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ORIGINAL ARTICLE a Clinical and Histopathological Study of Lichenoid Eruption of Skin in Two Tertiary Care Hospitals of Dhaka
ORIGINAL ARTICLE A Clinical and Histopathological study of Lichenoid Eruption of Skin in Two Tertiary Care Hospitals of Dhaka. Khaled A1, Banu SG 2, Kamal M 3, Manzoor J 4, Nasir TA 5 Introduction studies from other countries. Skin diseases manifested by lichenoid eruption, With this background, this present study was is common in our country. Patients usually undertaken to know the clinical and attend the skin disease clinic in advanced stage histopathological pattern of lichenoid eruption, of disease because of improper treatment due to age and sex distribution of the diseases and to difficulties in differentiation of myriads of well assess the clinical diagnostic accuracy by established diseases which present as lichenoid histopathology. eruption. When we call a clinical eruption lichenoid, we Materials and Method usually mean it resembles lichen planus1, the A total of 134 cases were included in this study prototype of this group of disease. The term and these cases were collected from lichenoid used clinically to describe a flat Bangabandhu Sheikh Mujib Medical University topped, shiny papular eruption resembling 2 (Jan 2003 to Feb 2005) and Apollo Hospitals lichen planus. Histopathologically these Dhaka (Oct 2006 to May 2008), both of these are diseases show lichenoid tissue reaction. The large tertiary care hospitals in Dhaka. Biopsy lichenoid tissue reaction is characterized by specimen from patients of all age group having epidermal basal cell damage that is intimately lichenoid eruption was included in this study. associated with massive infiltration of T cells in 3 Detailed clinical history including age, sex, upper dermis. distribution of lesions, presence of itching, The spectrum of clinical diseases related to exacerbating factors, drug history, family history lichenoid tissue reaction is wider and usually and any systemic manifestation were noted. -
Immunologic Adverse Reactions of Β-Blockers and the Skin (Review)
EXPERIMENTAL AND THERAPEUTIC MEDICINE 18: 955-959, 2019 Immunologic adverse reactions of β-blockers and the skin (Review) ALIN LAURENTIU TATU1, ALINA MIHAELA ELISEI1, VALENTIN CHIONCEL2, MAGDALENA MIULESCU3 and LAWRENCE CHUKWUDI NWABUDIKE4 1Medical and Pharmaceutical Research Unit/Competitive, Interdisciplinary Research Integrated Platform ‘Dunărea de Jos’, ReForm-UDJG; Research Centre in the Field of Medical and Pharmaceutical Sciences, Faculty of Medicine and Pharmacy, Department of Pharmaceutical Sciences, ‘Dunărea de Jos’ University of Galați, 800010 Galati; 2Department of Cardio-Thoracic Pathology, Faculty of Medicine, ‘Carol Davila’ University of Medicine and Phamacy, 050474 Bucharest; 3Department of Morphological and Functional Sciences, Faculty of Medicine and Pharmacy, ‘Dunarea de Jos University’ of Galati, 800010 Galati; 4Department of Diabetic Foot Care, ‘Prof. N. Paulescu’ National Institute of Diabetes, 011233 Bucharest, Romania Received September 11, 2018; Accepted November 16, 2018 DOI: 10.3892/etm.2019.7504 Abstract. β-Blockers are a widely utilised class of medica- use, as well as possible therapeutic approaches to these. This tion. They have been in use for a variety of systemic disorders short review will focus on those dermatoses resulting from including hypertension, heart failure and intention tremors. β-blocker use, which have an immunologic basis. Their use in dermatology has garnered growing interest with the discovery of their therapeutic effects in the treatment of haemangiomas, their potential positive effects in wound Contents healing, Kaposi sarcoma, melanoma and pyogenic granuloma, and, more recently, pemphigus. Since β-blockers are deployed 1. Introduction in a variety of disorders, which have cutaneous co-morbidities 2. Cutaneous side - effects of β-blockers such as psoriasis, their pertinence to dermatologists cannot be 3. -
