“Relationship Between Smoking and Plantar Callus
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Idiopathic Spiny Keratoderma: a Report of Two Cases and Literature Review
Idiopathic Spiny Keratoderma: A Report of Two Cases and Literature Review Jessica Schweitzer, DO,* Matthew Koehler, DO,** David Horowitz, DO*** *Intern, Largo Medical Center, Largo, FL **Dermatology Resident, Third Year, College Medical Center/Western University, Long Beach, CA ***Dermatology Residency Program Director, College Medical Center/Western University, Long Beach, CA Abstract Spiny keratoderma is a rare and likely underreported condition that presents with punctate hyperkeratotic growths localized to the palms and soles. We present two cases of clinically diagnosed spiny keratoderma. Although the lesions were asymptomatic, patients are at risk of an underlying internal malignancy with this condition, so diagnosis is crucial. Neither men were seeking treatment for the lesions when they were discovered, suggesting that this condition may be much more common than reported. Patients with histories of manual labor, increased UV exposure, and non-melanoma skin cancer (NMSC) may also be at higher risk for developing spiny keratoderma.1 The epidemiology, histopathologic features, differential diagnosis, and current treatments for spiny keratoderma are reviewed. Introduction Case 2 enthusiast for his entire life, spending significant Spiny keratoderma is a rare palmoplantar A 67-year-old Caucasian male presented with a time using his hands to maintain and fire his keratoderma that presents with keratotic, pinpoint one-year history of insidiously growing, pinpoint weapons and many hours outside without sun papules on the palms and soles. There are both hyperkeratotic papules projecting from his palms protection. The patient was referred back to his hereditary and acquired forms. When found, bilaterally (Figures 4-5). He presented to the clinic primary care physician for internal evaluation. -
White Lesions of the Oral Cavity and Derive a Differential Diagnosis Four for Various White Lesions
2014 self-study course four course The Ohio State University College of Dentistry is a recognized provider for ADA, CERP, and AGD Fellowship, Mastership and Maintenance credit. ADA CERP is a service of the American Dental Association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit hours by boards of dentistry. Concerns or complaints about a CE provider may be directed to the provider or to ADA CERP at www.ada.org/goto/cerp. The Ohio State University College of Dentistry is approved by the Ohio State Dental Board as a permanent sponsor of continuing dental education ABOUT this FREQUENTLY asked COURSE… QUESTIONS… Q: Who can earn FREE CE credits? . READ the MATERIALS. Read and review the course materials. A: EVERYONE - All dental professionals in your office may earn free CE contact . COMPLETE the TEST. Answer the credits. Each person must read the eight question test. A total of 6/8 course materials and submit an questions must be answered correctly online answer form independently. for credit. us . SUBMIT the ANSWER FORM Q: What if I did not receive a ONLINE. You MUST submit your confirmation ID? answers ONLINE at: A: Once you have fully completed your p h o n e http://dent.osu.edu/sterilization/ce answer form and click “submit” you will be directed to a page with a . RECORD or PRINT THE 614-292-6737 unique confirmation ID. CONFIRMATION ID This unique ID is displayed upon successful submission Q: Where can I find my SMS number? of your answer form. -
An Unusual Course in Bullous Morphea
