Ted Rosen, MD Professor of Dermatology Baylor College Of

Total Page:16

File Type:pdf, Size:1020Kb

Ted Rosen, MD Professor of Dermatology Baylor College Of Most Common Dermatological Problems in VA Ambulatory Care None Intrinsic aging of the skin Analogous to osteoporosis Regardless of external physical factors Regardless of disease states Ultimately leads to “skin failure” Dermatology 215:271 and 284, 2007 Int J Cosmet Sci.35:477-83, 2013 What reduces skin’s multipurpose functionality? Intrinsic Aging EPIDERMIS DERMIS Epidermis thins Reduced sebaceous gland activity Increased TEWL Reduced sweat gland activity Decreased SC lipids Reduced collagen synthesis Decreased melanocytes Reduced elastin synthesis (10% per decade) Shrinking collagen and elastin Fewer functional dendritic cells (1% per year after age 25) (Reduced immunosurveillance) Increased MMP activity due to decreased MMP inhibitors (destruction dermal fibrils) Reduced hyaluronic acid synthesis Dermatology 215:271 and 284, 2007 This may be the most obvious extrinsic factor in loss of skin integrity, but not the only one! Photoaging: UV exposure What reduces skin’s multipurpose functionality? Extrinsic Factors UV Light Smoking Sedentary life Extreme temps Stress Alcohol abuse Pollutants Drugs What reduces skin’s multipurpose functionality? Extrinsic Factors UV Light Smoking Sedentary life Extreme temps Stress Alcohol abuse Pollutants EPIDERMIS DERMIS Epidermis thins Collagen degeneration DNA damage: abnormal cells Elastin degeneration Destruction of dendritic cells Increased MMP (due to ROS) (Reduced immunosurveillance) Hyaluronic acid degeneration Pathol Biol 51:569, 2003 J Cut Med Surg 8:415, 2004 Arch Dermatol 143:397,2007 J Invest Dermatol 130:2719, 2012 Rhytids* Xerosis Sagging skin Skin fragility Solar elastosis Senile purpura Cutis rhomboidalis Patterned alopecia Solar lentigines Poliosis Actinic comedones Nail thinning/ridging Indian J Dermatol 57:343-52, 2012 It doesn’t stop with emphysema and lung cancer! Twin A 52.5 pack-years Twin B No smoking Arch Dermatol 143:1543-46, 2007 QUIT SMOKING Better yet, don’t start! Int J Dermatol 53:1205, 2014 Plast Reconstr Surg 132:1085, 2013 Exp Dermatol 22:349, 2013 Skin Res Technol 18:511, 2012 Lower skin oxygenation Vasoconstriction Lower telomerase Increased MMP activity Increased cytokines Skinmed 8:23-9, 2010 Rhytids Xerosis* Sagging skin Skin fragility Solar elastosis Senile purpura* Cutis rhomboidalis Patterned alopecia Solar lentigines* Poliosis Actinic comedones Nail thinning/ridging Indian J Dermatol 57:343-52, 2012 OLD: Bleach with 4% hydroquinone (+ retinoid or AHA) OLD: Liquid nitrogen cryospray NEW: Laser ablation Nd-Yag at wavelength 532nm IPL at wavelength 515nm Alexandrite at wavelength 755nm Xerosis: Dry Skin Most common skin “disorder” in mature adults May cause inflammation: Xerotic eczema Xerosis may itch… Cerave: Cream, Lotion, Wash Curel: “Rough Skin Rescue Lotion” Curel: “Advanced Ceramide Therapy” Eucerin: “Professional Repair” Cetaphil: “Restoradem” Aveeno: “Eczema Care” OBVIOUS ETIOLOGY ETIOLOGY UNCERTAIN Xerosis cutis Scabies incognito Classic Scabies Atypical contact Body lice (homeless) dermatitis DH, GA, Hives ID rxn Lichen planus, Psoriasis Unusual drug eruption Drug reaction Prurigo nodularis Pemphigoid (early, atypical) “Unclassified Contact dermatitis Endogenous Eczema” Atopic dermatitis Nummular eczema Tinea pedis/cruris/corporis Atypical in the Elderly