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  • CLINICAL CASES AND PEARLS BENJAMIN BARANKIN, MD, FRCPC ANIL KURIAN, MD
  • RAPID FIRE DERMATOLOGY Dr. Benjamin Barankin is a Toronto dermatologist, the Founder & Medical Director of Toronto Dermatology Centre (www.torontodermatologycentre.com). He is also the author of other dermatology books, including Derm Notes, Stedman’s Illustrated Dictionary of Dermatology Eponyms, Dermographies Volume 1 & 2, and Diagnostic Criteria in Dermatology. DR. ANIL KURIAN is a dermatology resident at the University of Alberta in Edmonton. At this early stage in his career, he has already co-authored more than 25 dermatology-related articles and also received a prestigious award from the Ontario Medical Association (OMA) for his patient advocacy work promoting a ban on indoor tanning services to minors.
  • Praise for Rapid Fire Dermatology “Rapid Fire Dermatology by Drs. Barankin and Kurian is an excellent state-of-the art guide to many of the common skin disorders that primary providers will encounter with regularity. The format differs from most other guides in that this book is actually fun to read. It also provides realistic medication and treatment options that are applicable to the primary care setting. It will have broad appeal to its targeted audience.” — Dr. David J. Elpern, Dermatologist, Williamstown, MA USA “Rapid Fire Dermatology is a wonderful learning tool and reference book for family physicians. Focusing on the most common dermatological conditions seen in a family physician office setting, this book offers clear pictures and an intriguing case presentation approach that allows you to test your knowledge with multiple choice questions. The explanations are clearly explained with a wonderful practical approach to treating these dermatological conditions. The treatment options are gauged at the family practice level, and more advanced dermatological approaches for more complex cases are discussed as well. It was an enjoyable learning experience to read this book.” — Dr. Monica Pearl, Family Physician, Toronto, ON Canada “Clinical cases are a key component in modern medical education, assisting the clinician to work through cases using best practice techniques. Dermatology is a highly visual subject requiring the health care provider to understand often very subtle differences in the presentation of patients. This new book will help define accurately the diagnostic and management criteria to base clinical decision-making on. I am very excited about the potential for this clinical reference tool!” — Dr. Robert Norman, Dermatologist, Associate Professor, Department of Dermatology, University of Central Florida College of Medicine, Tampa Bay, FL USA “Barankin and Kurian’s new book, Rapid Fire Dermatology, is an outstanding work for those interested in learning the basics of dermatology. The book focuses on some of the most common afflictions of men and women, providing practical advice on both differential diagnosis and management. The clinical photographs are wonderfully illustrative of common disease presentations, and the text is concise and easily read. If you are a family or other primary care provider, a resident or a medical student, you will see patients with these conditions. Rapid Fire Dermatology will prepare you to recognize and manage them.” — Dr. Steven R. Feldman, Dermatologist, Professor of Dermatology, Pathology & Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC USA ii
  • “The case-based Rapid Fire Dermatology is a great way to learn a wide variety of the most common skin diseases. The pictures are terrific and the text is concise and to the point. I highly recommend this book.” — Dr. Gary Goldenberg, Dermatologist, Assistant Professor, Dermatology and Pathology, Medical Director of the Dermatology Faculty Practice, Mount Sinai School of Medicine, New York, NY USA “Drs. Barankin and Kurian have put together the perfect pocket summary of the most common dermatologic conditions that a family physician, pediatrician, or nurse practitioner will see on a regular basis. Not only does the small book literally fit easily within a typical white coat pocket, it details 25 of the most common skin conditions seen in general practice using case presentations and Q&A format that allows for the rapid assimilation of the crucial information needed to make a definitive diagnosis, initiate appropriate therapy, or recognize when a referral to a dermatologist is warranted. This book is the ideal entry level text to help demystify the confusing world of dermatology to the primary care physician and other healthcare providers.” — Dr. Thomas G. Salopek, Dermatologist, Director, Associate Professor, Division of Dermatology & Cutaneous Sciences at University of Alberta, Edmonton, AB Canada Copyright © 2012 Benjamin Barankin and Anil Kurian All rights reserved. Except for the quotation of short passages for review purposes, no part of this publication may be reproduced in any form without prior permission of the authors. Print Design: Brenda Conroy
 iBook Design: Paul La Rue [Fission Media] Printed Copies of this book may be obtained from:
 Dr. Benjamin Barankin at benbarankin@gmail.com Library and Archives Canada Cataloguing in Publication iii
  • Authors Dr. Benjamin Barankin is a Toronto dermatologist specializing in medical, surgical, laser and cosmetic care of the skin. His undergraduate university training was in Life Sciences and Psychology at Queen’s University, followed by medical school at the University of Western Ontario, and dermatology residency at the University of Alberta. Dr. Benjamin Barankin is also a widely published author with more than 500 articles related to dermatology and he has gained international distinction as the author of 6 other books on dermatology. He has been honoured with being voted onto the Executive Board of the Canadian Dermatology Association (CDA) where he held the position of Secretary and Chair of the Membership & Awards Committee. He serves on the editorial boards of numerous medical journals and newspapers, and Dr. Barankin is also team dermatologist for the Toronto FC soccer team. He resides in Toronto with his physician wife and daughters. Dr. Anil Kurian is a dermatology resident at the University of Alberta. Prior to entering medicine, he had a career in nursing, working as a registered nurse and subsequently, a nurse practitioner. He completed his Bachelor of Science in Nursing degree from the University of Ottawa and his Master of Nursing degree from Dalhousie University. He completed his medical school training at McMaster University. Dr. Anil Kurian is already making an impact in the field of dermatology. At this early stage in his medical career, he has already co-authored more than 25 dermatology-related articles and also received a prestigious award from the Ontario Medical Association (OMA) for his patient advocacy work promoting a ban on indoor tanning services to minors. He is also project lead of many groundbreaking dermatology projects in Edmonton, including the innovative use of teledermatology in the ER department, the first of its kind in Canada. He resides in Edmonton with his family. iv
  • Introduction The idea of this book was developed through the very successful case-based columns and articles written by the book’s senior author, Dr. Benjamin Barankin, over the past decade. Dr. Barankin has spoken at many primary care conferences and aspires to educate family physicians about how important recognizing and treating dermatological conditions are in a primary care setting. Incorporating routine skin checks during a patient’s physical examination promotes greater surveillance for the diagnosis of pathological skin conditions and lesions, as well as proper treatment being implemented in a timely fashion. We aspired to integrate a large number of dermatological casebased conditions packaged into one succinct pocket-style book with quality dermatology images. Each case will be described in great detail and will provide the clinical practitioner with specific tips on the types of dermatological visual and tactile cues they should recognize and look for in each particular case, to improve their diagnostic acumen. We envisioned a practical book formatted to include exclusive Canadian medical content. We believe that this book would be relevant to family physicians and pediatricians, for use as a pocket reference in their clinic-based practices, as well as medical residents and students wishing to become familiar with various dermatological presentations. Case-based scenarios are a well-received and utilized style of learning among physicians and trainees. Dermatology is a highly visual field within medicine and recognition of visual cues and patterns, in conjunction with the clinical patient history, direct the practitioner to the correct diagnosis. The 25 dermatology cases presented within are common and important clinical concerns of patients that include skin cancers, skin infections, inflammatory and immunologic skin conditions, as well as benign lesions. Additionally, each dermatology case will have an interactive question and answer (Q&A) section where the reader can test their knowledge relating to the clinical case presented. This unique and interactive self-test will aid the reader to retain the primary teaching points of each of the cases featured. Rapid Fire Dermatology is a unique dermatology book tailored to the Canadian marketplace, including up-to-date, comprehensive information regarding dermatological diagnosis, as well as specific medication and treatment recommendations. Additionally, after each case presentation, there is an added “Clinical Pearls” section with informative dermatologist tips related to diagnosis or treatment aspects for that particular condition. Rapid Fire Dermatology is a great resource for Canadian physicians, medical residents or students. We hope you find it of value to your practice. If you have any comments about this book or suggestions for topics for the next edition, please contact Dr. Benjamin Barankin at: benbarankin@gmail.com Acknowledgements The authors would like to thank their respective families for their unconditional support of educational pursuits by the authors, specifically relating to dermatology education and research endeavours. We are also grateful for the efforts of our book designer, Brenda Conroy. The development and funding of this book has been made possible through a grant provided by Leo Pharma Inc. v
  • Question 1 of 3 1. What is her diagnosis? A. Allergic contact dermatitis B. Psoriasis C. Tinea corporis T HIGH RASH WITH CRUSTY LESIONS A 15 year-old girl presents with a mild fever and a moderately pruritic rash on her left and right thigh regions. The lesions began 3 days before as blisters discharging a clear yellowish fluid. The blisters progressively enlarged despite treatment with a topical antibiotic ointment. She is taking no other medications and her medical history is unremarkable. D. Bullous impetigo E. Bullous pemphigoid Check Answer Diagnosis & Information 6
  • Predisposing factors include skin abrasions, minor trauma, burns, poor hygiene, insect bites, diabetes mellitus, primary varicella infection, and pre-existing skin disease, such as eczema. Also, those with nasal or perineal Staphylococcal aureus colonization are at increased risk for developing impetigo. Diagnosis: Bullous impetigo Bullous impetigo commonly starts with small vesicles on the face, trunk, buttocks, perineum, or extremities, without surrounding erythema. These vesicles rapidly enlarge into flaccid, transparent bullae measuring from 1 to 5 cm in diameter. Bullae initially contain a clear yellow fluid that subsequently becomes dark yellow and turbid. Their margins are sharply demarcated, having no erythematous halo. The lesions heal more quickly than nonbullous lesions. The condition might be associated with fever, diarrhea, and weakness, but unlike nonbullous impetigo it is not associated with lymphadenopathy. Impetigo is a superficial skin infection encountered most frequently among children. It typically presents with multiple vesicular lesions on an erythematous base, which eventually crust over. There are 2 types: nonbullous and bullous. Both forms involve only the most superficial layers of the skin. The Nikolsky sign (sloughing of the epidermis with sliding pressure) is usually negative. Complications of impetigo include lymphadenitis, cellulitis, sepsis, or glomerulonephritis. The nonbullous form is the most common and is likely to be caused by a mixed staphylococcal and streptococcal infection. The bullous form, however, is a highly contagious condition caused by an epidermolytic toxin (produced most commonly by staphylococci) at the site of infection. Cultures of fluid from an intact blister or moist plaque should yield the causative agent; if the patient appears ill, blood cultures should also be obtained. The differential diagnosis primarily includes all of the herpes simplex viral infections, allergic contact dermatitis, thermal burns, bullous insect bite reactions, bullous pemphigoid and rarely pemphigus. 7
  • Prophylactic treatments to prevent staph infections include ‘bleach baths’. This is done by adding ¼ to ½ cup of common liquid bleach to approximately 40 gallons of bath water. Soaking in the bleach bath for about 10 minutes (2-3 times per week over 1-2 weeks), is an effective way to prevent the occurrence of cutaneous staphylococcal infections. This is especially helpful in children with recurrent impetigo or regular eczema flares. Local treatment of cutaneous lesions can be achieved with 2% mupirocin ointment (Bactroban®) or fusidic acid 2% cream (Fucidin® cream) and sodium fusidate 2% ointment (Fucidin® ointment). The former should be prescribed tid for 8-12 days, while the latter can be used 2-4 times daily for 8-12 days. In addition, local care, which includes cleansing, removal of crusts, and application of wet dressings, is sufficient to cure mild cases. Some studies have demonstrated that 2% mupirocin ointment is as safe and effective as oral erythromycin in the treatment of patients with impetigo, while another study showed that 2% fusidic acid was more effective than oral clindamycin, erythromycin or flucloxacillin in the treatment of soft tissue infections. It is important that duration of either individual topical therapy alone be limited as bacterial resistance can be seen with both local treatment options. Also, adding a mild topical steroid to antibiotic therapy, such as fusidic acid plus hydrocortisone found in Fucidin®H, is beneficial to deal with the underlying dermatitis and pruritus. Complicated, quickly spreading or widespread cases of bullous impetigo require 5 to 10 days of oral β-lactamase– resistant antibiotics, such as cephalexin (Keflex®) 250-500mg qid for 10 days or amoxicillin/clavulanate (Augmentin®) 250-500mg bid for 10 days. Clinical Pearl • Impetigo is highly contagious; patients should not touch the lesions or be discouraged by covering the lesion. The child should be kept at home until the lesions resolve if in an exposed area that other children may come in contact with. “When you are looking for the cause of disease, think food, bugs and drugs.” 
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 8
  • Question 1 of 3 What is the most likely diagnosis? A. Tinea corporis B. Sarcoidosis C. Granuloma annulare R EDDISH - BROWN LESIONS ON DORSAL HAND A 36 year-old male presents with erythematous-brown asymptomatic plaques on his dorsal hands. He is bothered by the cosmetic appearance, and would like to stop having to cover up the areas because of embarrassment. He occasionally takes ibuprofen and acetaminophen for tension headaches. D. Lichen planus E. Erythema annulare centrifugum Check Answer Diagnosis & Information 9
  • GA is an idiopathic condition, with controversial associations with infections, diabetes, and thyroid disease; there appears to be a hereditary component in some cases. Localized trauma and sunlight have also been hypothesized to play a role in its etiology. GA is often a clinical diagnosis. A punch or incisional biopsy is recommended for atypical or uncommon presentations, and especially if growing quickly and tender. Diagnosis: Granuloma annulare Granuloma annulare (GA) is a benign, inflammatory skin condition of dermal papules and annular plaques commonly affecting acral sites. GA occurs most commonly in women and in younger individuals (typically less than 30 years old). There are several clinical variants, including: localized GA (most common, especially in children & young adults), generalized GA (10%), subcutaneous GA, perforating GA (5%), and arcuate dermal erythema. Localized GA typically manifests as groups of small erythematous to brown papules, often in an annular arrangement (raised border, central clearing) over distal extremities, especially the hands, feet, and extensor limbs. Management involves reassurance that the condition is benign and spontaneous resolution of lesions typically occurs within 2 years in 50% of patients, especially of the localized clinical variant. Various treatment options have been utilized, but often have suboptimal clinical efficacy. Intralesional triamcinolone acetonide (Kenalog®, 2.5-5mg/ml q 4-6 weeks) is the most uniformly successful therapy. Potent topical steroids with or without occlusion can also be tried but have less efficacy. Cryotherapy in lighter skin types can also provide benefit alone or more commonly in combination with intralesional Kenalog®. While localized GA resolves after an average of 2 years duration, generalized forms of GA typically have a more chronic duration and unfortunately, are more resistant to treatment options. Phototherapy and oral retinoids are commonly employed in cases of generalized GA, and increasingly biologics are being used. Clinical Pearls • Granuloma annulare can be a frustrating condition to manage, as it is one of those conditions that develops for reasons that are not well understood, and similarly often resolves spontaneously. • Interestingly, some cases have been reported to disappear when oral antibiotics were given for sinus, fungal or other infections. 10
  • “Just because you have a diagnostic handle on a disease doesn’t mean you can handle it.” 