Case Report An Unusual Course in Bullous Morphea İlknur Kıvanç Altunay, MD, Hilal Kaya Erdoğan*, MD, Nurhan Döner, MD, Damlanur Sakız,1 MD. Address: Dermatology and 1Pathology Departments, Şişli Etfal Training and Research Hospital, Istanbul, 34377, Turkey. * Corresponding Author: Dr. Hilal Kaya Erdoğan, Şisli Etfal Training and Research Hospital. Istanbul, 34377, Turkey. E-mail: [email protected] Published: J Turk Acad Dermatol 2010; 4 (4): 04401c This article is available from: http://www.jtad.org/2010/4/jtad04401c.pdf Key Words: bullous morphea, drug reaction Abstract Observations: We report a 75-year-old woman with bullous morphea characterized by disseminated erythemato-pigmentous plaques and a few blisters on some morphea plaques at the beginning of first visit. While she was under narrow band UV therapy, she discontinued the treatment and refused to have any more after 13 sessions. One month later, she reapplied with extensive bullae and facial edema with severe itching. We learned that she had taken naproxen sodium one a day for two days ten days ago. Bullous drug reaction was diagnosed and systemic cortisone was started. She was in remission after fifteen days. The patient had very different clinical picture on her second visit with extensive, large and cadaverous bullae, facial eryhtema and edema. It seems to be a bullous drug reaction based on bullous morphea. However, it remains a mystery whether this clinical presentation is a peculiar drug reaction or is really a mere exacerbation of existed bullous morphea. Introduction noprost eye drop and tolterodine. These medicati- ons had been used for over a year. Her family his- Bullae formation in lesions of morphea is an tory was unremarkable. -
Foot Pain in Scleroderma
Foot Pain in Scleroderma Dr Begonya Alcacer-Pitarch LMBRU Postdoctoral Research Fellow 20th Anniversary Scleroderma Family Day 16th May 2015 Leeds Institute of Rheumatic and Musculoskeletal Medicine Presentation Content n Introduction n Different types of foot pain n Factors contributing to foot pain n Impact of foot pain on Quality of Life (QoL) Leeds Institute of Rheumatic and Musculoskeletal Medicine Scleroderma n Clinical features of scleroderma – Microvascular (small vessel) and macrovascular (large vessel) damage – Fibrosis of the skin and internal organs – Dysfunction of the immune system n Unknown aetiology n Female to male ratio 4.6 : 1 n The prevalence of SSc in the UK is 8.21 per 100 000 Leeds Institute of Rheumatic and Musculoskeletal Medicine Foot Involvement in SSc n Clinically 90% of SSc patients have foot involvement n It typically has a later involvement than hands n Foot involvement is less frequent than hand involvement, but is potentially disabling Leeds Institute of Rheumatic and Musculoskeletal Medicine Different Types of Foot Pain Leeds Institute of Rheumatic and Musculoskeletal Medicine Ischaemic Pain (vascular) Microvascular disease (small vessel) n Intermittent pain – Raynaud’s (spasm) • Cold • Throb • Numb • Tingle • Pain n Constant pain – Vessel center narrows • Distal pain (toes) • Gradually increasing pain • Intolerable pain when necrosis is present Leeds Institute of Rheumatic and Musculoskeletal Medicine Ischaemic Pain (vascular) Macrovascular disease (large vessels) n Intermittent and constant pain – Peripheral Arterial Disease • Intermittent claudication – Muscle pain (ache, cramp) during walking • Aching or burning pain • Night and rest pain • Cramps Leeds Institute of Rheumatic and Musculoskeletal Medicine Ulcer Pain n Ulcer development – Constant pain n Infected ulcer – Unexpected/ excess pain or tenderness Leeds Institute of Rheumatic and Musculoskeletal Medicine Neuropathic Pain n Nerve damage is not always obvious. -
Oral Frictional Hyperkeratosis (FK)
Patient information Oral frictional hyperkeratosis (FK) What is oral frictional hyperkeratosis? Hyperkeratinisation - excessive growth of stubbornly attached keratin (a fibrous protein produced by the body) - may happen for a number of reasons, and may be genetic (runs in the family), physiological e.g. due to friction from a sharp tooth, pre-malignant (pre-cancerous) and malignant (cancerous). The change may result from chemical, heat or physical irritants. Friction (the constant rubbing of two surfaces against each other) in the mouth may result in benign (non-cancerous) white patches. Various names have been used to describe particular examples of FK, including those resulting from excessive tooth-brushing force (toothbrush keratosis), the constant rubbing of the tongue against the teeth (tongue thrust keratosis), and that produced by the habit of chronic cheek or lip biting (cheek or lip bite keratosis). What are the signs and symptoms of FK? Most patients with FK are free of symptoms. A patient may notice a thickening of an area of skin in the mouth, or FK may be discovered by accident during a routine oral examination. What are the causes of FK? The white patches of FK that develop in the mouth are formed in the same way that calluses form on the skin of hands and feet. The most common causes are long term tissue chewing (biting the inside of the cheek or lips), ill-fitting dentures, jagged teeth, poorly adapted dental fillings or caps, and constant chewing on jaws that have no teeth. The constant irritation encourages the growth of keratin, giving the skin involved a different thickness and colour. -