Suspect scabies: mineral oil prep; Likely negative Suspect scabies but prep negative…. EVERY ELDERLY ADULT PRESENTING WITH NEW ONSET WIDESPREAD ITCH, NON-SPECIFIC RASH SHOULD BE ASSUMED TO HAVE SCABIES Ivermectin 1 mg/10 lbs + permethrin 5% cr Repeat in 1-2 week Treat close contacts with permethrin Address fabrics contacting skin prior week FROM: Nurse, Caregiver, Relative….OR… J Gerontol A Biol Sci Med Sci 56:424-7, 2001 Damn Viagra Given overall: risk of internal malignancy with pruritus is very low, if at all. Hematologic malignancy OR = 2 Bile duct CA OR = 3.73 Overall OR = 1.14 in itching patients J Am Acad Dermatol 70:651-8, 2014 Semin Cutan Med Surg 30:107-12, 2011 Am J Clin Dermatol 7:71-84, 2006 May be rare, but not impossible! Solar purpura Senile purpura Skin fragility Solar purpura Senile purpura NO RELIABLE THERAPY Skin fragility Arnica montana Inhibits hyaluronaidase Decreases capillary permeability Ascorbic acid Collagen synthesis Capillary strength Hesperidin Capillary stability Rutoside Inhibits elastase Decreases capillary permeability Eriocitrin Antioxidant Many choices; All OTC; All inexpensive…..What’s to lose? J Drugs Dermatol 10:718-22, 2011 Active Active Placebo Placebo J Drugs Dermatol 10:718-22, 2011 Superficial fungal infection: foot, groin, trunk Frequency increases with age Diabetes, Immunosuppression Trichophyton rubrum: 90% All forms itch Tinea pedis probably first, then spreads to groin, trunk ANY topical antifungal works Oral terbinafine 250mg/day Superficial fungal infection: foot, groin, trunk Diagnosis: KOH prep KOH the active border Obtain scale for fungal culture Topical therapy; Many agents to choose from and all work; be aware of dosing, which varies from agent to agent Vehicle important (cream, gel, lotion, foam) Azole: clotrimazole, econazole, ketoconazole luliconazole, oxiconazole, sertaconazole Allylamine: butenafine, naftifine, terbinafine Olamine: ciclopirox Br J Dermatol 166:927-33, 2012 Reservoir for fungi that cause other tinea infections Onychomycosis = 50% abnormal nails DIAGNOSIS: KOH, Culture In most patients, T. Rubrum Rarely Candida, Molds Can cause pain Can cause ulcers on nearby toes Can lead to cellulitis Rx: Terbinafine 250mg/d x 3-4 months Topical Rx: Efinaconazole, Tavaborole (Daily x 48 weeks!) What are these bumps? Seborrheic keratosis “Stuck on” appearing, rough and pigmented lesions; Familial Cherry angiomas Round, bright red to almost black growths; Familial Sebaceous hyperplasia Small, facial bumps with yellow color, central dip and surface blood vessels; Not familial SK Cherry Angiomas Sebaceous Hyperplasia Seborrheic keratosis, Sebaceous hyperplasia, Cherry Angioma All Rx with either light liquid nitrogen cryospray or by electrodestruction (“cooked”) or by snip + hemostasis SK: nitrogen > electrodesiccation >> snip Seb hyperplasia & cherry angioma Electrodesiccation > nitrogen >> snip TIP: With multiple lesions, a trial of each modality to see which works best! Skin Tags (Acrochordons) Skin Tags Snip at base Achieve hemostasis Pressure Drysol Light ED Immerse hemostat, forceps or needle holder in LN2 Grasp skin tag with frozen tip Keep in place ~10-15 seconds When multiple, associated with increased incidence of diabetes Int J Dermatol 46:1155, 2007 J Dtsch Dermatol Ges 6:852, 2008 When perianal: Sign of Crohn’s Disease J Clin Gastroenterol 44:151, 2010 Inflamm Bowel Dis 14:1236, 2008 When multiple, associated with pre-malignant colonic polyps????? YES! Ann Intrn Med 98:928, 1983 NO! Gastroenterology 95:1127, 1988 Venous Lake Venous Lake Venous Lake Closely related to senile angioma COMPRESS with PRESSURE Slowly refill May be very dark and resemble melanoma Arch Dermatol. 