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 11
  • Question 1 of 3 What is the most likely diagnosis? A. Pilomatricoma B. Epidermoid cyst C. Milia cyst S LOW GROWING BACK LUMP A 64 year-old male presents to clinic with a slowly growing nodule on his back. It has been present for at least a couple years, is asymptomatic, and has never had any bleeding or discharge. He has never had such a lesion before. D. Dermoid cyst E. Lipoma Check Answer Diagnosis & Information 12
  • pilosebaceous unit, HPV infection, or traumatic implantation of epidermal elements. A number of hereditary syndromes including nevoid basal cell carcinoma syndrome and Gardner syndrome have the feature of multiple epidermoid cysts. As well, idiopathic scrotal calcinosis may represent the end stage (calcification) of scrotal epidermoid cysts. Patients often present to clinic for a number of reasons relating to an epidermoid cyst. Reasons include the cosmetic appearance of a visible body ‘lump’, the malodorous cheese/curd-like material that can be extruded from the lesion, or because of lesional discomfort associated with either inflammation or infection. Clinically, the lesions appear as round, firm, flesh-coloured nodules (of various sizes), which quite often have a central punctum. Commonly affected areas on the body include the head, neck and trunk. Diagnosis: Epidermoid cyst Epidermoid cysts form as a result of the growth of epidermal cells within a focal area of the dermis. The material inside the cysts is chemotactic for neutrophils and can result in inflammation. Most epidermoid cysts do not cause any problems and grow rather slowly. However, cysts can become inflamed and less commonly infected which results in redness, tenderness and pain, due to trauma or other factors. Epidermoid cysts are more common in men during the young adulthood years but may be noted at any age. The pathogenesis of an epidermoid cyst is not completely clear, but some factors that may play a role include occlusion of the The diagnosis of an epidermoid cyst is typically made clinically. If infection of a cyst is of concern, a swab for bacterial culture can be sent. Diagnostic imaging is rarely necessary unless the lesion is in the midline of the body. In such a case, an ultrasound can be considered. Epidermoid cysts are benign lesions and require treatment only if symptomatic or for cosmetic purposes. A tender, inflamed, uninfected cyst often benefits from an intralesional triamcinolone acetonide (Kenalog®) injection. For cysts presumed or proven to be infected, incision and drainage is recommended following by a course of oral gram positive coverage antibiotics (eg. Keflex® 500mg qid x 7-10 days). Epidermoid cysts are excised using a classic large incision, mini incision, or trephination with a punch biopsy device. Incising and draining is a quick procedure, but has high recurrence risk since 13
  • the entire cyst wall is unlikely to be evacuated. Excision of the entire cyst, including the epidermal cyst wall lining, is the most definitive treatment, but even still recurrences may occur. Clinical Pearl • When removing epidermoid cysts, a punch biopsy instrument can be used that can result in a smaller scar than doing an elliptical excision. Along with trying to extrude the contents with forceps and pressure and undermining, inserting and moving back and forth a curette can be helpful in removing any remaining cyst wall contents to prevent recurrence. “Sometimes you have to wait for a disease to grow up before a diagnosis can be made.”
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 14
  • Question 1 of 3 What is the most likely diagnosis? A. Pityriasis alba B. Tinea versicolor C. Post-inflammatory hypopigmentation W HITE PATCH OVER KNEE A 40 year-old female presents with a two-year history of a white patch on her anterior knee and lower leg area. She has smaller white macules of this on her fingers and ankle. These lesions are asymptomatic. She has a history of pernicious anemia and a family history of thyroid disease. D. Vitiligo E. Nevus anemicus Check Answer Diagnosis & Information 15
  • Screening for these co-morbidities with periodic blood tests should be considered when a diagnosis of vitiligo is made. Vitiligo progresses without symptoms, though early lesions may occasionally be pruritic. Vitiligo presents as sharply demarcated patches that are cosmetically disturbing to most patients, especially those with darker skin colour where there is more contrast. After a few small white lesions appear, they increase in number and size, becoming confluent and having unusual shapes. Vitiligo is classified as having localized or generalized involvement. Although any area of skin can be affected, the most commonly affected areas include: face, neck, bony prominences, dorsal hands, and fingers. Hair in a patch of vitiligo will also depigment. A Wood’s lamp examination can help clarify the diagnosis as the depigmented white areas of vitiligo become accentuated under the light. Diagnosis: Vitiligo Vitiligo is an acquired, benign, depigmentation of the skin caused by destruction of melanocytes in skin and hair, resulting in white macules and patches. It affects 1-2% of the population with an equal gender distribution and most commonly onsets between 10-30 years of age. The etiology of vitiligo has not been fully elucidated, but the pathogenesis is multifactorial, likely having both genetic and autoimmune mechanisms. Melanocytes are destroyed in the skin and those in hair follicles can also be affected resulting in white hair. Vitiligo has been associated with other autoimmune conditions such as: pernicious anemia, alopecia areata, diabetes mellitus, Addison’s disease, and thyroid disease. Management options include potent topical steroids and topical calcineurin inhibitors (especially on areas with thin skin, such as the face or intertriginous areas). Phototherapy is commonly employed for more widespread involvement or resistant cases. Less commonly, excimer laser, repigmentation surgery, and depigmentation therapies are employed. A discussion of the use of cover up makeup (e.g. CoverFX, Dermablend™, Covermark®) and topical tanning creams should be considered. Management can be frustrating as improvement is slow and unpredictable. 16
  • Clinical Pearls • Vitiligo is a chronic and difficult condition to manage. Fortunately, areas such as the face typically respond well to treatment. Hands and feet are notoriously slow to respond to therapy. • Some dermatologists believe there is benefit to taking folic acid, vitamin C, and vitamin B12 in the treatment of vitiligo. Some have also observed improvement with long-term use of ibuprofen or acetylsalicylic acid. “The darker the skin, the more prominent the paler patches. 
 But for people of every shade, vitiligo can cause distress as strangers gawk and job interviews become sidetracked.”
 ~ Catherine Saint Louis, Journalist, New York Times 17
  • Question 1 of 3 What is the most likely diagnosis? A. Compound nevis B. Angiofibroma C. Basal cell carcinoma C HRONIC ERYTHEMATOUS FACIAL PAPULE A 74 year-old female presents with an erythematous and telangiectactic papule to her nose. She has been using topical steroid and antifungal creams for the past 2 months with minimal clinical improvement. D. Dermatofibroma E. Squamous cell carcinoma Check Answer Diagnosis & Information 18
  • previous actinic keratosis. Chronic sun exposure in a fair skin type is the major risk factor for the development of BCC. The most common sites are the head (especially nose) and neck, trunk, and arms and legs. Clinical presentation can vary based on subtype, which include: nodular BCC, superficial BCC, pigmented BCC, cystic BCC, and morpheaform/sclerosing BCC. BCC is largely a clinical diagnosis in many cases and no additional work-up is required. Diagnostic accuracy is enhanced by good lighting and magnification with a dermatoscope may be helpful. A biopsy of the lesion is indicated when clinical doubt as to the diagnosis exists or when the histological subtype of BCC may influence treatment selection and prognosis. Diagnosis: Basal cell carcinoma (BCC) This is the most common malignancy in humans, typically appearing on sun-exposed skin. BCCs can result in significant local destruction and even disfigurement, especially if located around the nose or eyes. They rarely metastasize (<0.1%). In Caucasians, there is approximately 25-35% lifetime risk of developing a BCC. These lesions are uncommon in dark skin types. Likelihood of BCCs increases with age, and they are considered uncommon under 35 years of age. Risk factors for BCC include a fair complexion, red or blond hair, light eye color, increased sun exposure during childhood years, ionizing radiation, UVA radiation, immunosuppression and BCC is a highly treatable form of skin cancer. Treatment of BCC can be surgical or nonsurgical. Surgical approaches with most definitive 5-year cure rates include surgical excision and Mohs micrographic surgery (99%) followed by curettage and electrodessication and cryosurgery (95%). Nonsurgical approaches include topical imiquimod, radiotherapy, and photodynamic therapy. Preventive measures for BCC include avoidance of the sun during peak hours and protection against sun exposure with a hat, clothing, and broad spectrum sunscreens. Avoiding tanning salons is also a must. Clinical Pearl • A patient with a history skin cancer complaining of a “sore that doesn’t heal” or “the lesion has scabbed and/or bled on a few occasions but won’t go away” is highly suggestive of the diagnosis of BCC. 19
  • “Inject xylocaine or saline into a suspect basal cell carcinoma to enhance its gross morphology.” 
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 20
  • Question 1 of 3 . What is your diagnosis? A. Melasma B. Lentigines C. Post-inflammatory hypermelanotic macules D ARK PATCHES ON CHEEKS A 42 year-old woman presented with brown macules that she has had for several years on both cheeks. She began to notice the macules during her pregnancy of her first child 4 years ago. She currently takes no medications, and her medical history is otherwise unremarkable. D. Addison’s disease E. Discoid lupus erythematosus Check Answer Diagnosis & Information 21
  • with darker complexions, including those of Hispanic, Middle Eastern, Asian, and Indian ethnicities. While most cases are idiopathic, melasma has also been associated with genetics, exposure to ultraviolet radiation, pregnancy, oral contraceptives, hormone replacement therapies, mild endocrine disturbances (e.g. ovarian or thyroid dysfunction), cosmetics, antiepileptic medications, and other photosensitizing drugs. Sun exposure tends to be the most important causative factor in all patients, so management options for melasma must always include avoidance of excessive exposure to sunlight. Diagnosis: Melasma Melasma is a common hypermelanosis that typically occurs on sun-exposed areas of the face. Melasma is characterized by symmetrically distributed macules with irregular borders ranging from light brown to dark brown to gray-brown. Common clinically distinct distributions include centrofacial (forehead, nose, chin, upper lip), malar (cheeks), and mandibular (lower jaw). Forearms are also occasionally affected. Pigmentation typically slowly evolves over many weeks or months. Melasma is rare before puberty and is noted more commonly in women of reproductive age. Men comprise approximately 10% of the affected population. Melasma is more prevalent among people Wood’s lamp examination is useful in diagnosis and can help classify melasma into epidermal, dermal, and mixed types. Epidermal pigmentation is the most common type of melasma where pigmentation is accentuated under Wood’s light examination. Dermal pigmentation decreases under Wood’s light examination, and mixed types show areas with increased (epidermal), absent, or decreased (dermal) pigmentation. Classifying the melasma type is a valuable indicator of prognosis. While epidermal pigmentation tends to respond better and faster to hypopigmenting agents (eg. hydroquinone), dermal pigmentation lesions show variable response, often with much less patient satisfaction. Melasma is a cosmetic problem that is difficult to treat. Current treatments include hypopigmenting compounds, exfoliative agents, and lasers. Topical hypopigmenting agents, such as hydroquinone 2% to 10%, arbutinin, lumixyl, retinoic acid or tretinoin, azelaic acid, vitamin C, mild-to-moderate strength topical corticosteroids, and combinations of these agents are effective. Exfoliative agents, such as alpha-hydroxy acid chemical peels or microdermabrasion, are useful adjuncts to therapy. In 22
  • recent years, various laser therapies have been used with mixed results. In some cases, melasma has spontaneously resolved several months postpartum or after cessation of oral contraceptives. If indicated, discontinuation of causative medications is appropriate. Treatment and prevention of melasma should always include avoiding excessive sun exposure and daily use of broad-spectrum sunscreens. Clinical Pearls • Granuloma annulare can be a frustrating condition to manage, as it is one of those conditions that develops for reasons that are not well understood, and similarly often resolves spontaneously. • Interestingly, some cases have been reported to disappear when oral antibiotics were given for sinus, fungal or other infections. “If you haven’t looked at it with the makeup off, 
 you haven’t looked at it.” 
