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342 Cards in this Set
- Front
- Back
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% of population that have a skin condition that would justify care
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30% of population that have a skin condition that would justify care
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# of patient that consult a primary care physician because of a skin problem
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1 out of 5
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% of inpatients in which skin reations to drugs occur
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3%
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consist of: macules, patches, papules, plaques, nodules, tumors, pustules, vesicles, bullae
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Primary lesions
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are important for accurate descriptions of skin lesions
Accurate descriptions relate the clinical findings to the histologic abnormality |
Primary lesions
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Are flat skin lesions that are less than 0.5cm in size
If you can palpate any part of the lesion, it is NOT this |
Macules
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Are flat skin lesions that are greater than 0.5 cm
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Patches
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are skin lesions that are palpable, raised lesions less that 0.5 cm
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Papules
If there is a part of the lesion that is raised and part that is flat, the raised part wins out Do NOT say “maculo-papular” rash |
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are skin lesions that are palpable, raised lesions that are greater that 0.5 cm
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Plaques
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are large protuberant lesions that are fuller in dimension than papules or plaques
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Nodules
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lesion is large and usually greater than several centimeters
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Tumor
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are blisters that are less that 0.5cm in size
can be found on the skin anywhere, including mucosal surfaces, scalp, hands and feet |
Vesicles
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blisters that are greater than 0.5cm in size
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Bullae
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Secondary skin lesions are those that have been altered in some way, (by the patient, natural course of the disease, physician, or treatment)
denuded areas of skin, superficial |
Excoriations
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Secondary skin lesions are those that have been altered in some way, (by the patient, natural course of the disease, physician, or treatment)
deep, denuded area of skin |
Ulceration
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include: biopsies, skin scrapings for tinea or yeast, Wood’s lamp illumination, Tzanck prep
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These tools are commonly used on a daily basis by all dermatologists
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Obtained by scraping the base of the ulceration and staining nuclei
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Tzanck preparation showing multinucleated giant cell
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No physiologic role
Important psychosocial role - Defines personality - Can define attractiveness to opposite sex - Can define success and health |
Role of hair in humans
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upper 1/3 of follicle
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Infundibulum
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Middle 1/3 of follicle
Begins below sebaceous duct to arrector pili muscle attachment |
Isthmus
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Lower 1/3 of follicle
Consists of hair bulb and matrix |
Bulbar or inferior region
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At level of the isthmus, layers of hair follicle from outermost to innermost layer:
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Surrounding connective tissue
Outer root sheath Inner root sheath l Henley’s layer, Huxley’s layer Shaft l Cuticle, Cortex, +/- Medulla |
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Scalp hair grows
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~ 0.5 mm/day
Shaving does NOT influence the growth rate of hair |
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Normal daily hair loss
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50 to 100 hairs/day
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Phases of hair growth cycle
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Anagen (growth), Catagen (transition), Telogen (resting)
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Anagen (growth) of hair
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3-5 years
90% hairs in this phase |
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Catagen (transition) of hair
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3 weeks
2% hairs in this phase |
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Telogen (resting) of hair
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3 months
8% hairs in this phase |
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Normal cycle of hair growth
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Anagen to Catagen to Telogen to Early-mid Anagen to Anagen
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Eumelanin
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Black and brown hair
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Phaeomelanin
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blonde and auburn hair
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Graying of hair
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lack of melanocyte function
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Premature graying without family history
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pernicious anemia, aging syndromes
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Poliosis - A patchy absence or lessening of melanin in hair of the scalp, brows, or lashes, due to lack of pigment in the epidermis; it occurs in several hereditary syndromes but may be caused by inflammation, irradiation, or infection such as herpes zoster
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vitiligo, alopecia areata, Waardenberg’s syndrome, Vogt-Koyanagi-Harada syndrome
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Generalized lack of hair pigment:
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albinism, Chediak-Hagashi syndrome
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Color changes
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nutritional deficiencies, phenylketonuria, chemical exposure
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Pull test - Tools for Hair and Scalp Exam
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Gently grasp 30-40 hairs between thumb and forefinger and apply even traction pulling out from the scalp
More than 2 hairs is a positive test |
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Androgen- dependent growth and development of hair in women in anatomic sites where such growth is considered secondary male characteristic
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Hirsutism