117:250 , 1981 Common sites: ear and lip Electrodesiccation or laser (YAG at 532; IPL at 560) All other cancers Melanoma BCC SCCA https://www.aad.org/media/stats/conditions/skin-cancer All other cancers 1,689,000 Melanoma 161,800 BCC SCCA 4,000,000 1,400,000 https://www.aad.org/media/stats/conditions/skin-cancer SCCA + BCC 3000 Melanoma 9730 All other cancers 587,490 https://www.cancer.org/research/cancer-facts-statistics/all-cancer-facts-figures/cancer-facts-figures-2017.html AK or SCCA Complete Rx Clearance Comment References How long Hautarzt 56:353, 2005 Cryosurgery 68-97% to freeze? Int J Derm 43:687, 2004 BID 4-6 Clin Ther 24:990, 2002 5-FU 0.5-5% 50%-96% Cutis 70:335, 2002 weeks Br J Derm 157(S):34, 2007 Imiquimod 45-85% 2 or 3x/wk JAAD 50:714, 2004 Cont? Cycle? Br J Derm 157(S):41, 2007 BID Int J Derm 40:709, 2001 Diclofenac 33-50% x 90 days Br J Derm 146:94, 2002 JAAD 56:125, 2007 PDT 69-93% ? Protocol Br J Derm 156:793, 2007 Pre-Rx 4 weeks End Rx (16 wk) 4 weeks post Epidemiology: Least dangerous Clinical course . Slow growing . Face, scalp, upper back and arms . Increasingly prevalent in elderly . Rarely metastasize….BUT . If neglected, can cause significant functional and cosmetic impairment . Given one BCC, lifetime risk for another >50%; 12-20% in first 12 months JEADV 20:698, 2006 Nodular Superficial Papule (elevated) Macule (flat) Translucent, Red and scaly Pearl-like Telangiectasia less Telangiectasia prominent on surface Painless Painless May Itch May bleed May bleed + Pigment + Pigment . If untreated may be very destructive! Second most common NMSC M:F = 2:1; Face, scalp, hands/arms and lips and ears More rapid growth; may metastasize Reddish, scaly, patches to firm plaques, to rock hard papules and nodules1 . May have ulcerated center . May develop keratin “horn” . May appear “wart like” SCCIS misdiagnosed as eczema or psoriasis Albino Chronic DLE Transplant Chronic Leg Ulcer Sometimes what is seen at the surface is only the tip of the iceberg Mohs micrographic surgery Classic scalpel excision (3-5mm margin) Curettage with electrodesiccation Radiotherapy Cryotherapy (liquid nitrogen) Topical therapy: 5-FU, Diclofenac Topical IRM: imiquimod Photodynamic therapy (ALA, MAL) (Intralesional interferon) (Laser ablation, Acid application) Any pigmented lesion should be viewed with suspicion since this can be fatal (20%) ABCDE: Asymmetry, Irregular border, Multiple colors, Large diameter, Evolving (growing) When in
Recommended publications
  • Level I Syllabus
    LEVEL I SYLLABUS 1 ACDT Course Learning Objectives Upon Completion, Those Enrolled Will Be MODULE Prepared To... The Language of Dermatology 1. Define and spell the following cutaneous lesions/descriptors: a. Macule b. Patch c. Papule d. Nodule e. Cyst f. Plaque g. Wheal h. Vesicle i. Bulla j. Pustule k. Erosion l. Ulcer m. Atrophy n. Scaling o. Crusting p. Excoriations q. Fissures r. Lichenification s. Erythematous t. Violaceous u. Purpuric v. Hypo­/Hyperpigmented w. Linear x. Annular y. Nummular/Discoid z. Blaschkoid aa. Morbilliform bb. Polycyclic cc. Arcuate dd. Reticular Collecting & Documenting Patient History Part I 1. Describe the importance of documentation and