Blistering, Papulosquamous, Connective Tissue and Alopecia Kathleen Haycraft, DNP, FNP/PNP-BC, DCNP, FAANP Objectives
Blistering, Papulosquamous, Connective Tissue and Alopecia Kathleen Haycraft, DNP, FNP/PNP-BC, DCNP, FAANP Objectives • Identify examples of papulosquamous disease and state treatment options • Identify examples of connective tissue disease and state treatment options • Identify examples of blistering diseases and state treatment options • Identify examples of alopecia and state treatment options Papulosquamous Psoriasis • Latin means “itchy plaque”. • In truth it is less itchy than yeast and eczema • Variable • Painful in high friction spots Psoriasis Plaque ©kathleenhaycraft Psoriasis ©kathleen haycraft ©kathleenhaycraft The clue to the vaginal pic ©kathleenhaycraft ©kathleenhaycraft Plantar Psoriasis ©kathleenhaycraft Palmar Psoriasis ©kathleenhaycraft Nivolumab induced Psoriasis ©[email protected] Psoriasis and its many forms • Plaque..85% • Scalp • Palmoplantar • Guttate • Inverse • Erythrodermic • Psoriatic arthritis • Psoriatic nails Cause • Affects 2 to 5% of the population • Many mediators including the T cell lymphocyte. • Many chemicals downstream including TNF alpha, PDE, Il 12, 23, 17 as well as a variety of inflammatory cytokines • These chemicals are distributed throughout the body • Imbalance between pro inflammatory and anti-inflammatory chemicals • Can be triggered by strep, HIV, Hepatitis, and a wide variety of infectious organisms Psoriasis causes • Koebner phenomenon after surgery or trauma • Drugs such as beta blockers, lithium, antimalarials • The cytokines result in proliferation of keratinocytes and angiogenesis (resulting in the Auspitz sign) • May be mild to severe and location of scalp, genitalia, face may trump degree of psoriasis (BSA- Comorbidities • Reviewed in the cutaneous manifestations of systemic disease • Range from depression to MI, psoriatic arthritis, malignancy, Dm • Future treatments may be based on how they treat the comorbids • Diagnose with visual or biopsy Treatment • Topical corticosteroids..caution to not over use particularly in high risk areas. -
Imatinib-Induced Lichenoid Eruption: a Case Report and a Review of Literature
Vol.33 No.4 Case report 329 Imatinib-induced lichenoid eruption: A case report and a review of literature. Thiraphong Mekwilaiphan MD, Natta Rajatanavin MD. ABSTRACT: MEKWILAIPHAN T, RAJATANAVIN N. IMATINIB-INDUCED LICHENOID ERUPTION: A CASE REPORT AND A REVIEW OF LITERATURE. THAI J DERMATOL 2017;33: 329-335. DIVISION OF DERMATOLOGY, DEPARTMENT OF MEDICINE, FACULTY OF MEDICINE, RAMATHIBODI HOSPITAL, MAHIDOL UNIVERSITY, BANGKOK, THAILAND. Imatinib is the first generation tyrosine kinase inhibitor which consisted of bcr-abl, c-kit, and platelet-derived growth factor receptors (PDGFRs). Its tolerability in the treatment of malignancies is higher than the conventional chemotherapy. However, various adverse cutaneous reactions are the most common side effect of imatinib. Nevertheless, lichenoid eruption is an uncommon cutaneous reaction from imatinib. The clinical manifestation is violaceous, flat-topped papules or plaques involving mainly trunk and extremities. Oral and genital mucosal involvement is a distinctive feature. There were no specific histopathological findings, but usually not a typical characteristic of lichen planus. Due to high prevalence of cutaneous rash, the pathogenesis may be related to pharmacological effect than hypersensitivity reaction. Dosage decrement of imatinib is a choice of treatment, or switch to the second or third generation tyrosine kinase inhibitors. Acitretin was successfully used to treat imatinib-induced lichenoid eruption in our patient and enabling the continuation of the high imatinib dosage for her hematologic malignancy. Key words: Imatinib, lichenoid eruption, tyrosine kinase inhibitor From: Division of Dermatology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University Corresponding author: Thiraphong Mekwilaiphan MD., email: [email protected] 330 Mekwilaiphan T et al Thai J Dermatol, October-December, 2017 บทคัดยอ: ธีรพงษ เมฆวิไลพันธุ, ณัฏฐา รัชตะนาวิน รายงานการเกิดผื่นชนิดไลเคนนอยด ในผูปวยที่ไดรับยาอิมมาทินิบ และ การทบทวนวรรณกรรม วารสารโรคผิวหนัง 2560; 33: 329-335. -