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic 23
  • Question 1 of 3 What is your diagnosis? A. Psoriasis B. Nummular eczema C. Allergic contact dermatitis I TCHY BUMPS TO LOWER ABDOMEN A 36 year-old male presents with a pruritic papular eruption to his lower abdomen. He had mild acne as a teenager, but no other skin problems. He has not used any topical agents to treat his abdomen and takes a proton-pump inhibitor (PPI) to treat his gastroesophageal reflux. D. Tinea corporis E. Fixed drug eruption Check Answer Diagnosis & Information 24
  • contact dermatitis”) as opposed to a specific sensitivity, in the case of ACD. Common causes of ACD include nickel, fragrances, preservatives, black hair dye, topical medications (e.g. neomycin, bacitracin), latex, rhus, cobalt, chromate, epoxy resin, rubber accelerators, rosin and many more chemical agents. Patients often complain of significant pruritus, and may have mild burning or discomfort. Lesions are typically edematous, erythematous, and welldemarcated. Diagnosis: Allergic contact dermatitis Allergic contact dermatitis (ACD) is a delayed type of induced sensitivity that occurs in individuals that have been previously sensitized to any of more than 3,000 chemicals, and is more likely in genetically predisposed individuals. The allergic reaction causes inflammation of the skin that is manifested by varying degrees of erythema, edema, and vesiculation. A reaction typically develops within 24-48hrs of a subsequent exposure, although it can occur up to 7 days later; it typically resolves after 2-3 weeks. The term “contact dermatitis” sometimes is used incorrectly as a synonym for ACD. Contact dermatitis is inflammation of the skin induced by chemicals that directly damage the skin (also known as “irritant Definitive treatment is the identification and removal of any potential causal agents; otherwise, the patient is at increased risk for chronic or recurrent dermatitis. Referral for skin patch testing (not skin prick testing; typically performed by a dermatologist) is appropriate. Online resources allow the physician to create a list of products free of allergens to which the patient is allergic, and should be avoided. Potent topical steroids are used, and occasionally if the reaction is severe or more widespread, a short course of oral steroids (e.g. Prednisone) can hasten resolution. Cool saline compresses, sedating antihistamines to aid in sleep, and topical immunomodulators (e.g. Protopic®, Elidel®) and emollients can provide benefit to the patient as well. 25
  • Clinical Pearls • A pruritic rash localized to the infra-umbilical area is an allergic contact dermatitis to nickel until proven otherwise. If this rash is not treated, it can eventually spread out to other areas of the body in an immune phenomenon termed the “id reaction.” • If a jean snap is a trigger for nickel contact (common), apply 1 coat of red nail polish on the inside of the snap and also encourage tucking in of one’s shirt. Once the red nail polish has disappeared (e.g. typically after 2 washings/dryings of the jeans), the absence of the red colour will remind you to repaint the jean snap. You can also cover it with duct tape. “In a particular clinic, the incidence of allergic contact dermatitis is determined by the interest the dermatologist takes in allergic contact dermatitis.” 
 ~ Drs. N. Hjorth & S. Fregert, Swedish and Danish Dermatologists 26
  • Question 1 of 3 What is the most likely diagnosis? A. Epidermoid cyst B. Milia cyst C. Digital mucous cyst U NCOMFORTABLE FINGER LESION A 50 year-old male is bothered by the appearance of a papule on his finger. It has grown very slowly over many months and doesn’t bleed. The lesion is tender only when it is firmly palpated or when he “accidentally bumps it.” D. Verruca vulgaris E. Cystic basal cell cancer Check Answer Diagnosis & Information 27
  • yellow-tinged. The lesions, which are usually solitary and appear lateral to the midline, are more common on dominant hands. Toes are less commonly involved. Although usually asymptomatic, pain can occur if there is impingement on nerve fibers, and rarely larger cysts can disfigure the affected digit. Nail deformities occur in many cases – called the “nail groove” sign. Women are more commonly affected (more than twice as often as men), as are those individuals between the ages of 50 and 70. Diagnosis: Digital mucous cyst Digital mucous cysts (DMCs) are benign and often asymptomatic ganglion cysts of the digits, typically located at the distal interphalangeal (DIP) joints or at the proximal nail fold. The etiology is uncertain, although it may relate to mucoid degeneration of connective tissue; this process seems to involve communication with the adjacent DIP joint and often is associated with osteoarthritis, and less commonly with antecedent trauma. Digital mucous cysts are translucent to flesh-coloured, solitary, round and dome-shaped semi-firm papulonodules. The cysts can be from a few millimeters to approximately one centimeter in diameter. The cysts contain a gelatinous thick fluid that is clear or Surgery or pseudo-surgical options are the standard of therapy and attempt to remove the cyst and any underlying stalk connected to the joint. Using conservative therapies, one can periodically needle the cyst with a wide-bore needles resulting in drainage and scarification until the cyst resolves. Aspirating the cyst contents followed by intralesional triamcinolone acetonide (10mg/ml) or liquid nitrogen cryotherapy is commonly employed. Less commonly, curettage +/- electrodessication, CO2 laser, or sclerotherapy techniques can be utilized. More aggressive surgical procedures using cold-steel surgical excision have been used which may require flaps or grafts. Another approach involves marsupialization, or excision of the whole proximal nail fold, with subsequent healing by secondary intention. Aggressive surgery to remove underlying osteophytes at the joint results in few recurrences. However, this procedure may slightly increase the risk of surgical complications (e.g. joint stiffness, reduced movement). Osteophyte removal alone (without removal of the cyst) has been reported to be effective. Nail deformities often resolve following osteophyte removal. While osteophyte 28
  • removal or open joint procedures are usually performed in the hospital setting, other management techniques can be performed in an office setting by primary care providers and dermatologists. Clinical Pearl • Puncturing a few holes into the lesion with a 25guage needle, extruding most of the viscous contents, and then applying cryotherapy is effective in many cases. As a backup, the patient can be given the needle that was used and instructed that if there is a recurrence, to boil the needle and repuncture the cyst and squeeze out its contents, eventually leading to permanent scarification and an end to the cyst. “Do not show your wounded finger, for everything will knock up against it.” ~ Baltasar Garcian, Spanish philosopher 29
  • Question 1 of 3 What is your diagnosis? A. Pigmented basal cell carcinoma B. Melanoma C. Dysplastic nevus D. Congenital melanocytic nevus D ARK SPOT ON CHEEK A 41 year-old woman presents with a dark lesion to her right cheek. The lesion causes no discomfort and it does not bleed or itch. The patient is not exactly sure how long the lesion has been present, but feels it has been at least a few months. She has a personal history of mild facial acne as a teenager and has no family history of skin problems. The patient worked as a lifeguard when she was a teenager and recalls several painful sunburns. She does not take any medications and has no known drug allergies. E. Blue nevus Check Answer Diagnosis & Information 30
  • respectively. However, mortality rates are higher in darker skin types due often to a more advanced presentation. There is little gender discrepancy. Older persons are more likely to acquire and die from melanoma, with a median age at diagnosis of 53. Primary risk factors for or clinical warning signs of melanoma include the following: • Changing mole (most important clinical warning sign; 
 the “E in Evolution”) • Clinical atypical/dysplastic nevi (particularly >5-10) • Large numbers of common nevi (>100) • Large (giant) congenital nevi (>20 cm diameter in an adult) • Previous melanoma • Sun sensitivity/history of excessive sun exposure Diagnosis: Melanoma • Melanoma in first-degree relative(s) Melanoma is a skin cancer of pigment-producing melanocytes that typically affects the skin, and less commonly the mucosae, eyes, leptomeninges and gastrointestinal tract. It account for approximately 5% of skin cancers, but 75% of deaths from skin cancer. It is believed that two-thirds of melanomas arise de novo, while one-third develop from pre-existing nevi. In Canada, approximately 5,000 people are diagnosed with melanoma each year, and approximately 950 will die of the disease. Detection and treatment in early stages provides the best opportunity for cure. • Prior nonmelanoma skin cancer (basal cell and squamous 
 cell carcinoma) • Male sex • Age older than 50 years • Presence of xeroderma pigmentosum or familial atypical 
 mole melanoma syndrome: These 2 genodermatoses confer a
 500- to 1000-fold greater relative risk of developing
 melanoma. Caucasians are most commonly afflicted, with black and Hispanic persons having one twentieth and one-sixth the prevalence, 31
  • The most common warning signs are a new or changing mole. Variation in the ABCDs (Asymmetry, Border irregularity, Color variegation, Diameter >6mm) is evident in more than 80% of lesions at diagnosis. Less commonly, one may note symptoms such as pruritus, pain, bleeding or ulceration. The letter “E” has been added to the ABCDs to signify “evolution” or change in an existing lesion. As well, the “ugly duckling” warning sign which signifies concern for a lesion that looks different from the rest is a beneficial adjunct to the ABCDE rule. The four main clinico-histopathologic subtypes of primary cutaneous melanoma are: superficial spreading melanoma (most common on trunk in men, and legs of women), nodular melanoma (15-30% of cases), lentigo maligna melanoma (slow-growing, usually head & neck of elderly), acral lentiginous melanoma (occurs on palms, soles or under nail plate; more common in darker skin types). Clinical Pearls • Any new black lesion on the skin should be strongly considered for biopsy or referral to a dermatologist. • Even after melanoma wide excision, these patients and those persons in their genetic lineage should be screened periodically for life and a much higher index of suspicion for biopsy is warranted for any new lesion or dark lesion on their skin. “It is easy to know a nevus. But to know a melanoma takes suspicion and excision, and remember that close observation can help prevent a lentiginous lesion from becoming a ‘litigenous’ one.” 
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis If detected early, melanoma can be cured with surgical excision. Stage 1 lesions (melanoma in situ) confer a 5 year survival rate of 95%, whereas, stage IV melanoma metastatic to skin, subcutaneous tissue or lymph nodes with normal LDH has a 5year survival rate of 19%. A stage IV melanoma that has metastasized to lungs has a 5 year survival rate of 7%. Most metastases occur within the first three years of a melanoma diagnosis, the most common locations for metastases are: lymph nodes, lung, liver, bone and brain. Patients diagnosed with melanoma must be followed for life not only because of risk of recurrence of their melanoma, but also because they are at increased risk of another primary melanoma. 32
  • Question 1 of 3 What is the most likely diagnosis? A. Large congenital melanocytic nevus B. Becker’s nevus C. Melanoma D. Acanthosis nigricans L ARGE BROWN HAIRY PATCH A 19 year-old male presents with a several year history of an increasingly evident hyperpigmented and hypertrichotic area to his left upper chest. The lesion is asymptomatic. He is healthy and takes no medications. E. Tinea versicolour Check Answer Diagnosis & Information 33
  • in the majority of cases a Becker’s nevus is considered a benign process. However, there have been a small number reported cases of melanoma within a Becker’s nevus. The diagnosis is usually clinical, although a skin biopsy can provide a histopathological diagnosis and helps distinguish it from other clinical entities, all of which are benign. Patients should be informed that this is a benign entity that does not require treatment except for cosmetic reasons. Patient concerns relate to the hyperpigmentation and/or the hypertrichosis. At present, it is quite difficult to remove the hyperpigmentation, although hypertrichosis can be safely and effectively removed by using laser hair removal or electrolysis. Clinical Pearl Diagnosis: Becker’s nevus A Becker’s nevus is an organoid nevus with hamartomatous elements, not a melanocytic nevus, predominantly affecting males. The nevus typically first appears as an irregular pigmentation (hyperpigmentation) on the torso or upper arm (though other areas of the body can be affected), and gradually enlarges irregularly, becoming thickened and often with hypertrichosis. There is an association with ipsilateral hypoplasia of breast and skeletal anomalies including scoliosis, spina bifida occulta, or ipsilateral hypoplasia of a limb that has been termed the Becker nevus syndrome, a sporadic condition. Other than the syndrome, • This benign late appearing birthmark is most common on the upper trunk and patients should be reassured as to its benign nature, and that currently we can clear the hypertrichosis, but that we are likely a few years away from being able to remove the hyperpigmentation with laser. “The skin is a diagnostician’s delight. Everything to be named is in full view. One has but to look, and recognize.” 
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists, Advanced Dermatologic Diagnosis 34
  • Question 1 of 3 What is your diagnosis? A. Alopecia secondary to irondeficiency B. Androgenetic alopecia C. Alopecia areata R OUND , BALD PATCHES ON SCALP A 29 year-old male is concerned with three round areas of hair loss to his posterior scalp that he has had for the previous two months. The areas are asymptomatic and he is otherwise healthy, though he hasn’t had a blood test in years. He had a similar round lesion on his scalp years ago that resolved on its own over a few months. D. Telogen effluvium E. Tinea capitis Check Answer Diagnosis & Information 35
  • round, well-defined, bald patches with “exclamation-mark hairs” at the periphery. AA has an unpredictable onset but most commonly affects the scalp. However, any of the hair-bearing areas of the body can be affected, including the eyebrows, eyelashes, beard, or even the body. Interestingly, there may also be nail pitting (similar to that found in psoriasis). It is typically asymptomatic, though occasionally mildly pruritic preceding the lesion development. Entire scalp involvement is termed alopecia totalis, while hair loss affecting the entire body is termed alopecia universalis. Diagnosis: Alopecia areata Alopecia areata (AA) is a non-scarring autoimmune condition that most commonly presents in young adulthood. AA, which affects men and women equally, affects 1.5-2% of the general population at some point in their lives. Most people with AA are healthy individuals, though they do have a higher risk of atopy, and autoimmune conditions such as thyroid disease and vitiligo; family members may have autoimmune conditions such as insulin-dependent diabetes, rheumatoid arthritis, thyroid disease or systemic lupus erythematosus. Although not life threatening, it can have a profound psychosocial impact on individuals. Lesions clinically present as one or more The differential diagnosis of AA should include other non-scarring alopecias such as telogen effluvium, androgenetic alopecia, and even tinea capitis. Occasionally a scalp biopsy or referral to a dermatologist is required to ascertain the diagnosis. Other autoimmune conditions including atopic dermatitis, vitiligo, thyroid disease, and pernicious anemia have been associated with AA, as has iron deficiency, and thus are often screened for on blood tests. The treatment of choice is intralesional triamcinolone acetonide (Kenalog®, 2.5-5mg/ml) injected in multiple sites 1cm apart on the affected areas every 4-6 weeks until regrowth. Hair growth usually becomes apparent in four weeks. Local skin atrophy, the predominant side effect, can be minimized by taking care to inject into the mid-dermis, rather than into the more superficial epidermis or the lower subcutaneous fat. Potent topical steroids are also used, as well as topical minoxidil (Rogaine®) and contact sensitizers such as diphencyclopropenone (DPCP) for more widespread involvement. Hair prostheses should be recommended for widespread involvement. 36
  • Clinical Pearl • In children with alopecia areata, in light of the often selflimited nature of this condition and the pain factor, starting treatment with a potent topical steroid often makes more sense than going straight to intralesional cortisone. “Hair brings one’s self-image into focus; it is vanity’s proving ground. Hair is terribly personal, a tangle of mysterious prejudices.”