Investigating Biomarkers of Keloid Scarring
Investigating Biomarkers of Keloid Scarring Zoe Drymoussi 2015 A thesis presented for the degree of Doctor of Philosophy Centre for Cutaneous Research, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London 1 Declaration I, Zoe Drymoussi, declare that the work presented in this thesis is my own and has not been submitted in any form for another degree or diploma at any university or other institute of tertiary education. Information derived from the published or unpublished work of others has been acknowledged in the text and a list of references is given. Zoe Drymoussi, PhD Student 1st August 2015 2 Abstract Keloids are fibroproliferative scars that form in response to abnormal healing processes. The extracellular matrix (ECM) remodelling of the dermis in the maturation phase of normal wound healing is insufficient in keloids, leading to excessive ECM proteins being deposited in the granulation tissue. Keloid scars are unique to humans, and show increased prevalence in darker skin types. Current treatments rarely lead to permanent regression, and despite decades of study, the key molecular processes responsible for keloid scarring are still largely elusive. The research presented in this thesis aims to investigate markers of keloid scars, and to examine the impact of both the dermis and epidermis in keloid pathogenesis. Histological examination of the keloid scars showed a thickened epidermis and densely collagenous dermis, both of which demonstrated a higher level of cell proliferation and myofibroblast expression, as compared to normal skin. Differences between the central and marginal regions of the scars were also noted. -
Fundamentals of Dermatology Describing Rashes and Lesions
Dermatology for the Non-Dermatologist May 30 – June 3, 2018 - 1 - Fundamentals of Dermatology Describing Rashes and Lesions History remains ESSENTIAL to establish diagnosis – duration, treatments, prior history of skin conditions, drug use, systemic illness, etc., etc. Historical characteristics of lesions and rashes are also key elements of the description. Painful vs. painless? Pruritic? Burning sensation? Key descriptive elements – 1- definition and morphology of the lesion, 2- location and the extent of the disease. DEFINITIONS: Atrophy: Thinning of the epidermis and/or dermis causing a shiny appearance or fine wrinkling and/or depression of the skin (common causes: steroids, sudden weight gain, “stretch marks”) Bulla: Circumscribed superficial collection of fluid below or within the epidermis > 5mm (if <5mm vesicle), may be formed by the coalescence of vesicles (blister) Burrow: A linear, “threadlike” elevation of the skin, typically a few millimeters long. (scabies) Comedo: A plugged sebaceous follicle, such as closed (whitehead) & open comedones (blackhead) in acne Crust: Dried residue of serum, blood or pus (scab) Cyst: A circumscribed, usually slightly compressible, round, walled lesion, below the epidermis, may be filled with fluid or semi-solid material (sebaceous cyst, cystic acne) Dermatitis: nonspecific term for inflammation of the skin (many possible causes); may be a specific condition, e.g. atopic dermatitis Eczema: a generic term for acute or chronic inflammatory conditions of the skin. Typically appears erythematous, -