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Increased hair density or length beyond normal in any area of the body
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Hypertrichosis
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Etiology of Increased Hair Growth - Hypertrichosis
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Idiopathic
Disease associated Part of congenital syndrome |
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Etiology of Increased Hair Growth - Hirsutism
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Idiopathic
Hormone-secreting tumor Male hormone excess Medications |
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Determine underlying cause and treat cause if possible
Electrolysis: electrical current passed via probe into hair follicle, only permanent method of hair removal Hair removal lasers: long term hair loss for use in select populations Shaving, depilatories, waxing, bleaching |
Treatment for Increased Hair Growth
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Hair coming out by roots vs. breaking off
Time course loss Thinning vs. increased fallen hairs Medical history 6-12 months Medications Family history of hair loss Hair care practices |
General Approach to Hair Loss - History
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General appearance of patient
Is the hair abnormality diffuse or localized? Scarring or nonscarring? Nails, lymph nodes, rest of skin Pull test results Hair shaft microscopy Biopsy findings |
Examination for hair loss
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Usually 4mm punch biopsy is performed in area of concern
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Tools for hair and scalp exam
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Androgenetic
Telogen Effluvium Chronic telogen effluvium Alopecia Areata Traction Trichotillomania Chemical Damage |
Non-scarring causes of hair loss
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Lichenplanopilaris
Discoid lesions of lupus Psuedopalade Follicular Degeneration Misc.—sarcoid, neoplasm, infection, temporal arteritis |
Scarring causes of hair loss
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Coming out by roots versus breakage
Scarring verus non-scarring Diffuse versus localized (or patchy) Scalp only or involving other body sites |
Categories of alopecia
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Etiology remains unknown
Hereditary factors important but inheritance patterns unclear Hormones influence clinical disease |
Androgenetic alopecia
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In women: rule out congenital adrenal hyperplasia, neoplasm, drug, polycystic ovary disease
Patient younger than 20 Patient with acute onset hair loss and clear signs of virilization |
Red Flags
Androgenetic Alopecia |
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Minoxidil 2% solution
Minoxidil 5% solution Oral 5-alpha reductase inhibitors Oral Anti-Androgens Hair Transplantation Surgical flap procedures Combinations of above |
Treatment of Androgenetic Alopecia
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Autoimmune process
Common, especially in patients < age 30 Can occur in localized or generalized manner Non-Scarring form hair loss |
Alopecia areata
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Biopsy
Usually not necessary Lymphocytic peribulbar perivascular inflammation surrounding anagen follicles |
Alopecia areata diagnosis
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Corticosteroids: topical, intralesional, short oral tapers, intramuscular
Anthralin cream – keratolytic Topical sensitizers Psoralen and ultraviolet A light |
Treatment of Alopecia Areata
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A form of traction alopecia
Characterized by a compulsion to pluck one’s hair Often linked with other psychiatric diagnoses |
Trichotillomania
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Common causes include:
Medications Iron deficiency Thyroid abnormalities Post-partum alopecia Weight loss Protein calorie malnutrition Physiologic stress (fever, systemic illness, surgery) |
Telogen Effluvium
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Diffuse non-scarring hair loss over scalp
Can be acute or chronic Usually begins 2-4 months after even/exposure If active, pull test is positive (>2/20 hairs between thumb and forefinger) |
Telogen Effluvium History and Clinical Exam
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Androgens
Angiotensin Converting Enzyme inhibitors Beta-blockers Gold H2 blockers Oral contraceptives Minoxidil Retinoids Sulfasalazine Vitamin A |
Drugs Associated with Telogen Effluvium*
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Often difficult to find a cause
Stop any potential medications or recommend change to a different class If applicable arrange nutrition counseling Consider short term Minoxidil Do not attribute hair loss to just “stress” Lab evaluations as appropriate |
Telogen Effluvium Treatment
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Anagen arrest with chemotherapeutic agents, radiation
Tinea capitis (can cause scarring if very inflammatory) Traction (can cause scarring if long-standing) |
Special Cases of Non-Scarring Alopecia
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Seen rarely
Hair in the growth phase shed instead of passing into the falling out phase Most commonly due to: - Heavy metals - Chemotherapeutic agents |
Anagen Effluvium
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Hair shaft abnormality
Most commonly due to weathering from hair care practices |
Hair breakage
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Numerous types and accompanying syndromes exist
Divided into categories Structural defects with fragility of the hair shafts Structural defects without fragility of the hair shaft Miscellaneous defects Treatment: treat the underlying condition, decrease manipulation, moisturizing shampoos and conditioners |
Hair shaft abnormalities
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Common occurrence from over-processing from chemicals, heat damage
Clinical exam: Brittle broken hairs of different lenghts Usually non-scarring |
Weathering of Hair Shafts
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Inflammatory scalp disease can cause: dissecting cellulitis, acne keloidalis
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Scarring forms of alopecia
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Lupus erythematosus
Neoplasms Trauma |
Other causes of hair loss that include scarring - scarring alopecia
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Rare, recessively inherited form of condition in Pakistani kindred
Linkage on chromosome 8 Human homolog of murine gene, hairless, found Hairless likely encodes a transcription factor protein |
Alopecia Universalis Associated with Mutation in the Human hairless Gene
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Can be helpful in diagnosis of systemic disease or skin disease
Often forgotten portion of the physical exam Fungal infections extremely common especially in the elderly Acute changes may signal severe disease |
Nails
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Greater than 180 degree angle of nail
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Clubbing with Lovibond's angle
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transverse grooves on the fingernails following severe febrile disease, malnutrition, trauma, myocardial infarction, or other disorders
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Beau's lines
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tiny longitudinal subungual hemorrhages typically seen in but not diagnostic of bacterial endocarditis, trichinosis, etc.