chart review, while properly collecting dermatology­specific medical history components, including: a. Chief Complaint b. Past Medical History c. Family History d. Medications e. Allergies Collecting & Documenting Patient History Part II 1. Demonstrate the proper collection of dermatology­specific medical history and explain the significance of the following: a. Social History b. Review of Systems c. History of Present Illness Anatomy 1. Spell and document the following directional indicators while applying them to the appropriate anatomical landmarks: a. Proximal/Distal b. Superior/Mid/Inferior c. Anterior/Posterior d. Medial/Lateral e. Dorsal/Ventral 2. Spell and identify specific anatomical locations involving the: a. Scalp b. Forehead c. Ears d. Eyes e. Nose f. Cheeks g. Lips h. Chin i. Neck j. Back k. Upper extremity l. Hands m. Nails n. Chest o. Abdomen p. Buttocks q. Hips r. Lower extremity s. Feet Skin Structure and Function 1. Identify and spell the three primary layers of skin: a.
    [Show full text]
  • Urticaria and Angioedema
    Challenging Cases in Allergy and Immunology Massoud Mahmoudi Editor Challenging Cases in Allergy and Immunology Editor Massoud Mahmoudi D.O, Ph.D. RM (NRM), FACOI, FAOCAI, FASCMS, FACP, FCCP, FAAAAI Assistant Clinical Professor of Medicine University of California San Francisco San Francisco, California Chairman, Department of Medicine Community Hospital of Los Gatos Los Gatos, California USA ISBN 978-1-60327-442-5 e-ISBN 978-1-60327-443-2 DOI 10.1007/978-1-60327-443-2 Springer Dordrecht Heidelberg London New York Library of Congress Control Number: 2009928233 © Humana Press, a part of Springer Science+Business Media, LLC 2009 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Humana Press, c/o Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made.
    [Show full text]
  • Copyrighted Material
    1 Index Note: Page numbers in italics refer to figures, those in bold refer to tables and boxes. References are to pages within chapters, thus 58.10 is page 10 of Chapter 58. A definition 87.2 congenital ichthyoses 65.38–9 differential diagnosis 90.62 A fibres 85.1, 85.2 dermatomyositis association 88.21 discoid lupus erythematosus occupational 90.56–9 α-adrenoceptor agonists 106.8 differential diagnosis 87.5 treatment 89.41 chemical origin 130.10–12 abacavir disease course 87.5 hand eczema treatment 39.18 clinical features 90.58 drug eruptions 31.18 drug-induced 87.4 hidradenitis suppurativa management definition 90.56 HLA allele association 12.5 endocrine disorder skin signs 149.10, 92.10 differential diagnosis 90.57 hypersensitivity 119.6 149.11 keratitis–ichthyosis–deafness syndrome epidemiology 90.58 pharmacological hypersensitivity 31.10– epidemiology 87.3 treatment 65.32 investigations 90.58–9 11 familial 87.4 keratoacanthoma treatment 142.36 management 90.59 ABCA12 gene mutations 65.7 familial partial lipodystrophy neutral lipid storage disease with papular elastorrhexis differential ABCC6 gene mutations 72.27, 72.30 association 74.2 ichthyosis treatment 65.33 diagnosis 96.30 ABCC11 gene mutations 94.16 generalized 87.4 pityriasis rubra pilaris treatment 36.5, penile 111.19 abdominal wall, lymphoedema 105.20–1 genital 111.27 36.6 photodynamic therapy 22.7 ABHD5 gene mutations 65.32 HIV infection 31.12 psoriasis pomade 90.17 abrasions, sports injuries 123.16 investigations 87.5 generalized pustular 35.37 prepubertal 90.59–64 Abrikossoff
    [Show full text]