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Massage Tocaloma Signature 80 min. $210 Seaweed Body Wrap 50 min. $130 Restore Moisture Miracle Facial 50 min. $170 A decadent massage fully customizable to your specific Helps release stored toxins and relieve fluid retention, as When skin is stressed and compromised, it needs a needs. Includes a hydrating hand treatment and scalp well as hormonal and adrenal balancing. A body brush is restorative moisture miracle. This anti-aging facial will massage for the ultimate relaxation. used to exfoliate dead skin cells. Next, a warmed infuse deep hydration while boosting firmness leaving your application of seaweed envelopes the body while a skin feeling soft, nourished and renewed. Swedish 20 mins. $80 | 50 min. $120 | 80 min. $180 relaxing scalp massage soothes stress. After a eucalyptus Acne Clarifying Facial 50 min. $140 This treatment is ideal when arriving at Tapatio to welcome shower, moisture-rich body lotion is applied to leave skin you and ground your energy. Therapists focus on areas silky smooth. Improve skin clarity while combating acne and unbalanced prone to tension after traveling while utilizing long, relaxing skin. Improve skin smoothness, balance oil production, Sedona Purification Body Wrap 50 min. $130 strokes of light to medium pressure, providing instant relief unclog pores and speed up skin cell turnover while creating of pain and stiffness. Rich in minerals from the Arizona desert and derived from an overall glow and revealing healthy skin. the clays of the Southwest, this treatment will nourish, tone Therapeutic 20 mins. $100 | 50 min. $140 | 80 min. $200 Lighten & Brighten Facial 50 min. $160 and purify your skin. -
Botulinum Toxin in the Treatment of Sweatworsened Foot Problems In
15 March 2005 Use of Articles in the Pachyonychia Congenita Bibliography The articles in the PC Bibliography may be restricted by copyright laws. These have been made available to you by PC Project for the exclusive use in teaching, scholar- ship or research regarding Pachyonychia Congenita. To the best of our understanding, in supplying this material to you we have followed the guidelines of Sec 107 regarding fair use of copyright materials. That section reads as follows: Sec. 107. - Limitations on exclusive rights: Fair use Notwithstanding the provisions of sections 106 and 106A, the fair use of a copyrighted work, including such use by reproduction in copies or phonorecords or by any other means specified by that section, for purposes such as criticism, comment, news reporting, teaching (including multiple copies for classroom use), scholarship, or research, is not an infringement of copyright. In determining whether the use made of a work in any particular case is a fair use the factors to be considered shall include - (1) the purpose and character of the use, including whether such use is of a commercial nature or is for nonprofit educational purposes; (2) the nature of the copyrighted work; (3) the amount and substantiality of the portion used in relation to the copyrighted work as a whole; and (4) the effect of the use upon the potential market for or value of the copyrighted work. The fact that a work is unpublished shall not itself bar a finding of fair use if such finding is made upon consideration of all the above factors. -
For Peer Review Only
Expert Opinion On Drug Metabolism & Toxicology For Peer Review Only Please download and read the Referee Guidelines Intravenous immunoglobulin: pharmacological properties and use in polyneuropathies Journal: Expert Opinion On Drug Metabolism and Toxicology Manuscript ID EOMT-2016-0106.R1 Manuscript Type: Review IVIg, CIDP, GBS, anti-idiotype antibodies, anti-ganglioside antibodies, Keywords: sialylation, IgG molecule., Fc receptors URL: http://mc.manuscriptcentral.com/eomt Email: [email protected] Page 1 of 60 Expert Opinion On Drug Metabolism & Toxicology 1 2 Abstract 3 4 Introduction: Intravenous immunoglobulin (IVIg) is increasingly used for the treatment of 5 6 autoimmune and systemic inflammatory diseases with both licensed and off-label indications. The 7 mechanism of action is complex and not fully understood, involving the neutralization of 8 9 pathological antibodies, Fc receptor blockade, complement inhibition, immunoregulation of 10 11 dendritic cells, B cells and T cells and the modulation of apoptosis. 