History of Psoriasis and Parapsoriasis
History of Psoriasis and Parapsoriasis By Karl Holubar Summary Parapsoriasis is «oï a disease entity. Jt is an auxiliary term introduced in J 902 to group several dermatoses w>itk a/aint similarity to psoriasis. Tlie liistorical development leading to tlie creation o/ t/ie term parapsoriasis is outlined and t/te Itistory o/psoriasis is 6rie/ly reviewed. Semantic and terminological considerations Obviously, para-psoriasis as a term has been created in analogy to psoriasis. We should remember similar neologisms in medical language, e. g. protein and para-protein; typhoid and para-typhoid, thyroid and para-thyroid, phimosis and para-phimosis, eventually, pemphigus and para-pemphigus (the latter in 1955 this term was to be employed instead of pemphigoid but was not accepted by the dermatological world). Literally, para is a Greek preposition, (with the genitive, dative and accusative), meaning: by the side of, next to something, alongside something. In medicine, para is used often as a prefix to another term, which designates a condition somewhat similar to the one under consideration. The same holds for psoriasis and parapsoria- sis. In detail, though, it is a bit more complicated. Parapsoriasis has more than one "/at/ier", three in fact: ideiurick /Iu.spitz f 1835—1886,), Paul Gerson Luna (A850—1929j and Louis Procç fI856—I928J. Auspitz, in 1881, had published a new system of skin diseases the seventh class of which was called epidermidoses, subdivided into liypcrlcfiratose.s, parakeratoses, kerato/y- ses, the characteristics of which were excessive keratinization, abnormal keratinization and insufficent keratinization. When Unna, in 1890®, pub- lished his two reports on what he called parakeratosis variegata, he referred to Auspitz' system and term when coining his own. -
Dermatological Indications of Disease - Part II This Patient on Dialysis Is Showing: A
“Cutaneous Manifestations of Disease” ACOI - Las Vegas FR Darrow, DO, MACOI Burrell College of Osteopathic Medicine This 56 year old man has a history of headaches, jaw claudication and recent onset of blindness in his left eye. Sed rate is 110. He has: A. Ergot poisoning. B. Cholesterol emboli. C. Temporal arteritis. D. Scleroderma. E. Mucormycosis. Varicella associated. GCA complex = Cranial arteritis; Aortic arch syndrome; Fever/wasting syndrome (FUO); Polymyalgia rheumatica. This patient missed his vaccine due at age: A. 45 B. 50 C. 55 D. 60 E. 65 He must see a (an): A. neurologist. B. opthalmologist. C. cardiologist. D. gastroenterologist. E. surgeon. Medscape This 60 y/o male patient would most likely have which of the following as a pathogen? A. Pseudomonas B. Group B streptococcus* C. Listeria D. Pneumococcus E. Staphylococcus epidermidis This skin condition, erysipelas, may rarely lead to septicemia, thrombophlebitis, septic arthritis, osteomyelitis, and endocarditis. Involves the lymphatics with scarring and chronic lymphedema. *more likely pyogenes/beta hemolytic Streptococcus This patient is susceptible to: A. psoriasis. B. rheumatic fever. C. vasculitis. D. Celiac disease E. membranoproliferative glomerulonephritis. Also susceptible to PSGN and scarlet fever and reactive arthritis. Culture if MRSA suspected. This patient has antithyroid antibodies. This is: • A. alopecia areata. • B. psoriasis. • C. tinea. • D. lichen planus. • E. syphilis. Search for Hashimoto’s or Addison’s or other B8, Q2, Q3, DRB1, DR3, DR4, DR8 diseases. This patient who works in the electronics industry presents with paresthesias, abdominal pain, fingernail changes, and the below findings. He may well have poisoning from : A. lead. B. -
The Lichenoid Reaction Pattern M Ramaml, Asha Kubba'?