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Splinter hemmorhages
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Suppurative inflammation of the nail fold surrounding the nail plate; may be due to bacteria or fungi, most commonly staphylococci and streptococci.
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Paryonychia
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Loosening of the nails, beginning at the free border, and usually incomplete.
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Onycholysis
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Very common fungus infections of the nails, causing thickening, roughness, and splitting, often caused by Trichophyton rubrum or T. mentagrophytes, Candida, and occasionally molds. Syn: ringworm of nails.
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Onychomycosis
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the distal 1–2 mm of the nail is of the normal pink color, but the rest of the nail is whitish, due to changes in the nail bed. Seen in patients with cirrhosis, chronic congestive heart failure, and diabetes.
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Terry nail
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division of the nail by a transverse line into a proximal dull white part and a distal pink or brown part; seen in uremia.
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Half and half nail
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A progressive condition characterized by symmetric proximal muscular weakness with elevated serum levels of muscle enzymes and a skin rash, typically a purplish-red erythema on the face, and edema of the eyelids and periorbital tissue; affected muscle tissue shows degeneration of fibers with a chronic inflammatory reaction; occurs in children and adults, and in the latter may be associated with visceral cancer or other disorders of connective tissue.
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Dermatomyositis
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periungual extension of brown-black pigmentation from longitudinal melanonychia onto the proximal and lateral nailfolds, is an important indicator of subungual melanoma. However, experience has demonstrated that this sign, although valuable, is not an infallible predictor of melanoma. Periungual pigmentation is present in a variety of benign disorders and, therefore, may lead to overdiagnosis of subungual melanoma
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Hutchinson's sign
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Actinic Keratosis
Squamous Cell Carcinoma Basal Cell Carcinoma |
Non-melanoma skin cancer (NMSC) 95%
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accumulation of mutations
+ genomic “instability” Less efficient DNA repair (bad helicases, etc) |
Carcinogenesis -
Multi-step/”multi-hit” process |
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penetrates to deep dermis
Not as effective as UVB in causing biological change Immediate tanning |
UVA
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penetrates epidermis to upper dermis
Responsible for most biological effects Reddens skin in ~6 hrs Delayed Tanning 48–72 hrs |
UVB
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Photoaging
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UVA
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Carcinogenesis
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UVB
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Pyrimidine dimers (cyclobutane and 3,4 photoproducts)
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Direct DNA damage (UVB)
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Reactive oxygen species created(H2O2, O)
Guanine most susceptible |
Indirect DNA damage (UVA)
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Direct DNA damage Mutations:
Affect cell cycle & division |
Initiation (UVB)
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Reactive oxygen species (ROS) -
Damage biological molecules |
Promotion (UVA/UVB)
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Additional mutation load
-Metastasis Loss of apoptosis |
Progression (UVB)
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Key tumor suppressor
Halts progression into S phase of damaged cells Promotes proofreading of damaged DNA Most commonly mutated gene in human cancer Expression elevated in Caucasians with chronic sun exposure 70% have clones with missense mutation Severe DNA damage=apoptosis Mutated clones are resistant to apoptosis |
p53
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Palmoplantar pits, odontogenic keratocysts, calcification of the falx cerebri, bifid ribs, meduloblastoma, macrocephaly, frontal bossing/wide nasal root/coarse facies
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Gorlin’s syndrome (Basal Cell Nevus Syndrome)
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Important in embryogenesis and many tumors (BCC, esp.)