  • Osteoporosis in Skin Diseases
    International Journal of Molecular Sciences Review Osteoporosis in Skin Diseases Maria Maddalena Sirufo 1,2, Francesca De Pietro 1,2, Enrica Maria Bassino 1,2, Lia Ginaldi 1,2 and Massimo De Martinis 1,2,* 1 Department of Life, Health and Environmental Sciences, University of L’Aquila, 67100 L’Aquila, Italy; [email protected] (M.M.S.); [email protected] (F.D.P.); [email protected] (E.M.B.); [email protected] (L.G.) 2 Allergy and Clinical Immunology Unit, Center for the Diagnosis and Treatment of Osteoporosis, AUSL 04 64100 Teramo, Italy * Correspondence: [email protected]; Tel.: +39-0861-429548; Fax: +39-0861-211395 Received: 1 June 2020; Accepted: 1 July 2020; Published: 3 July 2020 Abstract: Osteoporosis (OP) is defined as a generalized skeletal disease characterized by low bone mass and an alteration of the microarchitecture that lead to an increase in bone fragility and, therefore, an increased risk of fractures. It must be considered today as a true public health problem and the most widespread metabolic bone disease that affects more than 200 million people worldwide. Under physiological conditions, there is a balance between bone formation and bone resorption necessary for skeletal homeostasis. In pathological situations, this balance is altered in favor of osteoclast (OC)-mediated bone resorption. During chronic inflammation, the balance between bone formation and bone resorption may be considerably affected, contributing to a net prevalence of osteoclastogenesis. Skin diseases are the fourth cause of human disease in the world, affecting approximately one third of the world’s population with a prevalence in elderly men.
    [Show full text]
  • UV Light and Skin Aging
    See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/266027439 UV light and skin aging Article · September 2014 DOI: 10.1515/reveh-2014-0058 · Source: PubMed CITATIONS READS 4 73 2 authors, including: Jéssica EPS Silveira Natura Cosmeticos 5 PUBLICATIONS 21 CITATIONS SEE PROFILE Available from: Jéssica EPS Silveira Retrieved on: 13 April 2016 Rev Environ Health 2014; aop J é ssica Eleonora Pedroso Sanches Silveira * and D é bora Midori Myaki Pedroso UV light and skin aging Abstract: This article reviews current data about the rela- signs of aging. Physiological changes in aged skin include tionship between sun radiation and skin, especially with structural and biochemical changes as well as changes regards ultraviolet light and the skin aging process. The in neurosensory perception, permeability, response to benefits of sun exposition and the photoaging process are injury, repair capacity, and increased incidence of some discussed. Finally, the authors present a review of photopro- skin diseases (5) . tection agents that are commercially available nowadays. The skin aging process occurs in the epidermis and dermis. Although the number of cell layers remains stable, Keywords: photoaging; sun protection; ultraviolet (UV) the skin thins progressively over adult life at an accelerat- exposure. ing rate. The epidermis decreases in thickness by about 6.4% per decade on average, with an associated reduc- tion in epidermal cell numbers (6) , particularly in women. DOI 10.1515/reveh-2014-0058 Received August 4 , 2014 ; accepted August 15 , 2014 Further, dermis thickness decreases with age, and thin- ning is accompanied by a decrease in both vascularity and cellularity (5) .