 ~ Shana Alexander, former Journalist and Commentator on 60 Minutes 37
  • Question 1 of 3 What is your diagnosis? A. Impetigo B. Angular cheilitis C. Hand, foot and mouth disease D. Herpangina S ORES AT CORNER OF MOUTH A 24 year-old female presents with painful lesions at the corner of her mouth. Every few months, she develops tingling, burning and erosions to the area and is quite frustrated with topical antiviral therapy. E. Herpes simplex Check Answer Diagnosis & Information 38
  • such as those lining the eyes, vagina, cervix, or inside of the mouth. The skin around the blisters is often red. The diagnosis of HSV infection may be made clinically, but laboratory confirmation is recommended in patients presenting with primary or suspected recurrent infection. The gold standard of diagnosis is viral isolation by tissue culture, although this process can take as long as four to five days, and the sensitivity rate is only 70% to 80%. Despite these limitations, viral culture is still the diagnostic test of choice for HSV skin infections. Serologic testing is extremely sensitive but is not helpful during primary infection because of the delay in antibody development. Polymerase chain reaction enzyme-linked immunosorbent assay (PCR-ELISA) is extremely sensitive (96%) and specific (99%) but expensive. For this reason, it is not used for the diagnosis of skin lesions but is the laboratory test of choice for diagnosing HSV encephalitis. Diagnosis: Herpes simplex Herpes simplex virus (HSV) is a DNA virus presenting as grouped vesicles on an erythematous base. Typically infections will be recurrent in the same location. While oral herpes labialis is usually caused by HSV-1, genital involvement is more commonly due to HSV-2, although we now see both strains in both locations. Transmission occurs when an actively shedding individual (with clinical lesions or not) contacts mucous membranes which may be open or abraded. The virus then travels to sensory dorsal root ganglion where latency is established. Various stimuli can elicit outbreaks, including: trauma, fever, stress, hormonal fluctuations, and immunosuppression (e.g. from UV radiation). An eruption of tiny vesicles appears on the skin or on the mucous membranes, Susceptible patients without existing antibodies to HSV develop primary infection after first exposure to HSV. Any recurrence of HSV is termed “recur-rent infection.” About 20% to 40% of the general population experience recur-rent infection of the lips or perioral region. Herpes viruses establish lifelong infections and the virus cannot currently be eradicated from the body. Treatment usually involves antiviral drugs (acyclovir, valacyclovir, famciclovir; valacyclovir (Valtrex®) has the highest percentage bioavailability at 70%) that interfere with viral replication, reducing the physical severity of outbreak-associated lesions and lowering the chance of transmission to others. Resistance to antiviral drugs in immunocompetent individuals is rare. Treatment is most effective 39
  • if started early (within 12 hours of the start of symptoms such as burning or tingling sensation is ideal, although within 72 hours is part of the formal indication) and can help symptoms resolve a day or two sooner (“episodic therapy”). Studies of vulnerable patient populations have indicated that daily use of antivirals can reduce reactivation rates. For people who have frequent, painful attacks, reactivation rates can be reduced by continuous therapy (“chronic suppressive” or “maintenance therapy”) with antiviral drugs. Docosanol (Abreva®) is an over-the-counter cream used for recurrent oral-facial herpes simplex episodes (cold sores or fever blisters). It is used 5 times per day for up to 10 days. Acyclovir 5% cream (Zovirax®) is a prescription antiviral topical agent used to treat cold sores. It is used 5 times per day for 4 days once tingling sensation or erythema is noticed to the mouth region. Oral antiviral therapy is considered significantly more effective than topical therapy. Analgesic medications are also commonly used to manage painful lesions. Clinical Pearl • Episodic therapy is sufficient for patients with only the occasional herpes simplex eruption, though for patients with frequent eruptions or who want to lessen the risk of transmission to others, chronic suppressive therapy is advised. “An inefficient virus kills its host. A clever virus stays with it.” ~ Professor James Lovelock, Independent scientist and ecologist 40
  • Question 1 of 3 What is the most likely diagnosis? A. Verruca vulgaris B. Squamous cell carcinoma C. Basal cell carcinoma D. Prurigo nodularis R APIDLY EVOLVING HAND PLAQUE A 78 year-old female presents with a three month history of a rapidly growing large plaque with central crust on her dorsal hand, and which is occasionally tender. She has mild hypertension, but is otherwise healthy. She has no history of skin cancer, but has had “things burned off.” E. Keratoacanthoma Check Answer Diagnosis & Information 41
  • KAs typically affect elderly Caucasians, especially men. Several variants of this tumor exist, including: eruptive keratoacanthoma of Grzybowski (multiple non-involuting KAs), and multiple Ferguson-Smith keratoacanthoma (rare, autosomal dominant, self-healing, affecting young adults). Treatment options are largely surgical. If left untreated, many KA lesions can resolve spontaneously over a period of a few months. However, due to a small metastatic potential as evidenced by rare instances of metastases or invasion (possibly misdiagnosed SCC), surgical excision of the lesion is warranted in many cases. Occasionally systemic retinoids are employed for multiple KAs. For poor surgical candidates or those with lesions that due to size and location are difficult to excise, intralesional methotrexate, 5FU or bleomycin can be effective. Aggressive liquid nitrogen cryotherapy can also be considered and may need to be repeated. Clinical Pearls Diagnosis: Keratoacanthoma (KA) A keratoacanthoma (KA) is a common, low-grade tumor that can clinically resemble a squamous cell carcinoma. Some experts believe KA to be a variant of squamous cell carcinoma, and thus suggest similar treatment. A keratoacanthoma is characterized by its rapid growth velocity (over weeks to months). There is often a solitary, firm skin to red-coloured papule with a central crateriform keratin plug (“volcano” appearance). Etiologic factors for this tumor are multifold, including: ultraviolet radiation, immunosuppression, smoking, human papilloma virus, tar or pitch exposure, trauma, and genetic factors. • Although some KAs can self-resolve even if left alone, because the lesion is often unsightly or uncomfortable, and because of the potential that the lesion is actually a squamous cell carcinoma, KAs are typically treated for cure. Additionally, the scar left after spontaneous resolution is typically not as cosmetically acceptable as a surgical scar. • A rapid growing scaly tumour that looks like a mini-volcano is likely a KA. 
 “People don’t get checked enough. What scares me is that a lot of people with skin cancer came in for something different and I just happened to see the tumor. ” 
 ~ Dr. Quang Le, American Dermatologist 42
  • Question 1 of 3 What is the most likely diagnosis? A. Lichen planus B. Lichen simplex chronicus C. Pityriasis rosea D. Pustular psoriasis I TCHY PAPULES ON WRISTS A 33 year-old male presents with numerous pruritic papules on his wrists, shins and ankles. The patient finds the rash very bothersome and recently has difficulty sleeping. He takes occasional migraine medications, and has no drug allergies. E. Nummular eczema Check Answer Diagnosis & Information 43
  • Lesions slowly develop over weeks and months, often starting on the wrists. Pruritus is common and worse in the hypertrophic form (often on the shins). Oral lesions can be asymptomatic or cause burning and pain. Most cases will resolve within two years, although oral involvement often implies a longer duration. Along with cutaneous involvement, scalp (lichen planopilaris can cause scarring and permanent alopecia), nails (10% of patients; nail plate thinning, grooving and ridging, scarring), oral (tongue, buccal) and genitals (vulva, glans) can be affected. Diagnosis: Lichen planus Lichen planus (LP) is a pruritic papulosquamous disease of planar, polygonal, and purple/violaceous papules (5 P’s). Common sites of involvement include the flexor surfaces of the arms and wrists, shins, ankles, genitalia, and oral mucosa (lacy white “Wickham striae”). There is no gender or racial predilection, and while LP can occur at any age, those age 30-60 years-old are most commonly afflicted. Several clinical subtypes have been observed: hypertrophic, atrophic, erosive, follicular, annular, linear, vesiculobullous, lichen planus pemphigoides, and actinic. The diagnosis of LP is often clinical, although histopathology may be required to confirm the diagnosis. LP appears to be an idiopathic immunologically-mediated inflammatory disorder. Stress may play a role in triggering this condition. Different variants exist, which have different presentations and symptomatology. Hypertrophic LP is particularly pruritic, and often affects the shins. The oral erosive form of lichen sclerosus has been associated in some cases with Hepatitis C viral infection. Ulcerative lesions of the mouth and vulva, unlike the cutaneous lesions, have a small risk of malignant transformation into squamous cell carcinoma. Other conditions with altered immunity may co-exist with LP, including alopecia areata, vitiligo, lichen sclerosis and myasthenia gravis. LP is a self-limited condition that usually resolves within 1-2 years. Most patients are treated symptomatically and with potent topical steroids. Oro-genital involvement can benefit from topical calcineurin inhibitors, such as tacrolimus (Protopic®). Less commonly, oral metronidazole (Flagyl®), oral acitretin (Soriatane®), phototherapy, and systemic steroids are employed by dermatologists for resistant or generalized LP. 44
  • Clinical Pearl • Both psoriasis and lichen planus commonly present in men on the glans penis (remember the P’s of lichen planus: purple, polygonal, planar, pruritic papules….and penis!). While STDs are important to rule out in lesions affecting the glans, remember these two immunologic conditions as well. “Ordinarily, lichen planus is as easily recognizable as an old friend. He greets you with an itch and wears iridescent purple patches in all the old familiar places on wrist and ankle….then with experience you will learn to recognize your friend by his masks. You will come to know him sans itch, sans papule, and sans Wickham’s striae.” 
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 45
  • Question 1 of 3 The most likely diagnosis is? A. Tinea corporis B. Cutaneous lupus erythematosus C. Chronic form of nummular dermatitis S CALY , ERYTHEMATOUS RASH ON ELBOWS A 63 year-old woman presented with a scaly, erythematous rash on her elbows and buttocks. She has been using daily moisturizers and 1% hydrocortisone cream without much clinical improvement. Her past medical history includes hypertension and dyslipidemia. She is currently taking ramipril (Altace®), atorvastatin (Lipitor®), and a multivitamin on a daily basis. D. Psoriasis vulgaris 
 (mild-to-moderate type) E. Mycosis fungoides Check Answer Diagnosis & Information 46
  • About 35% of patients with psoriasis have a family history of the disease. Several environmental factors can trigger psoriasis in susceptible individuals: infection (most commonly streptococcal infection); trauma to the skin (surgery, sunburn, scratching; known as “Koebner phenomenon”); drug reaction (e.g., lithium, beta blockers, anti-malarial drugs, non-steroidal antiinflammatory drugs, and glucocorticoids); and stress. Diagnosis: Psoriasis vulgaris 
 (mild-to-moderate type) Psoriasis is a chronic, recurring inflammatory disease that can affect the skin, scalp, nails and joints. The typical lesions are pruritic, erythematous, and present as well-demarcated papules and plaques with silvery-white scales. Psoriasis affects about 2% of the population and ranges in severity from mild to severe; patients with moderate to severe disease can experience a significant impact on quality of life. It affects men and women equally. The age of onset of psoriasis follows a bimodal distribution (peaks between ages 20 to 30 years and again between the ages of 50 to 60). Both genetic and environmental factors have been implicated in the pathophysiology of psoriasis. The clinical presentation of psoriasis varies depending on the morphologic subclass. Plaque psoriasis (Psoriasis vulgaris) is the most common subtype and is usually concentrated on the extensor surfaces (i.e., elbows, knees, and lumbar back), scalp, genital areas, palms, and soles. Removal of scale causes sites of punctate bleeding (Auspitz sign), a diagnostic sign of historic note. Therapy varies depending on disease severity, as determined by the degree of body surface area involvement (BSA). Mild psoriasis involves <2% of the BSA, moderate psoriasis covers 2% to 10% of the BSA, and severe psoriasis covers >10% of the BSA. However, the vast majority of patients (approximately 80-90%) presents with relatively mild disease and have only limited involvement of the skin, which can be well-controlled with topical therapy alone. Patients with scalp, face, genital, and palmoplantar involvement in particular can have a very significant impact on their quality of life. Diagnosis of psoriasis is mainly made on clinical grounds. History and physical examination are usually diagnostic and should include a screen for arthritis because up to 30% of patients with psoriasis have or will develop joint involvement (psoriatic arthritis). Skin biopsy can be helpful in difficult cases. The differential diagnosis includes pityriasis rosea, seborrheic dermatitis, lichen simplex chronicus, tinea infections, 47
  • psoriasiform drug eruptions, mycosis fungoides, and nummular eczema. Mild-to-moderate psoriasis is typically treated using topical agents. Useful topical preparations include those including corticosteroids, vitamin D analogues, combinations of these, and calcineurin inhibitors. Corticosteroids remain the mainstay of topical treatment for mild-to-moderate psoriasis. In choosing an appropriate corticosteroid potency and vehicle, the physical location being treated and patient preference should be considered. Psoriatic patients with thick, chronic plaques often require treatment with the highest potency corticosteroids (+/LCD tar or salicylic acid) and/or intralesional triamcinolone acetonide. Topical vitamin D modulators are among the most widely used medications for the treatment of mild-to-moderate psoriasis. Dovonex® (calcipotriol ointment and cream) and Silkis® (calcitriol 3 µg/g) ointment are synthetic topical vitamin D analogs with a great safety profile. Dovobet® (calcipotriol/ betamethasone proprionate) ointment combines the benefits seen in both a topical vitamin D analog and a topical corticosteroid. Mechanistically, this refers to the anti-proliferative/ prodifferentiating effects of the vitamin D analog component and the anti-inflammatory effects of the corticosteroid component. Clobex® spray (clobetasol propionate) is another good and elegant option for plaque psoriasis. of calcineurin inhibitors in some patients are a burning sensation and pruritus with initial treatments; however, the discomfort generally diminishes with ongoing use. The aforementioned topical therapies can be applied once or twice daily for up to 8 weeks. If insufficient improvement is noted, consider referral to a dermatologist. For recalcitrant mild-to-moderate or for more extensive psoriasis, psoralen plus ultraviolet-A topical therapy administered 2 to 3 times a week or more commonly narrow-band (311 nm) ultraviolet-B therapy are effective options and typically covered under provincial plans. Several systemic agents have been used as therapy for moderate psoriasis not controlled by topical therapy alone. Methotrexate, acitetrin, and less commonly cyclosporine are most widely used. Rotating ultraviolet light and systemic medications can help prevent toxicity from continuous use of any one therapy alone. Increasingly, biologic therapies (e.g. adalimumab, etanercept, infliximab, and ustekinumab) are also being used for moderate plaque psoriasis. There are two topical preparations of calcineurin inhibitors: Protopic® (tacrolimus ointment 0.03% and 0.1%) and Elidel® (pimecrolimus cream 1.0%). Tacrolimus and pimecrolimus have been used in areas of skin where greater topical penetration is improved, such as in flexural or facial skin. The main side-effects 48
  • Clinical Pearls • Make sure to use the right vehicle in the right location. For instance, for the scalp or other hair bearing areas, lotions, foams or gels are great vehicles, while for very thick or fissured plaques of psoriasis, an ointment is a better fit. Also, ask your patients if they have a specific preference. • Psoriasis skin is very thick, so patients need to understand that although “steroids thin the skin,” in psoriasis this is a very wanted side effect! • For patients asking about more natural or lifestyle options, there is evidence to support the benefits of weight reduction, smoking cessation, reducing alcohol, and consuming more fish or fish oil capsules. • For patients with a significant impact on their quality of life, consider more aggressive therapeutic options and/or referral to a dermatologist. “Psoriasis is an acronym for a Pitting, Scaling, Ongoing, Red, Inflammatory, Anguishing, Symmetrical, Inherited Skin disease.” 