The lichenoid reaction Pattern M Ramaml, Asha Kubba'? Sri Lanka lournal of Dermatology, 2002, 6,20-26 There is some confusion about the origin of the It is easier to bring these diverse conditions term lichen to describe skin diseases but it appears to together based on the histopathological appearance. characteristic of lichenoid have been a popular name for many conditions. An Histologically, the defining cell damage2-3. The damage impressive list of dermatoses that begin with the term tissue reactions is basal or liquefactive degeneration, Iichen or lichenoid could be colled from the index of a occurs by apoptosis processes that appear to be mediated by different major textbook (Table 1)1. It is difficult to conceive of a pathogenetic mechanisms. Apoptosis, a special type way to unify atl these conditions but there are some of single cell death, consists of the condensation features that some of these diseases share. These fea- of single cells followed by active budding and tures are also shared by diseases that do not have fragmentationa. Unlike necrosis, cell membranes and lichen in their names. Briefly, the common clinical organelles remain intact till late in the apoptosis. On denominator is the presence of small papules, purple light microscopy, apoPtotic keratinocytes appear as and histologically, damage to the or skin coloured, pink, shrunken globules (known as Civatte bodies) basal keratinocytes. which may show pyknotic nuclear remnants. The Civatte bodies may be phagocytosed by other keratinocytes and macrophages or may drop down into the papillary dermis as colloid bodies. Liquefac- Table 1. tive degeneration leads to keratinocyte damage by the Lichen amyloidosus accumulation of fluid within basal cells. -
Desensitization to Hydroxychloroquine: Alternative Interpretations
Editorial Desensitization to Hydroxychloroquine: Alternative Interpretations Considering the increasingly important role of the amino- Psoriasis (exacerbation) quinoline antimalarials (AA) in the management of systemic Pustular eruption lupus erythematosus (SLE) and rheumatoid arthritis (RA), Rash [sic] Mates and coworkers are to be congratulated for addressing Stevens-Johnson syndrome an important clinical issue in the management of antimalar- Toxic epidermal necrolysis ial cutaneous adverse reactions1. However, their report rais- Urticaria es several important issues not commented upon by these Vasculitis investigators. We wish to offer an alternative interpretation to the results of their proposed desensitization protocol and An exanthem is the most commonly noted cutaneous provide a broader perspective on clinical issues related to adverse reaction pattern to all drugs, ranging between 51% AA cutaneous adverse drug reactions. and 95% in various series5,6; it is also the most common A pruritic maculopapular eruption that was presumably cutaneous adverse reaction to AA7. symmetrically distributed on the trunk and extremities Other than the suggestion that hydroxychloroquine- occurring 1–2 weeks after starting hydroxychloroquine (pre- induced exanthems might be more common in dermato- sumably hydroxychloroquine sulfate; HCQ) was reported in myositis than in other disease settings7, drug-induced exan- all 4 cases described by Mates, et al. Although skin biopsy thems produced by AA are not significantly different in results were not presented, this pattern of cutaneous hyper- clinical features or prognosis from drug-induced exanthems sensitivity would appear to be best classified as a simple produced by a host of other more commonly employed drug-induced exanthem (synonymous with exanthematous agents including antibiotics, anticonvulsants, antiinflamma- drug rash/eruption, maculopapular drug rash/eruption, mor- tories, and allopurinol. -
Differential Diagnosis in Dermatology
Differential Diagnosis in Dermatology ZohrehTehranchi Dermatologist COMMON ACNE AND CYSTIC ACNE Rosacea Rosacea PERIORAL DERMATITIS ECZEMA/DERMATITIS Chronic irritant dermatitis Dyshidrotic eczematous dermatitis Childood atopic dermatitis Autosensitization dermatitis (“id” reaction): dermatophytid Seborrheic dermatitis PSORIASIS VULGARIS Pemphigus vulgaris BULLOUS PEMPHIGOID (BP) Pityriasis rosea small-plaque parapsoriasis Large-plaque parapsoriasis (parapsoriasis en plaques) LICHEN PLANUS (LP) GRANULOMA ANNULARE (GA) Erythema multiforme ERYTHEMA NODOSUM Actinic keratoses Bowen disease (Squamous cell carcinoma in situ) Bowen disease and invasive SCC Squamous cell carcinoma: invasive on the lip Squamous cell carcinoma, well differentiated Squamous cell carcinoma, undifferentiated Squamous cell carcinoma, advanced, well differentiated, on the hand Keratoacanthoma showing different stages of evolution BASAL CELL CARCINOMA (BCC) Basal cell carcinoma, ulcerated: Rodent ulcer A large rodent ulcer in the nuchal and Bas cell calarcinoma: sclerosing type retroauricular area extending to the temple Basal cell carcinoma, sclerosing, nodular, Superficial basal cell carcinoma: solitary lesion and multiple lesions Superficial basal cell carcinoma, invasive Basal cell carcinoma, pigmented Dysplastic nevi Superficial spreading melanoma: arising within a dysplastic nevus Congenital nevomelanocytic nevus Melanoma: arising in small CNMN Melanoma in situ: lentigo maligna Melanoma in situ, superficial spreading type Superficial spreading melanoma, vertical -