    [Show full text]
  • Geriatric Dermatology
    10/18/2020 Participants will be able to: • Describe the skin changes that occur with aging • Perform the appropriate work-up and Geriatric Dermatology initiate management of pruritus Objectives • Steve Daveluy MD Recognize and treat common inflammatory skin diseases Wayne State Department of Dermatology • [email protected] Recognize potential skin cancers and counsel on risk reduction 1 2 • Skin changes with aging • Itch and Rash • Tumors – benign and malignant • I have no relevant conflicts of interest for • Sun Protection Disclosure this session Outline • Elder Abuse 3 4 Elderly Population Skin Changes with Aging • Baby Boomers 1946-1964: 65.2 million in 2012 • Intrinsic • In 2029, youngest boomers reach 65: • Extrinsic: UV exposure, smoking • Census estimates: 71.4 million in US > 65 • Epidermal Barrier Defects • 20% of US population (14% in 2012) • Immunosenescence • Altered wound healing capacity • 65-74 years old: 40% skin problem requiring treatment by physician US Census Bureau Chang. JAMDA 14 (2013) 724-730 Beauregard. Arch Dermatol 123:1638–1643, 1987 5 6 1 10/18/2020 Cutis Rhomboidalis Nuchae Skin Changes with Aging Skin Changes from UV Exposure Favre-Racouchot • Wrinkled, lax, increased fragility • Thinner Poikiloderma of Civatte • Decreased blood flow, sweat glands, subQ fat -> thermoregulation Solar Purpura Southern Medical Journal Nov 2012; 105 (11) Dermatology. 2018 Elsevier 7 8 Pruritus • Incidence: 12% in 65+; 20% in 85+ • Associated sleep disturbance, depression • Berger et al proposed 2 visit algorithm • Visit
    [Show full text]
  • Diagnosis and Management of Leukocytoclastic Vasculitis
    Internal and Emergency Medicine https://doi.org/10.1007/s11739-021-02688-x IM - REVIEW Diagnosis and management of leukocytoclastic vasculitis Paolo Fraticelli1 · Devis Benfaremo1 · Armando Gabrielli1 Received: 14 October 2020 / Accepted: 23 February 2021 © The Author(s) 2021 Abstract Leukocytoclastic vasculitis (LCV) is a histopathologic description of a common form of small vessel vasculitis (SVV), that can be found in various types of vasculitis afecting the skin and internal organs. The leading clinical presentation of LCV is palpable purpura and the diagnosis relies on histopathological examination, in which the infammatory infltrate is composed of neutrophils with fbrinoid necrosis and disintegration of nuclei into fragments (“leukocytoclasia”). Several medications can cause LCV, as well as infections, or malignancy. Among systemic diseases, the most frequently associated with LCV are ANCA-associated vasculitides, connective tissue diseases, cryoglobulinemic vasculitis, IgA vasculitis (formerly known as Henoch–Schonlein purpura) and hypocomplementemic urticarial vasculitis (HUV). When LCV is suspected, an exten- sive workout is usually necessary to determine whether the process is skin-limited, or expression of a systemic vasculitis or disease. A comprehensive history and detailed physical examination must be performed; platelet count, renal function and urinalysis, serological tests for hepatitis B and C viruses, autoantibodies (anti-nuclear antibodies and anti-neutrophil cytoplasmic antibodies), complement fractions and IgA staining in biopsy specimens are part of the usual workout of LCV. The treatment is mainly focused on symptom management, based on rest (avoiding standing or walking), low dose corticos- teroids, colchicine or diferent unproven therapies, if skin-limited. When a medication is the cause, the prognosis is favorable and the discontinuation of the culprit drug is usually resolutive.
    [Show full text]
  • British Journal of Dermatology
    British Journal of Dermatology July 2007 - Vol. 157 Issue s1 Page1-138 Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Foreword pages iv–iv Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Disclaimer pages vi–vi Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Guest Speakers pages xx–xx Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Main Plenary Sessions Main Plenary Sessions: Summaries of Papers pages 1–9 Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Registrars’ Symposium pages 10–13 Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Clinicopathological Cases Clinicopathological Cases: Summaries of Papers pages 14–22 Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Bristol Cup Posters Bristol Cup Posters: Summaries of Posters pages 23–73 Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Historical Archive Symposium Historical Archive Symposium: Summaries of Papers pages 74–80 Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Contact Dermatitis British Contact Dermatitis Society: Summaries of Papers pages 81–93 Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K. 10-13 July 2007 Dermatopathology British Society for Dermatopathology: Summary of Papers pages 94–105 Abstracts for the British Association of Dermatologists 87th Annual Meeting Birmingham, U.K.