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 49
  • Question 1 of 3 What is the most likely diagnosis? A. Fordyce glands B. Flat warts C. Xanthelasma D. Syringomas P ERIOCULAR PAPULES A 34 year-old female is bothered by the appearance of papules under her eyes that she has had for several years. She mentions that an aunt had similar asymptomatic, flesh-coloured papules which increased in number over time. She is healthy and takes no medications. E. Milia Check Answer Diagnosis & Information 50
  • include the axilla, chest, abdomen, and genitals. Syringomas have been associated with Down syndrome. Where clinical uncertainty as to a diagnosis exists, a skin biopsy or referral to a dermatologist can be beneficial. Patients should be reassured as to the benign nature of these lesions. Treatment is primarily for cosmetic reasons only, with the goal of having complete destruction of lesions without evidence of scars. Syringomas can be treated with local excision, electrodessication, dermabrasion or cutaneous resurfacing with a carbon dioxide or erbium-yag laser. Clinical Pearl Diagnosis: Syringomas • Syringomas are benign, cosmetically unappealing skincoloured to yellowish small papules most commonly found in females, especially in my experience in Asian skin. The lower eyelids have many more lesions than the upper eyelids. Syringomas, considered benign adnexal tumors, are fairly common lesions more commonly affecting females, and predominantly of cosmetic concern. Lesions typically first appear around the time of puberty. • Even with treatment, patients should be warned that lesions can recur and/or new lesions may develop over time, so multiple treatments would be typical over one’s lifetime. Syringomas are asymptomatic flesh-colored to yellow small dermal papules that can also appear translucent. The lesional surface is either flat-topped or round, and the lesions typically are quite small, having a diameter of less than 4mm. Syringomas are distributed symmetrically in clusters, usually involving the lower eyelids and upper cheeks. Other less commonly affected areas “You’ll never get the big picture without looking at the little details.” ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 51
  • Question 1 of 3 What is the most likely diagnosis? A. Verruca vulgaris B. Papular dermatitis C. Molluscum contagiosum D. Corns F INGER PAPULES E. Acquired digital fibrokeratomas A 32 year-old male presents with a seven month history of papules growing and multiplying on his hand. They are asymptomatic, but unsightly. Check Answer Diagnosis & Information 52
  • Warts are transmitted by direct or indirect contact, and disruption of the epithelial barrier is a predisposing factor. A subset of HPV types has been associated with the development of malignancies: HPV 6, 11, 16, 18, 31, and 35; malignant transformation is most common in those with genital warts or those who are immunocompromised. There are now two HPV vaccines authorized for use in Canada: Gardasil® and Cervarix®. Gardasil® is approved for use in females and males aged 9-26, and provides protection against four HPV types: HPV-6, HPV-11, HPV-16 and HPV-18. Cervarix® was recently approved for use in Canada for females aged 10 to 25. At this time Cervarix® has not been approved for use in males in Canada. Cervarix® provides protection against the two HPV types: HPV-16 and HPV-18. Diagnosis: Verruca vulgaris (Warts) Cutaneous warts, one of the most common skin diseases, are a frequent presenting complaint to family practice and dermatology clinics. Warts are benign proliferations of skin and mucosa confined to the epithelium caused by one of the more than 150 types of the double-stranded DNA human papilloma virus (HPV). Common, plantar and flat warts are cutaneous manifestations of the human papillomavirus (HPV). Certain HPV types tend to occur at particular anatomic sites; however, warts of any HPV type may occur at any site. Clinically, HPV manifests itself as either: common warts, flat warts, genital warts, or palmoplantar warts. The treatment of warts poses a therapeutic challenge for physicians as no general consensus on monotherapy to achieve complete remission in all patients has been reached. As a result, many different approaches to wart therapy exist with varying mechanisms of action and efficacy. A ‘watch-and-wait approach’ is the first option to consider, since 65% of warts are believed to regress spontaneously within two years. Non-treatment in patients with extensive, spreading, or symptomatic warts is not advised. The first line of therapy is the topical agents, particularly salicylic acid, which is effective for non-genital warts. Many salicylic acid preparations are available over the counter (e.g. Soluver plus®, Duofilm™) at concentrations up to 40%, can be applied at home, and have cure rates from 70-80%. Dermatologists may prescribe even stronger compounded acid mixtures containing trichloroacetic acid, salicylic acid and lactic acid. Topical vitamin A acid/retinoids can also be considered in the therapeutic armamentarium. 53
  • There are several topical agents that are applied only in the physician’s office, and they include catharidin and powerful sensitizing agents such as diphencyprone in a treatment referred to as immunotherapy. Cryotherapy destroys warts by thermal cytolysis. It can be used to treat warts in any location. An experienced physician applies liquid nitrogen with a cotton applicator or the more aggressive cryospray. Cryotherapy has been shown to be superior in the treatment of common warts. 5fluorouracil (5-FU), such as Efudex®, is a chemotherapeutic agent that interferes with DNA and RNA synthesis, and both topical and intralesional compounds have been used to treat genital warts. Imiquimod (Aldara®, Zyclara®) has also been used for hand warts with some success, although it is more useful for mucosal warts where absorption is much greater. For persistent and refractory warts, intralesional injections, most commonly Bleomycin or candida antigen, can be performed by an experienced physician. Clinical Pearl • Make clear to your patients that there is no quick and easy fix as far as warts are concerned. • Evidence-based medicine for non-mucosal warts best supports liquid nitrogen cryotherapy and salicylic acid preparations. • Consider oral zinc therapy as an immune booster for stubborn warts – start at 50mg/day with food (studies show it can be increased as tolerated up to 600mg/day). “Of all the futile disorders of the skin, it would be hard to find any that are regarded with greater contempt by the lay public and yet capable of resisting a greater variety of treatment than the group of papillary lesions commonly known as warts.” 
 ~ Dr. W.W. Lempiere, Australian Dermatologist The treatment of warts continues to pose a therapeutic challenge. Many different approaches to wart therapy exist with varying mechanisms of action and efficacy. The treatment options are extremely heterogeneous and no single treatment or group of treatments is standard. Patients are often dissatisfied with recurrence, as a therapeutic regimen to achieve complete remission in all patients has not yet been developed. Additional clinical trials of the many therapeutic options will help to clarify the best treatment choices for cutaneous warts. 54
  • Question 1 of 3 What is the most likely diagnosis? A. Subungual wart B. Psoriatic nail C. Onychomycosis D. Traumatic nail changes T HICK , YELLOW TOENAILS A 56 year-old male has slowly changing nails over the past 10 years. They have gotten thicker, yellow in colour, and occasionally cause him discomfort. He finds cutting his toenails to be increasingly difficult. E. Pseudomonas nail infection Check Answer Diagnosis & Information 55
  • dermatophyte molds. However, the clinical appearance is indistinguishable between the different fungal species. The main subtypes include: distal lateral subungual onychomycosis (DLSO), white superficial onychomycosis (WSO), proximal subungual onychomycosis (PSO), and candidal onychomycosis. Clinically, onychomycosis manifests with an increased nail thickness, an opacified nail plate, subungual thickening, and/or onycholysis. There is also often discoloration of the nail ranging from white to yellow to brown in colour. Diagnosis is usually clinical, although the nail changes of psoriasis or lichen planus and the effects of aging can have a similar appearance. Further testing such as direct microscopy with 20% potassium hydroxide (KOH) testing can be beneficial, and a fungal culture is often used to identify the causative organism. Diagnosis: Onychomycosis Onychomycosis is a fungal infection that most commonly affects the toenails. It can affect any component of the nail unit, including the nail matrix, nail bed, or nail plate. The majority of the time, the concern is primarily cosmetic in nature, but occasionally, there can also be discomfort and pain. The prevalence of onychomycosis is approximately 6% and it accounts for half of all nail disorders. Onychomycosis is uncommon in childhood, but is seen with prevalence rates up to 90% in the elderly. The most common microorganism implicated is the dermatophyte Trichophyton rubrum. Onychomycosis is caused by 3 main types of fungi: dermatophytes, yeasts, and non- Topical therapy is beneficial in mild cases involving the very distal nail plate and when few nails are involved. Topical therapy is also considered in combination with systemic therapy or where the patient is on multiple oral medications. The best topical therapy option is likely ciclopirox olamine 8% nail lacquer solution (Penlac®). Ciclopirox lacquer is usually applied to the affected nails once daily at bedtime or at least 8 hours before washing the affected area. Apply daily over the previous coat. Once a week, remove the lacquer with rubbing alcohol. Loose nail material should be filed and nails trimmed, as required. Treatment of onychomycosis (especially multiple nails or of long duration) is largely systemic with terbinafine (Lamisil®) considered by most to be the drug of choice. Less commonly, itraconazole pulse therapy or nail avulsion is employed. Not treating the nails is a common and important option to discuss. 56
  • Clinical Pearls • Onychomycosis and tinea pedis are often important to treat in diabetic patients since the fissures or maceration caused by tinea can provide an entry point for bacteria, and ultimately risk for cellulitis, sepsis, or amputation. • For patients with recurrent tinea cruris (“jock itch”), always check their toenails as there is often a concomitant onychomycosis. “You can tell a lot from a person’s nails. When a life starts to unravel, they’re among the first to go.” 
 ~ Ian McEwan, critically-acclaimed author and Man Booker Prize winner 57
  • Question 1 of 3 What is the most likely diagnosis? A. Scalp psoriasis B. Severe seborrheic dermatitis C. Mycosis fungoides S CALY , ERYTHEMATOUS PLAQUES ON HEAD A 54 year-old man comes to your clinic with a longstanding history of ‘dandruff’ that is pruritic and he is unable to get under control. He has tried using many shampoos advertised on television and recommended by his pharmacist but has seen no clinical improvement. He also has scaly plaques to his elbows and knees. He is otherwise healthy and takes no medications. D. Tinea capitis E. None of the above Check Answer Diagnosis & Information 58
  • white or gray scale and may extend beyond hair margins, affecting the forehead, neck, ear and retroauricular area. Quality of life can be severely compromised, particularly if lesions are visible, scales fall onto clothes, and when pruritus is intense. Hair loss secondary to poorly managed scalp psoriasis can occur. Thick accumulated scale and hair, particularly with very thick hair, may be obstacles to medications reaching the scalp. The diagnosis of scalp psoriasis is most often made clinically. In some cases, it may be difficult to differentiate between scalp psoriasis and seborrheic dermatitis, but the presence of psoriasis in other locations may aid its diagnosis in the scalp. Localization of disease past the scalp margins and sharply demarcated plaques may help differentiate scalp psoriasis from seborrheic dermatitis, as seborrhea usually does not extend beyond the scalp margins but may be found in the central facial region or central chest. Diagnosis: Scalp psoriasis Psoriasis affects approximately 2% of the population, and in 50-80 percent of cases, the scalp is affected. Scalp involvement may occur in isolation, with plaque psoriasis located elsewhere (most common), or with erythrodermic, pustular or guttate psoriasis, and/or psoriatic arthritis. In 25-50 percent of affected patients, psoriasis presents initially on the scalp. Family history may predispose patients to scalp psoriasis. Mild forms of scalp psoriasis involve minimal scaling, while severe disease may be associated with thick, crusted plaques that are frequently associated with moderate to severe itch. Classic scalp lesions are asymmetric, sharply demarcated, covered with silver- Scalp psoriasis is a chronic inflammatory disease and cure is not a realistic treatment expectation. Instead, the clinician’s focus should be on enhancing the patients’ skin-related quality of life. Non-pharmacological physical therapies which include moist occlusion to plaques and gentle debridement of scalp scaling are useful in some patients. Occlusion therapy involves first applying skin products, such as moisturizers to the skin then wrapping the skin with plastic wrap and tape. Occlusion helps keep the area moist and increases the effectiveness of medicated creams. Topical agents are the mainstay of pharmacologic treatments, with clinically proven efficacy. Scalp psoriasis can be managed with topical preparations of tar and salicylic acid, such as Sebcur/ T™ (10% tar with 4% salicylic acid) and Neutrogena® T/Gel® (0.5% tar) medicated shampoos, Derma-smoothe/FS® scalp oil (fluocinolone topical oil) overnight with shower cap, Dermovate® 59
  • lotion (clobetasol 17 - propionate), or Diprosalic® lotion (0.05% betamethasone and 2% salicylic acid). The retinoic acid derivative Tazorac® (0.1% tazarotene gel), applied nightly, can be helpful for scalp psoriasis, but must be used in combination with steroids to prevent irritation. Newer topical agents for scalp use are being used currently with better patient satisfaction and compliance. Dovobet® gel is a new lipophilic gel specially formulated for the scalp and contains the active ingredients calcipotriol 0.005% (synthetic vitamin D analogue) and betamethasone dipropionate 0.05% (potent corticosteroid).” Clobex® (Clobetasol proprionate) 0.05% shampoo is also efficacious and safe for the management of moderate scalp psoriasis; it is often prescribed twice weekly (alternating with other psoriasis shampoos) and effectively helps to prevent the relapse of scalp psoriasis; this 15 minute shortcontact shampoo formulation can be safely utilized for extended periods and weaned as necessary. Topical therapies may be used in combination with sunlight or ultraviolet light (phototherapy) for moderate psoriasis that affects less than 20% of the skin surface. Brief exposures to ultraviolet B light (UVB), and less commonly UVA, improves psoriasis and treatments are usually conducted three times per week. As an alternative to topical application, corticosteroids administered through intralesional injection (e.g. Kenalog® (triamcinolone acetonide), 5-10 mg/mL) to recalcitrant scalp lesions may provide some patients with a reduction of symptoms, often lasting several months. Systemics used for management of psoriasis include cyclosporine (least common), methotrexate and acitretin; and although these therapies may be effective, each involves inherent limitations. Biologics have become an important modality for the treatment of moderate-to-severe chronic plaque psoriasis and may be an effective approach to management of difficult plaque psoriasis of the scalp. Current biologics on the market for psoriasis include the tumour necrosis factor-alpha blockers Enbrel® (etanercept), Remicade® (infliximab), and Humira® (adalimumab). One of the newest biologics is Stelara® (ustekinumab), a human monoclonal antibody directed against interleukin (IL)-12 and IL-23. Many new biologics are in the pipeline. Clinical Pearls • For stubborn scalp psoriasis, consider multi-modal treatment, meaning shampoo and overnight gel or lotion use. For very stubborn plaques, consider intralesional Kenalog®. • Scalp psoriasis can have a tremendous impact on quality of life and can be difficult to control, and so occasionally systemics or biologics are employed even if this is the only area affected by psoriasis. Phototherapy can also be considered, especially in those persons with little or no hair. “I have long had the idea that God created psoriasis and warts to teach dermatologists the merits of humility.”
