a diagnosis of melanoma. Rather, monitoring is detecting actual melanomas, but earlier than is possible by observation of morphology alone. Most issues regarding monitoring are clarified if this fact is kept in mind; what one is monitoring is potentially already a melanoma. A "back of the envelope" calculation shows malignant transformation in a nevus is a very rare event. If one assumes that populations with lighter skin phototypes have an average of 20 nevi per person and the incidence of melanoma in this group is 20 per 100,000 persons per year, then, one may anticipate 200 mel- anomas per year in a population of 1 million. Given approximately 20 % of melanomas arise in a pre-existing nevus, of these 200 melanomas, 40 would have arisen in a pre-existing nevus. As these 40 melanomas have arisen in a population with 20 million nevi, the annual risk of a single nevus undergoing malignant transformation is therefore 1:500,000. In other words, one would have to observe 500,000 nevi for a year in order to detect a single melanoma emerging in a pre-existing nevus, or one would have to prophylactically excise 500,000 nevi in order to prevent one melanoma per year. Even if the actual rate of transformation was 10 times this estimate, the basic argument remains valid as the observation or excision of even "only" 50,000 lesions to detect or prevent one melanoma annually is still absurd. The strategy of monitoring of nevi for malignant transformation is therefore only feasible if the clinician is able to identify lesions which are hundreds or even thousands of times more likely than the average nevus to undergo malignant transformation. Unfortunately, the morphology of a nevus says nothing about its risk of malignant transformation (9. However, there is a risk that a lesion thought to be an "atypical" or "dysplastic" nevus may actually be a melanoma, but not recognized as such. That is, these terms are used when there is diagnostic uncertainty regarding the distinction between these lesions and melanoma. Once this has been understood, the concept of the "dysplastic" or "atypical" nevus loses meaning. Digital monitoring is of most utility for small and flat melanocytic lesions that demonstrate no obvious clues to melanoma, in a patient with multiple pigmented lesions. Lesions selected must be flat, to avoid the possibility of monitoring a thick melanoma. Firstly, lesions can be selected on the basis of criteria which are considered to suggest that the lesion has some likelihood of being an early melanoma. Monitoring is generally restricted to one or a few lesions, with a shorter monitoring interval, usually 3 months. Lesions to be monitored are flat and nearly symmetrical, and have either a) no clues to malignancy but have changed according to the patient or b) a certain "architectural disorder" which falls short of clear-cut clues to malignancy. The clinical image on the left shows a melanoma that developed in a pre-existing nevus. On the right one can see digital dermatoscopic images of four nevi of the same patient. Can you predict by morphology which nevus is the precursor lesion of the melanoma on the left The concept of the "dysplastic" or "atypical" nevus is flawed fundamentally because the morphology of a nevus is not predictive of its biological fate. A second type of monitoring may be used for high risk patients with multiple nevi (9. Lesions to be monitored are selected randomly, with as many lesions as possible documented at the initial examination and re-imaged at each consultation (4). One therefore relies on chance and increases the likelihood of identifying a melanoma by documenting as many lesions as possible and confining the investigation to high-risk patients. This type of monitoring is an alternative to indiscriminate excision of nevi in patients with multiple nevi. Short term monitoring, however, will only increase the specificity by reducing the number of excisions. To find additional false negatives one must include inconspicuous lesions (long term monitoring). Because inconspicuous lesions are monitored one needs to monitor a lot of lesions to detect one melanoma, more than 1000 in some settings. Long term monitoring, however, will increase specificity and sensitivity because it will detect melanomas that do not have any clues and cannot be diagnosed otherwise. A third possible approach is to identify new or changed pigmented lesions by comparison of serial clinical total body photographs, and then subjecting these lesions to digital monitoring. Monitoring by digital dermatoscopy is especially suitable for patients with multiple nevi. It is an appropriate but time-consuming alternative to indiscriminate excision of nevi.