12 13 14 Areas covered:For First, this Peerreview describes Review the pharmacological propertiesOnly of IVIg, including the 15 16 composition, mechanism of action, and adverse events. The second part gives an overview of some 17 of the immune-mediated polyneuropathies, with special focus on the pathomechanism and clinical 18 19 trials assessing the efficacy of IVIg. A literature search on PubMed was performed using the terms 20 21 IVIg, IVIg preparations, side effects, mechanism of action, clinical trials, GBS, CIDP. 22 23 24 Expert opinion: Challenges associated with IVIg therapy and the treatment possibilities for 25 26 immune-mediated polyneuropathies are discussed. The availability of IVIg is limited, the expenses 27 are high, and, in several diseases, a chronic therapy is necessary to maintain the immunomodulatory 28 29 effect. -
Basal Cell Papilloma, Senile Keratosis, Seborrheic Wart)
ATLAS OF HEAD AND NECK PATHOLOGY SEBORRHEIC KERATOSIS SEBORRHEIC KERATOSIS (BASAL CELL PAPILLOMA, SENILE KERATOSIS, SEBORRHEIC WART) These lesions, often multiple, and occurring for the most part after 50 years of age, are most common on the face and upper body. They are brownish to black, slightly greasy, slightly raised, with either a smooth or mildly verrucous surface and a “stuck-on” appearance. They measure from a few millimeters to several centimeters in diameter. Microscopically, there is variance in appearance but all types show hyperkerato- sis, acanthosis (thickening of the epidermis) and a papillary formation sharply demar- cated from the adjacent epidermis. Generally a straight line drawn from one edge of the lesion to the other will pass just under the deeper part of the tumor. Horny invaginations from the epidermis appear on cross-section as pseudo- horn cysts and there are also true horn cysts. Both of these cysts show complete keratinization, concentrically arranged, and only a thin granulosal cell layer. Melanin is prevalent in many tumors and accounts for the dark appearance as seen clinically. Both squamous and basal (“basaloid”) cells are seen in this lesion and they are ar- ranged in sheets. In some types of seborrheic keratoses there are interwoven tracts of basal cells and in others the basal cells are in nests. Intercellular bridges are common. Seborrheic keratosis, showing how the tumor tends to have a straight edge along its deep margin. Also seen are acantho- sis (large arrow), papillary projections (triangles), and hyperkeratosis (small arrows). Several cysts are present with keratin concentrically arranged. Most of the epithelial cells here are dark and, having the appearance of epidermoid basal cells, are called basaloid cells. -
Seborrheic Keratosis
Benign Epidermal and Dermal Tumors REAGAN ANDERSON, DO- PROGRAM DIRECTOR, COLORADO DERMATOLOGY INSTITUTE, RVU PGY3 RESIDENTS- JONATHAN BIELFIELD, GEORGE BRANT PGY2 RESIDENT- MICHELLE ELWAY Seborrheic Keratosis Common benign growth seen after third/fourth decade of life Ubiquitous among older individuals Tan to black, macular, papular, or verrucous lesion Occur everywhere except palms, soles, and mucous membranes Can simulate melanocytic neoplasms Pathogenesis: Sun exposure- Australian study found higher incidence in the head/neck Alteration in distribution of epidermal growth factors Somatic activating mutations in fibroblast growth factor receptor and phosphoinositide-3-kinase Seborrheic Keratosis Sign of Leser-Trelat: Rare cutaneous marker of internal malignancy • Gastric/colonic adenocarcinoma, breast carcinoma, and lymphoma m/c • Abrupt increase in number/size of SKs that can occur before, during, or after an internal malignancy is detected • 40% pruritus • M/C location is the back • Malignant acanthosis nigricans may also appear in 20% of patients • Should resolve when primary tumor is treated, and reappear with recurrence/mets Seborrheic Keratosis 6 Histologic types Acanthotic Hyperkeratotic Reticulated Irritated Clonal Melanoacanthoma Borst-Jadassohn phenomenon Well-demarcated nests of keratinocytes within the epidermis Seborrheic Keratoses Treatment Reassurance Irritated SKs (itching, catching on clothes, inflamed) Cryotherapy, curettage, shave excision Pulsed CO2, erbium:YAG lasers Electrodessication Flegel