 ~ Vincent Joseph Derbes, Dermatologist and former Editor, International Journal of Dermatology 60
  • Question 1 of 3 What is the most likely diagnosis? A. Basal cell carcinoma B. Actinic keratosis C. Keratoacanthoma D. Irritated seborrheic keratosis L ARGE SCALY SCALP PLAQUE A 67 year-old male presents with a scaly plaque on his scalp. It has slowly enlarged in the past year, and is otherwise asymptomatic. He has a history of actinic keratoses, and worked in construction. E. Squamous cell carcinoma Check Answer Diagnosis & Information 61
  • involvement and invasion of dermis). The diagnosis of squamous cell carcinoma is based on clinical suspicion and confirmed by a histopathological diagnosis on biopsy. Treatment options include surgical excision, as well as curettage and electrosurgery (similar cure rates). For well-differentiated small SCCs (<2cm), a 4mm margin is recommended, whereas in larger tumors in high risk sites require at least a 6mm margin. Larger SCCs and those that are poorly differentiated have a higher incidence of local invasion and metastases. Mohs micrographic surgery is indicated for aggressive subtypes of SCC, recurrent tumors, or highly aggressive features (e.g. SCC in a burn scar). Other treatment options include radiation and cryosurgery in patients with impaired clotting disorders or tumors in difficult to excise areas. Diagnosis: Squamous cell carcinoma (SCC) Squamous cell carcinoma is currently the second most common skin cancer in Caucasians, and the most common type in black individuals. SCC can develop in the setting of actinic keratoses, leukoplakia, lichen sclerosus, radiation dermatitis, chronic arsenic exposure, scars, burns, chronic ulcers or sinuses (e.g. hidradenitis suppurativa). Prevention of SCC is similar to preventative treatment of actinic keratoses (AKs). Effective measures include avoidance of excessive sun exposure, especially during peak day-time hours, avoidance of artificial sources of ultraviolet (UV) light such as tanning beds or prolonged UV treatments, wearing protective clothing, applying sunscreen with at least 30 SPF over sunexposed areas a few times per day. Additionally, proper management of AKs and aggressively managing other underlying conditions (e.g. lichen sclerosus) is important. There is thought to be a spectrum of keratinocyte malignant transformation: actinic keratoses (atypical keratinocytes in up to one-half of the epidermis), Bowen disease or SCC-in-situ (full epidermal keratinocyte atypia), and invasive SCC (full epidermal 62
  • Clinical Pearls • An SCC on a dark-skinned individual will often present on the lower leg as a benign-appearing hyperpigmented scaly plaque. • Both coffee and Cox-2 inhibitors may prevent non-melanoma skin cancer like SCC. “Skin cancer, if caught early, can be treated fairly straightforwardly, and it’s not that big a deal. But once skin cancer has spread, effectively nothing works. So it’s particularly important to catch skin cancer early.”
 ~ Dr. Darrell Rigel, American dermatologist 63
  • Question 1 of 3 What is your diagnosis? A. Impetigo B. Molluscum contagiosum C. Juvenile xanthogranuloma D. Milia P APULES ON THE ABDOMEN A 5 year-old boy was brought into clinic by his mother because of a concern regarding papules that were developing on his abdomen, chest and upper arms. These papules were mildly pruritic, and had been present for 2 months and new papules were still appearing. There were no sick contacts, and the child felt well otherwise. E. Common Warts Check Answer Diagnosis & Information 64
  • typically occur on the chest, arms, trunk, legs, and face. Mucous membrane involvement is rare, and the palmoplantar area is spared. Patients with a history of atopic dermatitis are more prone to MC and may develop a large number of lesions. Approximately 10% of all patients will develop eczema around the lesions. In adults, MC is most commonly a sexually transmitted disease and presents as a few scattered lesions often limited to the perineum, genitalia, inner thighs, lower abdomen, or buttocks. MC in healthy children and adults is usually a self-limited disease, but may persist for several months and even up to a few years. Widespread, persistent, and atypical MC may occur in patients who are significantly immunocompromised or have acquired immunodeficiency syndrome (AIDS) with low CD4 T-lymphocyte counts. Diagnosis: Molluscum contagiosum Molluscum contagiosum (MC) is a viral infection of the skin caused by a DNA poxvirus called the molluscum contagiosum virus (MCV), which is a benign and generally self-limited viral infection. Skin lesions typically consist of multiple dome-shaped, pink to skin-colored papules 2-6 mm in diameter of which some lesions show the classic feature of umbilication. MC is usually asymptomatic, although individual lesions can occasionally be tender or pruritic. MC is encountered most commonly in children who become infected through direct skin-to-skin contact or indirect skin contact with fomites, as well as by auto-inoculation. Lesions Diagnosis is usually clinical and based on the distinctive central umbilication of the dome-shaped papule. If diagnosis is uncertain, papules can be biopsied and sent for histopathologic identification. Adult patients should be questioned about sexual history and where appropriate, evaluated for other concomitant STDs. Always consider testing for HIV infection in patients with large or facial MC lesions. Patients and their families should be educated as to the benign and self-limited nature of this condition and that treatment is not a necessity. For the most part, the main concern is temporary adverse cosmetic results and embarrassment. Most lesions resolve with no permanent residual skin defect; however, occasional lesions may produce a slightly depressed scar, especially if excoriated. Although treatment is not required, it can help reduce autoinoculation or transmission to close contacts and improve clinical appearance. More than one treatment session is frequently required. 65
  • In healthy children, a major goal is to limit physical discomfort. Often, no medical intervention or minor direct trauma is appropriate. Cryotherapy or curettage (can apply topical anesthetic cream pre-procedure) are very effective therapies for older children. For younger children, Cantharidin applied carefully to the lesions and washed off after 15 minutes to 2 hours can be effective. Similarly, tretinoin/vitamin-A acid applied topically only to the lesions (e.g. with a toothpick) can be used. Another treatment option to consider, with variable benefit, is topical imiquimod (e.g. Aldara™, Zyclara™), a topical immune response modifier and a potent inducer of anti-viral interferons. “What perhaps should receive more attention is the effect of the treatment on the virus.” ~ Luc Montagnier, French virologist and 2008 Nobel Prize Winner (Discovery of HIV) In adults who are more motivated to have their lesions treated, cryotherapy or curettage of individual lesions is effective and well tolerated. In immunocompromised individuals, MC can be extensive and difficult to treat. The prognosis of patients with MC is generally excellent because the disease is benign and self-limited. In healthy patients, 1-4 treatments are usually effective to see complete resolution of the lesions. Clinical Pearl • Be careful when treating self-limited conditions such as molluscum or warts in individuals with more pigmented skin as the treatments can result in hyper or hypo-pigmentation which often bother the patient even more than the original problem and can have medico-legal ramifications. 66
  • Question 1 of 3 What is his diagnosis? A. Linear IgA disease B. Herpes simplex C. Herpes zoster D. Dermatitis herpetiformis P AINFUL , VESICULAR RASH A 30 year-old male presents with a painful vesicular rash to his right lateral flank region. He has been experiencing generalized malaise and myalgias to the affected area for the past 2 days. E. None of the above Check Answer Diagnosis & Information 67
  • Diagnosis: Herpes zoster Herpes zoster (shingles) is an acute, painful dermatomal dermatitis that affects approximately 10% to 20% of adults, often in the presence of immunosuppression. Herpes zoster is a viral infection caused by the same virus (varicella) that causes chicken pox. During the course of varicella, the virus travels from the skin and mucosal surfaces to the sensory ganglia, where it lies dormant for a patient’s lifetime. Reactivation often follows immunosuppression, illness, emotional stress, trauma, and irradiation or surgical manipulation of the spine, producing a dermatomal dermatitis. Herpes zoster is primarily a disease of adults and typically begins with pain and paresthesia in a dermatomal or bandlike pattern followed by grouped vesicles within the dermatome several days later. Occasionally, fever and malaise occur. The thoracic area accounts for more than half of all reported cases. When zoster involves the tip and side of the nose (cranial nerve V) nasociliary nerve involvement can occur (30%-40%). Great care is needed if the blisters involve the eye because permanent eye damage can result, and so an ophthalmology consultation should be strongly considered. Most patients with zoster do well with only symptomatic treatment, but postherpetic neuralgia is common in the elderly. Disseminated zoster is uncommon and occurs primarily in immunocompromised patients. Since 2008, a live, injectable, attenuated herpes zoster vaccine (Zostavax™) has been authorized for use in Canada for the prevention of herpes zoster (shingles) infection in adults aged 60 years and older. Since its inception, the vaccine has greatly reduced the number of cases of postherpetic neuralgia and reduced the severity and duration of pain and discomfort associated with shingles. Diagnosis is by clinical presentation, viral culture, or direct fluorescent antibody from a skin biopsy. Prompt treatment reduces the extent and duration of symptoms as well as the risk of chronic sequelae. Antiviral agents (such as acyclovir, valacyclovir and famciclovir) promote healing of cutaneous lesions and prevent or reduce the severity of postherpetic neuralgia. The recommended adult dose of valacyclovir (Valtrex®) to treat shingles is 1000 mg tid for 7 days. The treatment should be initiated within 72 hours of the onset of the rash for better management of clinical sequelae. Narcotic and non-narcotic topical and oral analgesics, anti-convulsants, and tricyclic 68
  • antidepressants can be used for acute zoster-associated neuralgias. The use of oral corticosteroid therapy is controversial. Botulinum toxin (Botox®) is also effective for management of pain caused by postherpetic neuralgia. The analgesic effects are not dependant on changes in muscle tone. Clinical benefit with Botox® is seen for at least 14 weeks after it is given. Local anesthetics applied directly to the skin of the painful area affected by postherpetic neuralgia are also effective. Lidocaine (Xylocaine®) is available in a patch that has been approved for use specifically in postherpetic neuralgia. It can be used to the affected area every 4-12 hours as needed. Topical local anesthetics stay in the skin and therefore do not cause problems such as drowsiness or constipation. Capsaicin (Zostrix®) cream may be somewhat effective and is available over the counter. It can be applied to the affected area 3-5 times daily. However, patients often find that it causes a burning pain during application. Clinical Pearl • Be careful when treating self-limited conditions such as molluscum or warts in individuals with more pigmented skin as the treatments can result in hyper or hypo-pigmentation which often bother the patient even more than the original problem and can have medico-legal ramifications. “In making a dermatologic diagnosis, look for the distinctive face of the disease, not its featureless arms, legs and trunk.” ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 69
  • Question 1 of 3 What is the diagnosis? A. Inverse psoriasis B. Atopic dermatitis C. Mycosis fungoides D. Contact dermatitis I TCHY , ROUGH PATCHES ON LEGS A 41 year-old woman presents with a 6 month history of pruritic lesions affecting the popliteal fossae. She notices the lesions are more painful and itchy in the winter. She has tried some over the counter moisturizers that have only slightly helped. She had asthma and mild exzema as a child but is otherwise healthy and takes no medications. She has an older sister with a history of eczema. E. Nummular eczema Check Answer Diagnosis & Information 70
  • disease may have periods of complete remission, particularly in adolescence, and may then recur in early adult life. In the adult population, the rate of AD frequency is 1%, but onset may be delayed until adulthood. Persistent pruritus is the major symptom of AD and children often scratch themselves uncontrollably. Although pruritus may be present in the first few weeks of life, parents become more aware of the itch as the itch-scratch cycle matures when the patient is aged approximately 3 months. The disease typically has an intermittent course with flares and remissions occurring, often for unexplained reasons. Flares may be associated with seasonal changes (e.g. winter dry air), stress, activity, staphylococcal infection, or contact allergy. Diagnosis: Atopic dermatitis Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in early infancy (an adult-onset variant is also recognized). Pruritus, eczematous lesions, xerosis, and lichenification characterize this condition. AD may be associated with other atopic diseases (e.g. asthma, allergic rhinitis, urticaria, acute allergic reactions to foods). AD has significant morbidity, and the incidence and prevalence appear to be increasing. The prevalence rate for AD is 10-12% in children and 1% in adults. In addition, individuals of African or Asian background visit more frequently for AD than Caucasians. In 85% of cases, AD presents in the first year of life; in 95% of cases, it occurs before age 5 years. The incidence of AD is highest in early infancy and childhood. The Primary findings of AD include xerosis, lichenification, and eczematous lesions. Excoriations and crusting are common. The eczematous changes and its morphology are seen in different locations depending on the age of the patient. The following is a constellation of criteria commonly used for the diagnosis of AD: pruritus, eczematous changes that vary with age, chronic and relapsing course, early age of onset, atopy (IgE reactivity), xerosis, personal history of atopy, family history of atopic diseases in a first-degree relative, and onset younger than age 2 years. A firm diagnosis of AD depends on excluding conditions such as scabies, allergic contact dermatitis, seborrheic dermatitis, cutaneous lymphoma (mycosis fungoides), ichthyosis, psoriasis, immunodeficiency, and other primary disease entities. Patients with AD require frequent moisturization. Patients benefit from daily short (5-10 minutes) lukewarm baths to hydrate the skin. Adding emulsifying oils (e.g. Oilatum®) keeps the water on the skin and prevents evaporation to the outside environment. 71