Highly conserved (studied in Drosophila sp.) |
Patched - Hedgehog Signaling
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>1,000,000 estimated in 2007
(~2,000 deaths) Nearly $2.5 billion in 2005 (mostly direct costs) ~60,000 estimated in 2007 (>8k deaths) > $3 billion in 2005 (mostly indirect) Special populations: Outdoor workers OTR population ~6% die from cutaneous SCC |
Scope of NMSC and melanoma problem in US
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Skin Cancer Incidence Is a Function of
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Age
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“Resistant” versus “Proof”
Physical (Titanium Dioxide, Zinc Oxide) Scatter, messy, less irritancy Chemical (avobenzone, cinnamates, salicylates) Absorb, poor photostability (unless complexed) ?Increased risk of skin cancer?????? Ecamsule (Mexoryl SX®)---Anthelios® from L’Oreal |
Sunscreens
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SPF system based on ratio of MED in protected skin to unprotected skin
SPF measures only erythema, not other deleterious effects (collagen, immunosuppression, etc.) SPF based on application of 2mg/cm2 Typical application 0.5-1mg/cm2 UVA coverage currently designated by “Broad Spectrum” labeling Bottom line = only work if applied properly |
SPF and sunscreens
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Pink, relatively poorly demarcated, scaly patches & plaques on the sun-exposed skin
Symptomatic at times Increasing prevalence with age (>80% over 60yo) |
Actinic Keratoses
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Prognosis:
Spontaneous regression Persistence Evolve into SCC 1-3% chance progression to invasive SCC Comparison with CIN staging SCC may occur de novo |
Actinic Keratoses
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Lies between normal skin and squamous cell carcinoma
Restless epithelium concept |
Actinic Keratosis: Natural history
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Cryotherapy for an isolated lesion
Field treatment: topical 5-fluorouracil cream Aldara (imiquimod) TCA Photodynamic Tx Broad spectrum sunscreens Prevents and allows resolution Surgery? |
Actinic Keratosis: Treatment
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In-situ and invasive forms
Painful, erythematous keratotic plaques/ nodules sometimes with ulceration Head, Neck, arms/hands of men Chronic ulcers HPV link (immunosuppressed) 65-fold increased risk in OTR |
Squamous Cell Carcinoma
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Risk Factors:
Skin type UV or ionizing radiation Cumulative and recent sunlight (esp. AKs) Heredity (genomics) Smoking? Arsenic exposure HPV Immunosuppression & OTRs |
Squamous Cell Carcinoma
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> 2cm 9% vs 30%
>4mm invasion Anatomic location 11% lip Immunosuppression ~6% of mortality in OTRs Perineural involvement Bad histology Recurrence 25-45% Etiology~20% (Marjolin’s ulcer) |
SCC: Metastases
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Standard Excision
Curettage and Electrodesiccation Mohs Imiquimod Cryosurgery Radiation Therapy PDT Laser 5-FU |
SCC: Treatment
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Most common malignancy period
Incidence near 1 million annually 80% of all nonmelanoma skin cancer Rare Syndromes: Gorlins(BCNS) Rombo XP Bazex Albinism(OCA1-4) |
Basal Cell Carcinoma
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Risk factors: skin type, UV or ionizing radiation exposure, heredity, arsenic exposure, immunosuppression?
**10 fold increase for 2nd occurence** Many flavors: nodular, pigmented, cystic, superficial, morpheaform |
Basal Cell Carcinoma
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Curettage and Electrodesiccation
Standard Excision Mohs Imiquimod Cryosurgery Radiation Therapy PDT Laser 5-FU No Treatment |
BCC: Treatment
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Excision with margin control
99% cure long term Tissue sparing 2 vs 4-6 mm margins Abused? Fellowship training Indications: Recurrent tumors Location (peri-nasal, orbital, auricular, oral, hands, genitalia) Indistinct margins Aggressive histology (high recurrence risk) |
Mohs Micrographic Surgery
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a nevus exceeding 5 mm in diameter, with irregular, indistinct, or notched borders and mixed tan-to-black and pink-to-red color. Microscopically these are basally nested and scattered intraepidermal melanocytes with hyperchromatic nuclei larger than those of basal keratinocytes. If multiple and associated with a family history of melanoma, these nevi have a high risk of malignant change, but isolated dysplastic nevi in the absence of a family history of melanoma are less frequently premalignant.