    [Show full text]
  • Pharmaceutical Cream Compositions Comprising Oxymetazoline to Treat Rosacea
    (19) TZZ¥___ __T (11) EP 3 181 121 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 21.06.2017 Bulletin 2017/25 A61K 9/10 (2006.01) A61K 31/4174 (2006.01) A61K 47/10 (2017.01) A61K 47/14 (2017.01) (2006.01) (21) Application number: 16196317.8 A61K 9/00 (22) Date of filing: 01.12.2011 (84) Designated Contracting States: • POWALA, Christopher AL AT BE BG CH CY CZ DE DK EE ES FI FR GB Radnor GR HR HU IE IS IT LI LT LU LV MC MK MT NL NO Pennsylvania 19087 (US) PL PT RO RS SE SI SK SM TR • RIOS, Luis Pembroke Pines (30) Priority: 03.12.2010 US 419693 P Florida 33029 (US) 03.12.2010 US 419697 P (74) Representative: Hoffmann Eitle (62) Document number(s) of the earlier application(s) in Patent- und Rechtsanwälte PartmbB accordance with Art. 76 EPC: Arabellastraße 30 11794911.5 / 2 645 993 81925 München (DE) (71) Applicant: ALLERGAN, INC. Remarks: Irvine, CA 92612 (US) •This application was filed on 28-10-2016 as a divisional application to the application mentioned (72) Inventors: under INID code 62. • SHANLER, Stuart D. •Claims filed after the date of receipt of the divisional Pomona application (Rule 68(4) EPC). New York 10970 (US) (54) PHARMACEUTICAL CREAM COMPOSITIONS COMPRISING OXYMETAZOLINE TO TREAT ROSACEA (57) Embodiments relating to cream formulations as baceous glands, such as acne, perioral dermatitis, and well as oxymetazoline creams and methods for treating pseudofolliculitis barbae; disorders of sweat glands, such rosacea and symptoms associated with rosacea, includ- as miliaria, including, but not limited
    [Show full text]
  • 2011 Board Review Course
    2011 Board Review Course 48th Annual Meeting October 20-23, 2011 Sheraton Seattle Seattle, Washington 2011 Board Review The American Society of Dermatopathology Faculty: Thomas N. Helm, MD, Course Director State University of New York at Buffalo Alina Bridges, DO Mayo Clinic, Rochester Klaus J. Busam, MD Memorial Sloan-Kettering Cancer Center Loren E. Clarke, MD Penn State Milton S. Hershey Medical Center/College of Medicine Tammie C. Ferringer, MD Geisinger Medical Center Darius R. Mehregan, MD Pinkus Dermatopathology Lab PC Diya F. Mutasim, MD University of Cincinnati Rajiv M. Patel, MD University of Michigan Margot S. Peters, MD Mayo Clinic, Rochester Garron Solomon, MD CBLPath, Inc. COURSE OBJECTIVES Upon completion of this course, participants should be able to: Identify board examination requirements. Utilize new technology to assist with various diagnoses and treatment methods. Structure and Function of the Skin Alina Bridges, DO Mayo Clinic, Rochester Structure and Function of the Epidermis Alina G. Bridges, D.O. Assistant Professor, Department of Dermatopathology, Division of Dermatopathology and Cutaneous Immunopathology, Mayo Clinic, Rochester, MN I. Functions A. Protection B. Sensory reception C. Thermal regulation D. Nutrient (Vitamin D) metabolism E. Immunologic surveillance 1.Keratinocytes produce interleukins, colony stimulating factors, tumor necrosis factors, transforming growth factors and growth F. Repair II. Epidermis A. Derived from ectoderm B. Keratinizing stratified squamous epithelium from which arise cutaneous appendages (sebaceous glands, nails and apocrine and eccrine sweat glands) 1. Rete 2. Dermal papillae C. Comprises the following layers a) Stratum germinativum (Basal cell layer) b) Stratum spinosum (Spinous Cell layer) c) Stratum granulosum (Granular layer) d) Stratum corneum (Horny cell layer) e) Stratum lucidum present in areas where the stratum corneum is thickest, such as the palms and soles.