  • After coming out of the bath, patients should pat dry with a towel (no rubbing), and within 2-3 minutes, apply a thick emollient (e.g. ceramide-based moisturizers, petroleum jelly) all over the body while damp, to seal in moisture. Topical steroids are currently the mainstay of medical treatment in AD. In association with moisturization, responses have been excellent. Initial therapy consists of 1-2.5% hydrocortisone applied od-bid to lesions on the face and in the folds, or if insufficient, the next level of potency such as desonide. A mid-strength topical steroid (e.g. betamethasone valerate (Betnovate®)) is applied odbid to lesions on the trunk until the eczematous lesions clear; sometimes more potent topical steroids are needed for chronic or severely inflamed lesions. Steroids are discontinued when lesions disappear and are resumed when new pruritic patches arise. Tacrolimus (Protopic®) is an immunomodulator that acts as a calcineurin inhibitor and is indicated for childen over 2 years of age. Tacrolimus is available in two strengths, 0.1% for adults and 0.03% for children. Tacrolimus is an ointment and is indicated for moderate-to-severe AD. A stinging sensation may occur following application in the acute setting, but this can be minimized by applying the medication on dry skin only. Pimecrolimus 1% (Elidel®) is also an immunomodulator and calcineurin inhibitor. Pimecrolimus is produced in a cream base for use twice a day. It is indicated for mild AD in persons older than 2 years and is particularly useful on the face. Along with benefits for use on thin areas of skin (face, axillae, groin), topical calcineurin inhibitors are also useful as maintenance therapy twice per week to prevent, delay and minimize flare-ups of atopic dermatitis. optimal combination of ceramides, cholesterol, and fatty acids that mimic those naturally found in the skin. EpiCeram® was approved by Health Canada in 2009 for use as a non-steroidal lipid barrier emulsion to manage burning and itching symptoms associated with dry skin conditions, such as AD. Studies have shown Epiceram® to have similar efficacy (though slower onset) to mid-strength topical corticosteroids in children with moderate to severe AD. Epiceram® has a favourable safety profile and does not appear to have substantial restrictions for use, such as treatment duration or patient age. Exacerbations of AD for which Staphylococcal infection should be suspected as a causative factor exhibit clinical signs such as crusting of lesions and/or erythema. For flares of AD in which these signs of infection are present, short-term use of a topical antibiotic such as fusidic acid (Fucidin®) or mupirocin (Bactroban®) is justified. A combination therapy with a topical antibiotic and topical steroid (e.g. fusidic acid and hydrocortisone acetate (Fucidin®-H)) may also be used. Other treatments for AD, which have shown possible effectiveness in studies to date, include probiotics, UV-A and UV-B phototherapy. In patients with severe disease, and particularly in adults, phototherapy, methotrexate, azathioprine (Imuran®), cyclosporine (Neoral®), and mycophenolate mofetil (CellCept®) have been used with success. Both hydroxyzine (Atarax®) and diphenhydramine hydrochloride (Benadryl®) provide a certain degree of relief from itching (especially at night), but are not effective without other treatments. Prescription ceramide-based moisturizers have been shown to be efficacious for patients with AD. These moisturizers consist of an 72
  • Clinical Pearls • Medicated creams and ointments can be made more soothing by compounding 1/4-1/2% menthol or camphor into them; best for chronic eczematous areas since acute areas with microscopic fissures will find these agents sting. • Medicated creams and ointments can also be made more soothing by placing them in the refrigerator 15 minutes before applying them. • Ointments have fewer ingredients and preservatives than creams or lotions and thus are better tolerated on acute eczematous areas. “If people are desperate, they will try anything. If they are angry, their anger can make them unreasonable. If they are depressed, nothing will seem to matter anyway. Unfortunately, these are the symptoms of chronic skin disease that are hardest to treat.” 
 ~ Irene A. Crosby, Board of Directors, National Eczema Association Support Community (EASE) 73
  • Question 1 of 3 What is your diagnosis? A. Squamous cell carcinoma B. Seborrheic keratoses C. Bowen disease S CALY LESIONS ON SCALP A 67 year-old Caucasian male presents with scaly and erythematous papules scattered throughout his scalp. The lesions are asymptomatic, but are increasing in number over time. Sam is a retired mailman, and takes a few medications which he can’t recall for his high blood pressure. Sam has never had skin problems or any history of skin cancer, but does state both his parents had some skin lesions on their faces treated. D. Actinic keratoses E. Porokeratosis Check Answer Diagnosis & Information 74
  • base, and can often be more easily palpated than visualized. They range from 3-8mm in diameter, and can gradually enlarge and thicken over time. If left untreated, over the course of many years, there is a very small risk that some of these lesions will develop into squamous cell carcinomas (SCCs). However, it is currently impossible to determine which AKs will progress to SCCs; therefore, all AKs should be treated. Diagnosis is made by clinical inspection and a high-level of clinical suspicion is relevant for patients with older age, excessive sun exposure, and fair skin type. No blood work or imaging is required. A biopsy of lesions with pronounced erythema, hyperkeratosis and induration is warranted to rule out an AK that has progressed to a SCC. Lesions not responding to typical therapy or those that are recurrent should also be sampled. Diagnosis: Actinic keratoses Actinic keratoses (AK) are the most common pre-cancer lesions in humans, most commonly found in individuals older than forty years of age, have Fitzpatrick skin type I or II – fair skinned, tan poorly and burn easily, and have had occupations or interests that resulted in significant sun exposure over many years. Patients will often also demonstrate a background of solar-damaged skin with telangiectases, blotchy colour, elastosis, and lentigines. Actinic keratoses are most commonly found on sun-exposed areas of the face, ears, forearms, and dorsum of the hands; however, they can be found anywhere that chronic sun exposure has taken place. They appear as rough, scaly lesions with an erythematous Prevention is the most important treatment modality for AKs. Effective measures include avoidance of excessive sun exposure, especially during peak day-time hours, avoidance of artificial sources of ultraviolet (UV) light such as tanning beds or prolonged UV treatments, wearing protective clothing, applying sunscreen with at least 30 SPF over sun-exposed areas a few times per day. The type of treatment of actinic keratoses depends on the number, location, and thickness of lesions. A small number of AKs can often be treated with several seconds of liquid nitrogen cryotherapy (Q-tip or canister). The actinic keratoses are irritated, may erode, ulcerate, or scab and slough off in the days following treatment. Cryotherapy treatments may need to be repeated for complete resolution of lesions. Often, semiannual or annual monitoring and treatment are advised. Thicker lesions can be removed by curettage or excision, although biopsy may be warranted. 75
  • Multiple AK lesions can be treated in several ways, depending on individual patient tolerance and acceptability (including acceptability of associated costs) of several modalities. Topical therapies such as imiquimod 3.75% (Zyclara™), imiquimod 5% (Aldara™), and 5-fluorouracil (Efudex®) can be used for treating an entire area (“Field Therapy”) since there is often microscopic, but widespread damage to the surrounding area, termed “subclinical lesions.” During the treatment phase, AKs become increasingly erythematous, and small subclinical lesions become highlighted. Field treatment can be temporarily uncomfortable and unsightly, with erythematous ulcerations and crust formation. However, if treatment is completed, the skin that previously had AKs usually heals within 2 weeks of discontinuing treatment, the complexion becomes smooth, and actinic keratoses disappear. Treatment will often need to be repeated periodically in subsequent years. Lesions not responding to treatment warrant a biopsy for further histopathological evaluation. Additional therapies of benefit for multiple actinic keratoses include photodynamic therapy, chemical peels (glycolic, trichloroacetic acid), topical retinoids, and less commonly dermabrasion and laser resurfacing. Clinical Pearls • Actinic keratoses are rough, pink scaly lesions, more easily felt than seen. Patients with these lesions should be educated that the sun damage that created these lesions was from many years ago, and that they are likely to develop new lesions in the future. • Predictable risk factors for AK and SCC include ultraviolet exposure, increasing age, male sex, and immunosuppression. • Two main approaches to treating AK are lesion-directed therapy, typically surgical or ablative methods targeted to one lesion, and field-directed therapy, typically topical drugs applied to multiple lesions or an entire area at risk. • Cryotherapy, the most common lesion-directed therapy, is very effective and reasonably well tolerated. • If extensive photodamage is evident, field-directed therapy should be considered given the strong likelihood of additional subclinical AKs present (Imiquimod, 5fluorouracil, and photodynamic therapy are highly effective field-directed therapies). “Young people need to know that they can significantly reduce their risk of getting skin cancer later if they start protecting their skin from the sun now.” ~ Dr. Jeffrey Koplan, Vice President Global Health, Emory University 76
  • Question 1 of 3 What is the most likely diagnosis? A. Atopic dermatitis B. Pityriasis rosea C. Guttate psoriasis D. Tinea corporis I TCHY RASH ON TRUNK An 11 year-old female presents with a 2 week history of an erythematous, mildly pruritic eruption with mild scaling, predominantly on the trunk, but with some additional lesions to her thighs. She is otherwise healthy and has had a normal childhood development. She does recall recently having the “sniffles.” She has a family history of eczema and diabetes. E. Nummular dermatitis Check Answer Diagnosis & Information 77
  • note a recent upper respiratory infection and lymphadenopathy. Additionally, a primary herald patch with subsequent development of a diffuse finely scaled rash is seen on the skin in 50-90% of cases a week or more before the onset of the eruption of smaller lesions. This secondary eruption occurs 2-21 days later, is generalized on the trunk, and often runs parallel to Langer’s skin lines, resulting in a “Christmas tree” pattern. Mild pruritus is common in the first few weeks of the rash. The diagnosis of PR is clinical, and laboratory tests are rarely indicated. If only a herald patch is evident, a potassium hydroxide (KOH) test searching for fungal etiology (e.g. tinea corporis) is reasonable. If the palms or soles are involved in a sexually active individual, testing for secondary syphilis is warranted (e.g. VDRL). A skin biopsy can also be helpful when the diagnosis is unclear. Diagnosis: Pityriasis rosea Pityriasis rosea (PR) is a benign and common skin disorder observed in otherwise healthy children and young adults. It presents as an acute, self-limiting, papulosquamous eruption with an average of 6- to 8-weeks duration (and up to 3-6 months). Lesions are salmon-coloured to erythematous and slightly scaly (“collarette of scale”). This is an idiopathic condition, although the strongest suggestion is for an infectious etiology. Most recently, there has been a suggested role for human herpes viruses, namely HHV-6 and HHV-7. Management of PR involves education and reassurance as this is a self-limited condition with minimal sequelae other than some temporary post-inflammatory hyperpigmentation. Patients with pruritus will benefit from symptomatic relief with calamine, menthol, pramoxine or oatmeal containing products. Oral antihistamines may be tried (e.g. diphenhydramine (Benadryl®) or hydroxyzine (Atarax®)). Additionally, mild to moderate potency topical steroids are helpful. The use of natural sunlight or UVB phototherapy can also be beneficial. Oral antiviral therapy (e.g. acyclovir) used for one to two weeks immediately after the initial rash development, may hasten its resolution. Clinical history reveals a small number of patients with prodromal symptoms such as fatigue, nausea, or arthralgias. Patients may 78
  • Clinical Pearl • Where you would normally see scaling in lighter skin types, you may conversely see papules in darker skin; this clinical variant is known as “papular pityriasis rosea.” “The diagnosis of pruritus should arouse an itch in you to find the cause.”