Papular Pityriasis Rosea
Continuing Medical Education Papular Pityriasis Rosea 2nd Lt Ronald M. Bernardin, MSC, USAF; Maj Steven E. Ritter, MC, FS, USAF; Lt Col Michael R. Murchland, MC, FS, USAF GOAL To describe a case of papular pityriasis rosea (PR) OBJECTIVES Upon completion of this activity, dermatologists and general practitioners should be able to: 1. Outline the varying clinical presentations of PR. 2. Discuss the theoretical etiologies of PR. 3. Describe therapy for PR. CME Test on page 48. This article has been peer reviewed and Medicine is accredited by the ACCME to provide approved by Michael Fisher, MD, Professor of continuing medical education for physicians. Medicine, Albert Einstein College of Medicine. Albert Einstein College of Medicine designates Review date: June 2002. this educational activity for a maximum of 1.0 hour This activity has been planned and implemented in category 1 credit toward the AMA Physician’s in accordance with the Essential Areas and Policies Recognition Award. Each physician should claim of the Accreditation Council for Continuing Medical only those hours of credit that he/she actually spent Education through the joint sponsorship of Albert in the educational activity. Einstein College of Medicine and Quadrant This activity has been planned and produced in HealthCom, Inc. The Albert Einstein College of accordance with ACCME Essentials. Pityriasis rosea (PR) is a seasonal papulosqua- and treatment options. Papular PR is atypical, pre- mous disorder that can be easily confused with a senting in a minority of patients, and may pose a wide variety of similar appearing cutaneous disor- diagnostic challenge. Being familiar with these ders. -
Pediatric Psoriasis
Pediatric Papulosquamous and Eczematous Disorders St. John’s Episcopal Hospital Program Director- Dr. Suzanne Sirota-Rozenberg Dr. Brett Dolgin, DO Dr. Asma Ahmed, DO Dr. Anna Slobodskya, DO Dr. Stephanie Lasky, DO Dr. Louis Siegel, DO Dr. Evelyn Gordon, DO Dr. Vanita Chand, DO Pediatric Psoriasis Epidemiology • Psoriasis can first appear at any age, from infancy to the eighth decade of life • The prevalence of psoriasis in children ages 0 to 18 years old is 1% with an incidence of 40.8 per 100,000 ppl • ~ 75% have onset before 40 years of age What causes psoriasis? • Multifactorial • Genetics – HLA associations (Cw6, B13, B17, B57, B27, DR7) • Abnormal T cell activation – Th1, Th17 with increased cytokines IL 1, 2, 12, 17, 23, IFN-gamma, TNF-alpha • External triggers: – Injury (Koebner phenomenon) – medications (lithium, IFNs, β-blockers, antimalarials, rapid taper of systemic corticosteroids) – infections (particularly streptococcal tonsillitis). Pediatric Psoriasis Types: • Acute Guttate Psoriasis – Small erythematous plaques occurring after infection (MOST common in children) • 40% of patients with guttate psoriasis will progress to develop plaque type psoriasis • Chronic plaque Psoriasis – erythematous plaques with scaling • Flexural Psoriasis – Erythematous areas between skin folds • Scalp Psoriasis – Thick scale found on scalp • Nail Psoriasis – Nail dystrophy • Erythrodermic Psoriasis– Severe erythema covering all or most of the body • Pustular Psoriasis – Acutely arising pustules • Photosensitive Psoriasis – Seen in areas of sun -
Photochemotherapy
Photochemotherapy Policy Number: Original Effective Date: MM.02.015 11/09/2004 Line(s) of Business: Current Effective Date: HMO; PPO; QUEST Integration June 1, 2016 Section: Medicine Place(s) of Service: Home; Office I. Description Photochemotherapy utilizing ultraviolet light type A (UVA) therapy is a treatment that involves exposing the patient to a photosynthesizing agent (psoralens) through oral ingestion or through bath water in conjunction with ultraviolet A light (sunlight or artificial light) for photochemotherapy of skin conditions. UVA therapy utilizing psoralens is also known as PUVA therapy. Photochemotherapy utilizing ultraviolet light type B (UVB) therapy is a treatment that involves exposing the patient to ultraviolet light type B or middle-wave ultraviolet light. It is generally used in combination with tar or anthralin. II. Criteria/Guidelines A. Photochemotherapy utilizing UVA therapy is covered (subject to Limitations/Exclusions and Administrative Guidelines) for the following diagnoses: 1. Pinta 2. Cutaneous T-cell lymphoma 3. Chronic Graft versus Host Disease refractory to standard immunosuppressive drug treatment 4. Psoriasis 5. Parapsoriasis 6. Atopic dermatitis 7. Lichen planus 8. Pityriasis rosea B. Bath water PUVA is covered if all of the following are met: 1. Patient has extensive, severe psoriasis 2. Patient had prior inability to tolerate systemic PUVA therapy and other conventional therapies. 3. Patient had no prior treatment involving carcinogenic materials (with the exception of methotrexate) including tar and UVB treatments, radiation therapy, and arsenic therapy. Photochemotherapy 2 C. Photochemotherapy utilizing UVB therapy is covered (subject to Limitations/Exclusions and Administrative Guidelines) for the following diagnoses: 1. Psoriasis 2. Parapsoriasis 3.