    [Show full text]
  • Report Generated on Sep 5, 2021
    Report generated on Sep 26, 2021: Report Generated Sep 26, 2021 To Submit Corrections email [email protected] Last Name First Name Title Accepting Phone Fax Number Specialty Clinical Interests Address City State Zip New Number Patients Aalsma Matthew PhD, Hospital- Pediatrics, Adolescent Mental Health Care of Delinquent HSPP Based Medicine Youth; ***; 2BSORCO Provider Only Aaron Vasantha MD Hospital- Nuclear Medicine, Based Radiology Provider Only Abbasi Rania MD Accepting 317.944.9981 Pediatric Congenital Cardiac Anesthesia New Patients Anesthesiology Team; ***; 2BSORCO Abbott Daniel MD Accepting 765.448.8100 765.838.4345 Urology Benign prostatic hyperplasia, IU Health Arnett Hospital Medical Lafayette IN 47905 New Patients Prostate cancer, Nephrolithiasis, Office Building Erectile disfunction, Overactive 5177 McCarty Lane bladder, Robotic surgery Abdeljawad Khaled MD Accepting 317.880.5475 317.880.0315 Gastroenterology - ***; 2BSORCO IU Health Physicians Digestive & Indianapolis IN 46202 New Patients Hepatology Liver Disorders 720 Eskenazi Ave. IU Health Physicians Digestive & Indianapolis IN 46202 Liver Disorders 705 Riley Hospital Dr. IU Health Physicians Digestive & Zionsville IN 46077 Liver Disorders 6866 W. Stonegate Dr., Ste 104 Abebe Sheila NP Not 317.962.5820 317.962.3916 Pulmonary - Critical IU Health Physicians Pulmonary & Indianapolis IN 46202 Accepting Care Critical Care New Patients 1801 N. Senate Blvd., Ste 230 Abeleda Aris Rodel MD Accepting 317.865.6700 317.865.6707 Family Medicine IU Health Physicians Family Indianapolis IN 46217 New Patients Medicine - South 8820 S. Meridian St., Ste 120 Abell Marielle PA-C Not 812.353.3719 812.353.3713 Palliative Care IU Health Southern Indiana Bloomington IN 47403 Accepting Physicians New Patients 514 W.
    [Show full text]
  • I Have No Relevant Conflicts of Interest
    7/23/2019 Common Dermatological Issues in the Elderly Lauren Graham, MD, PhD, FAAD Assistant Professor University of Alabama at Birmingham Alabama Medical Directors Association Annual Conference July 26, 2019 I have no relevant conflicts of interest. PI for clinical trial for Pfizer, consultant for UCB, speaker for psoriasis foundation Thank you to American Geriatric Society/Dr. Sara Steirman and Dr. Tracy Donahue OBJECTIVES Know and understand: Normal age-related changes in skin and photoaging The diagnosis and treatment of skin conditions common in older adults Recognizing benign vs concerning skin problems in the elderly 1 7/23/2019 DERMATOLOGIC CHANGES WITH AGING Epidermal and dermal changes Reduced lipids Slower wound healing Lower immune function Reduced collagen Hair changes EPIDERMAL AGING In youth, epidermis interdigitates with dermis With aging, the interdigitations flatten, resulting in: Reduced contact between epidermis and dermis Decreased nutrient transfer Increased skin fragility Easy bruising https://commons.wikimedia.org/wiki/File:Epidermis- delimited.JPG#/media/File:Epidermis-delimited.JPG LIPIDS AND AGING Aging is associated with decreased lipids in the top skin layer Decreased sebaceous gland and sweat gland activity Reduction in SQ fat • Dryness and roughness • Decreased barrier function 2 7/23/2019 IMPAIRED HEALING AND IMMUNE FUNCTION WITH AGING Slower turnover of epidermal cells may account for slower rate of wound healing Lower number of immune antigen- presenting cells (such as Langerhans)
    [Show full text]