 ~ Drs. Walter & Dorinda Shelley, American Dermatologists and authors of Advanced Dermatologic Diagnosis 79
  • Dermatology is a highly visual field within medicine, and recognition of visual cues and patterns, in conjunction with the clinical patient history, direct the practitioner to the correct diagnosis. The 25 dermatology cases presented, with colour photographs, are common and important clinical concerns of patients that include skin cancers, skin infections, inflammatory and immunologic skin conditions, as well as benign lesions. Rapid Fire Dermatology is a unique book, tailored to the Canadian marketplace and including up-to-date, comprehensive information regarding dermatological diagnosis, as well as specific medication and treatment recommendations. At the end of each case presentation, a “Clinical Pearls” section gives informative tips related to diagnosis and treatment. Rapid Fire Dermatology is an excellent resource for Canadian physicians, medical residents and students. “Drs. Barankin and Kurian have put together the perfect pocket summary of the most common dermatologic conditions that a family physician, pediatrician, or nurse practitioner will see on a regular basis. Not only does the small book literally fit easily within a typical white coat pocket, it uses case presentations and Q&A format that allow for the rapid assimilation of the crucial information needed to make a definitive diagnosis, initiate appropriate therapy, or recognize when a referral to a dermatologist is warranted. This book is the ideal entry level text to help demystify the confusing world of dermatology to the primary care physician and other healthcare providers.” — Dr. Thomas G. Salopek, Dermatologist, Director, Associate Professor, Division of Dermatology & Cutaneous Sciences at University of Alberta, Edmonton, AB Canada
  • Actinic keratoses Actinic keratoses (AK) are the most common pre-cancer lesions in humans, most commonly found in individuals older than forty years of age, have Fitzpatrick skin type I or II – fair skinned, tan poorly and burn easily, and have had occupations or interests that resulted in significant sun exposure over many years. Patients will often also demonstrate a background of solar-damaged skin with telangiectases, blotchy colour, elastosis, and lentigines. Related Glossary Terms Drag related terms here Index Find Term
  • Allergic contact dermatitis Allergic contact dermatitis (ACD) is a delayed type of induced sensitivity that occurs in individuals that have been previously sensitized to any of more than 3,000 chemicals, and is more likely in genetically predisposed individuals. The allergic reaction causes inflammation of the skin that is manifested by varying degrees of erythema, edema, and vesiculation. A reaction typically develops within 24-48hrs of a subsequent exposure, although it can occur up to 7 days later; it typically resolves after 2-3 weeks. The term “contact dermatitis” sometimes is used incorrectly as a synonym for ACD. Contact dermatitis is inflammation of the skin induced by chemicals that directly damage the skin (also known as “irritant contact dermatitis”) as opposed to a specific sensitivity, in the case of ACD. Related Glossary Terms Drag related terms here Index Find Term Section 7 - Itchy bumps to lower abdomen
  • Alopecia areata Alopecia areata (AA) is a non-scarring autoimmune condition that most commonly presents in young adulthood. AA, which affects men and women equally, affects 1.5-2% of the general population at some point in their lives. Most people with AA are healthy individuals, though they do have a higher risk of atopy, and autoimmune conditions such as thyroid disease and vitiligo; family members may have autoimmune conditions such as insulin-dependent diabetes, rheumatoid arthritis, thyroid disease or systemic lupus erythematosus. Related Glossary Terms Drag related terms here Index Find Term Section 11 - Round, bald patches on scalp
  • Atopic dermatitis Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in early infancy (an adult-onset variant is also recognized). Pruritus, eczematous lesions, xerosis, and lichenification characterize this condition. AD may be associated with other atopic diseases (e.g. asthma, allergic rhinitis, urticaria, acute allergic reactions to foods). AD has significant morbidity, and the incidence and prevalence appear to be increasing. The prevalence rate for AD is 10-12% in children and 1% in adults. In addition, individuals of African or Asian background visit more frequently for AD than Caucasians. In 85% of cases, AD presents in the first year of life; in 95% of cases, it occurs before age 5 years. The incidence of AD is highest in early infancy and childhood. The disease may have periods of complete remission, particularly in adolescence, and may then recur in early adult life. In the adult population, the rate of AD frequency is 1%, but onset may be delayed until adulthood. Related Glossary Terms Drag related terms here Index Find Term Section 23 - Itchy, rough patches on legs
  • Basal cell carcinoma (BCC) This is the most common malignancy in humans, typically appearing on sun-exposed skin. BCCs can result in significant local destruction and even disfigurement, especially if located around the nose or eyes. They rarely metastasize (<0.1%). In Caucasians, there is approximately 25-35% lifetime risk of developing a BCC. These lesions are uncommon in dark skin types. Likelihood of BCCs increases with age, and they are considered uncommon under 35 years of age. Related Glossary Terms Drag related terms here Index Find Term Section 5 - Chronic erythematous facial papule
  • Becker’s nevus A Becker’s nevus is an organoid nevus with hamartomatous elements, not a melanocytic nevus, predominantly affecting males. The nevus typically first appears as an irregular pigmentation (hyperpigmentation) on the torso or upper arm (though other areas of the body can be affected), and gradually enlarges irregularly, becoming thickened and often with hypertrichosis. Related Glossary Terms Drag related terms here Index Find Term Section 10 - Large brown hairy patch
  • Bullous impetigo Impetigo is a superficial skin infection encountered most frequently among children. It typically presents with multiple vesicular lesions on an erythematous base, which eventually crust over. There are 2 types: nonbullous and bullous. Both forms involve only the most superficial layers of the skin. Related Glossary Terms Drag related terms here Index Find Term Section 1 - Thigh rash with crusty lesions
  • Digital mucous cyst Digital mucous cysts (DMCs) are benign and often asymptomatic ganglion cysts of the digits, typically located at the distal interphalangeal (DIP) joints or at the proximal nail fold. The etiology is uncertain, although it may relate to mucoid degeneration of connective tissue; this process seems to involve communication with the adjacent DIP joint and often is associated with osteoarthritis, and less commonly with antecedent trauma. Related Glossary Terms Drag related terms here Index Find Term Section 8 - Uncomfortable finger lesion
  • Epidermoid cyst Epidermoid cysts form as a result of the growth of epidermal cells within a focal area of the dermis. The material inside the cysts is chemotactic for neutrophils and can result in inflammation. Most epidermoid cysts do not cause any problems and grow rather slowly. However, cysts can become inflamed and less commonly infected which results in redness, tenderness and pain, due to trauma or other factors. Epidermoid cysts are more common in men during the young adulthood years but may be noted at any age. Related Glossary Terms Drag related terms here Index Find Term Section 3 - Slow growing back lump
  • Granuloma annulare Granuloma annulare (GA) is a benign, inflammatory skin condition of dermal papules and annular plaques commonly affecting acral sites. GA occurs most commonly in women and in younger individuals (typically less than 30 years old). There are several clinical variants, including: localized GA (most common, especially in children & young adults), generalized GA (10%), subcutaneous GA, perforating GA (5%), and arcuate dermal erythema. Localized GA typically manifests as groups of small erythematous to brown papules, often in an annular arrangement (raised border, central clearing) over distal extremities, especially the hands, feet, and extensor limbs. Related Glossary Terms Drag related terms here Index Find Term Section 2 - Reddish-brown lesions on dorsal hand
  • Herpes simplex Herpes simplex virus (HSV) is a DNA virus presenting as grouped vesicles on an erythematous base. Typically infections will be recurrent in the same location. While oral herpes labialis is usually caused by HSV-1, genital involvement is more commonly due to HSV-2, although we now see both strains in both locations. Transmission occurs when an actively shedding individual (with clinical lesions or not) contacts mucous membranes which may be open or abraded. The virus then travels to sensory dorsal root ganglion where latency is established. Various stimuli can elicit outbreaks, including: trauma, fever, stress, hormonal fluctuations, and immunosuppression (e.g. from UV radiation). An eruption of tiny vesicles appears on the skin or on the mucous membranes, such as those lining the eyes, vagina, cervix, or inside of the mouth. The skin around the blisters is often red. Related Glossary Terms Drag related terms here Index Find Term Section 12 - Sores at corner of mouth
  • Herpes zoster Herpes zoster (shingles) is an acute, painful dermatomal dermatitis that affects approximately 10% to 20% of adults, often in the presence of immunosuppression. Herpes zoster is a viral infection caused by the same virus (varicella) that causes chicken pox. During the course of varicella, the virus travels from the skin and mucosal surfaces to the sensory ganglia, where it lies dormant for a patient’s lifetime. Reactivation often follows immunosuppression, illness, emotional stress, trauma, and irradiation or surgical manipulation of the spine, producing a dermatomal dermatitis. Related Glossary Terms Drag related terms here Index Find Term Section 22 - Painful, vesicular rash
  • Keratoacanthoma (KA) A keratoacanthoma (KA) is a common, low-grade tumor that can clinically resemble a squamous cell carcinoma. Some experts believe KA to be a variant of squamous cell carcinoma, and thus suggest similar treatment. A keratoacanthoma is characterized by its rapid growth velocity (over weeks to months). There is often a solitary, firm skin to redcoloured papule with a central crateriform keratin plug (“volcano” appearance). Etiologic factors for this tumor are multifold, including: ultraviolet radiation, immunosuppression, smoking, human papilloma virus, tar or pitch exposure, trauma, and genetic factors. Related Glossary Terms Drag related terms here Index Find Term Section 13 - Rapidly evolving hand plaque
  • Lichen planus Lichen planus (LP) is a pruritic papulosquamous disease of planar, polygonal, and purple/ violaceous papules (5 P’s). Common sites of involvement include the flexor surfaces of the arms and wrists, shins, ankles, genitalia, and oral mucosa (lacy white “Wickham striae”). There is no gender or racial predilection, and while LP can occur at any age, those age 30-60 years-old are most commonly afflicted. Several clinical subtypes have been observed: hypertrophic, atrophic, erosive, follicular, annular, linear, vesiculobullous, lichen planus pemphigoides, and actinic. The diagnosis of LP is often clinical, although histopathology may be required to confirm the diagnosis. Related Glossary Terms Drag related terms here Index Find Term Section 14 - Itchy papules on wrists
  • Melanoma Melanoma is a skin cancer of pigment-producing melanocytes that typically affects the skin, and less commonly the mucosae, eyes, leptomeninges and gastrointestinal tract. It account for approximately 5% of skin cancers, but 75% of deaths from skin cancer. It is believed that two-thirds of melanomas arise de novo, while one-third develop from pre-existing nevi. In Canada, approximately 5,000 people are diagnosed with melanoma each year, and approximately 950 will die of the disease. Detection and treatment in early stages provides the best opportunity for cure. Related Glossary Terms Drag related terms here Index Find Term Section 9 - Dark spot on cheek
  • Melasma Melasma is a common hypermelanosis that typically occurs on sun-exposed areas of the face. Melasma is characterized by symmetrically distributed macules with irregular borders ranging from light brown to dark brown to gray-brown. Common clinically distinct distributions include centrofacial (forehead, nose, chin, upper lip), malar (cheeks), and mandibular (lower jaw). Forearms are also occasionally affected. Pigmentation typically slowly evolves over many weeks or months. Related Glossary Terms Drag related terms here Index Find Term Section 6 - Dark patches on cheeks
  • Molluscum contagiosum Molluscum contagiosum (MC) is a viral infection of the skin caused by a DNA poxvirus called the molluscum contagiosum virus (MCV), which is a benign and generally self-limited viral infection. Skin lesions typically consist of multiple dome-shaped, pink to skin-colored papules 2-6 mm in diameter of which some lesions show the classic feature of umbilication. MC is usually asymptomatic, although individual lesions can occasionally be tender or pruritic. Related Glossary Terms Drag related terms here Index Find Term Section 21 - Papules on the abdomen
  • Onychomycosis Onychomycosis is a fungal infection that most commonly affects the toenails. It can affect any component of the nail unit, including the nail matrix, nail bed, or nail plate. The majority of the time, the concern is primarily cosmetic in nature, but occasionally, there can also be discomfort and pain. Related Glossary Terms Drag related terms here Index Find Term Section 18 - Thick, yellow toenails
  • Pityriasis rosea Pityriasis rosea (PR) is a benign and common skin disorder observed in otherwise healthy children and young adults. It presents as an acute, self-limiting, papulosquamous eruption with an average of 6- to 8-weeks duration (and up to 3-6 months). Lesions are salmoncoloured to erythematous and slightly scaly (“collarette of scale”). This is an idiopathic condition, although the strongest suggestion is for an infectious etiology. Most recently, there has been a suggested role for human herpes viruses, namely HHV-6 and HHV-7. Related Glossary Terms Drag related terms here Index Find Term Section 25 - Itchy rash on trunk
  • Psoriasis vulgaris Psoriasis is a chronic, recurring inflammatory disease that can affect the skin, scalp, nails and joints. The typical lesions are pruritic, erythematous, and present as well-demarcated papules and plaques with silvery-white scales. Psoriasis affects about 2% of the population and ranges in severity from mild to severe; patients with moderate to severe disease can experience a significant impact on quality of life. It affects men and women equally. The age of onset of psoriasis follows a bimodal distribution (peaks between ages 20 to 30 years and again between the ages of 50 to 60). Both genetic and environmental factors have been implicated in the pathophysiology of psoriasis. Related Glossary Terms Drag related terms here Index Find Term Section 15 - Scaly, erythematous rash on elbows
  • Scalp psoriasis Psoriasis affects approximately 2% of the population, and in 50-80 percent of cases, the scalp is affected. Scalp involvement may occur in isolation, with plaque psoriasis located elsewhere (most common), or with erythrodermic, pustular or guttate psoriasis, and/or psoriatic arthritis. In 25-50 percent of affected patients, psoriasis presents initially on the scalp. Family history may predispose patients to scalp psoriasis. Related Glossary Terms Drag related terms here Index Find Term Section 19 - Scaly, erythematous plaques on head
  • Squamous cell carcinoma (SCC) Squamous cell carcinoma is currently the second most common skin cancer in Caucasians, and the most common type in black individuals. SCC can develop in the setting of actinic keratoses, leukoplakia, lichen sclerosus, radiation dermatitis, chronic arsenic exposure, scars, burns, chronic ulcers or sinuses (e.g. hidradenitis suppurativa). Related Glossary Terms Drag related terms here Index Find Term Section 20 - Large scaly scalp plaque
  • Syringomas Syringomas, considered benign adnexal tumors, are fairly common lesions more commonly affecting females, and predominantly of cosmetic concern. Lesions typically first appear around the time of puberty. Related Glossary Terms Drag related terms here Index Find Term Section 16 - Periocular papules
  • Verruca vulgaris (Warts) Cutaneous warts, one of the most common skin diseases, are a frequent presenting complaint to family practice and dermatology clinics. Warts are benign proliferations of skin and mucosa confined to the epithelium caused by one of the more than 150 types of the double-stranded DNA human papilloma virus (HPV). Common, plantar and flat warts are cutaneous manifestations of the human papillomavirus (HPV). Certain HPV types tend to occur at particular anatomic sites; however, warts of any HPV type may occur at any site. Clinically, HPV manifests itself as either: common warts, flat warts, genital warts, or palmoplantar warts. Related Glossary Terms Drag related terms here Index Find Term Section 17 - Finger papules
  • Vitiligo Vitiligo is an acquired, benign, depigmentation of the skin caused by destruction of melanocytes in skin and hair, resulting in white macules and patches. It affects 1-2% of the population with an equal gender distribution and most commonly onsets between 10-30 years of age. The etiology of vitiligo has not been fully elucidated, but the pathogenesis is multifactorial, likely having both genetic and autoimmune mechanisms. Melanocytes are destroyed in the skin and those in hair follicles can also be affected resulting in white hair. Vitiligo has been associated with other autoimmune conditions such as: pernicious anemia, alopecia areata, diabetes mellitus, Addison’s disease, and thyroid disease. Related Glossary Terms Drag related terms here Index Find Term Section 4 - White patch over knee