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Dyplastic nevi
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A benign, acquired brown macule resembling a freckle except that the border is usually regular and microscopic elongation of rete ridges is present, with increased melanocytes and melanin pigment in the basal cell layer
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Lentigo
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Freckle
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Ephelides
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a nevus first seen as an irregular pigmentation of the shoulders, upper chest, or scapular area, gradually enlarging irregularly and becoming thickened and hairy
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Becker's nevus
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pigmentation of the sclera and skin around the eye, usually unilateral; seen especially in women of Asian descent
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Nevus of ota
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a dark blue or blue-black nevus covered by smooth skin and formed by heavily pigmented spindle-shaped or dendritic melanocytes in the reticular dermis
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Blue nevus
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a benign, sometimes multiple, melanocytic nevus in which involution occurs with a central brown mole surrounded by a uniformly depigmented zone or halo
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Halo nevus
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a form of (flat) nevus pigmentosus
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Nevus spilus
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a benign, slightly pigmented or red superficial small skin tumor composed of spindle-shaped, epithelioid, and multinucleated cells that may appear atypical; most common in children, but also appearing in adults
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Spitz nevus
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a melanocytic nevus that is visible at birth, is often larger than an acquired nevus, and more frequently involves deeper structures. Larger than 20.0 cm in diameter have a 6–12% lifetime risk of developing melanoma.
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Congenital nevus
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Asymmetry
Border Irregularity Color variation Diameter Evolution |
ABCDE’s of Melanoma
*not fool-proof |
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Most occur on the face
Usually start as a noninvasive process Any thickening suggests the progression to invasive melanoma |
Lentigo Maligna Melanoma
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Nevi may meet criteria
History of change or symptom most important |
Superficial spreading melanoma
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Isolated nodule without typical pigment spread
Poor prognosis |
Nodular melanoma
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Melanoma of the volar hands and feet
Radial growth first |
Acral-Lentiginous Melanoma
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Variant of acral-lentiginous melanoma
Manifested by streaks of pigmentation on the nail as well as pigmentation emerging from under and around the nail |
Nail bed melanoma
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an anaplastic melanoma consisting of cells derived from melanocytes but not forming melanin.
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Amelanotic melanoma
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Surgical treatment
Adjunctive therapy |
Melanoma treatment
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Early identification and removal are key
Appropriate surgical margins determined by tumor thickness The thicker the tumor, the worse the prognosis No controlled study has shown elective lymph node dissection improves survival Recurrence has been noted decades after removal |
Surgical treatment of melanoma
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No overall survival benefit demonstrated
May provide prognostic information Significant morbidity with basin dissection Less sensitive in H&N cases of melanoma In the end, a highly individual decision |
Sentinal Lymph Node Biopsy
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Circumscribed
Fluid containing Epidermal elevations Size < 5 mm Lose identity in short time bullae ( > 5 mm) or pustule |
Vesicles
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Rounded or irregularly shaped lesions
Fluid filled elevations serous or seropurulent material 0.5 cm < X < 1.0 cm Y > 1 cm Unilocular or multilocular |
Bullae/blisters
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Circumscribed
Raised lesion May vary in size and shape Contains a purulent exudate Pus is composed of leukocytes with or without cellular debris, may contain bacteria or may be sterile |
Pustules
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Herpes Simplex
Varicella Herpes Zoster Scabies Dyshidrosis Contact Dermatitis |
Diseases with Vesicles
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X-1 (orolabial); X-2 (genital)
Clinical: clustered small vesicles Recurrent episodes Course: 5-14 days per episode Viral shedding until crusted 4-7 days Genital version asymptomatic shedding between outbreaks Diagnosis: Tzanck smear, culture, PCR Treatment: sunscreen, symptomatic, acyclovir, famciclovir, valacyclovir |
Herpes Simplex Virus
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“Cold sore” or “Fever blister”
HSV-1 in 95% of cases Prodrome: tingling, itching or burning Variable symptomatology: local discomfort, headache, nasal congestion, flu-like symptoms Sun exposure trigger Recurrences: cheeks, eyelids, earlobes, intraorally |
Orolabial herpes
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HSV-2 in 85% of cases
Spread by sexual contact Primary infection: grouped blisters and erosions in the vagina, rectum, penis x 7-14 days Fever, flu-like symptoms, vaginal pain and dysuria Management should be individualized |
Genital herpes
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Tenderness and erythema on the lateral nail fold
Deep-seated blisters develop 24-48 hours later 55% of cases between 20-40 yo More often seen in dentist, dental hygienists and health care workers |
Herpetic Whitlow
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Common cause of blindness in USA
Punctate or marginal keratitis or dendritic corneal ulcer disciform keratitis scars Topical corticosteroids perforation of the cornea Recurrences are common |
Herpetic keratoconjunctivitis
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90% of cases in children < 10 yo
Incubation period is 10-21 days Transmission: direct contact with lesions and respiratory route Clinical: Fever, malaise, single vesicles on trunk and face “Dew drops on a rose petal” Spreads out as first lesions heal Old lesions become umbilicated |
Varicella Zoster Virus - Chicken Pox
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Complications: secondary bacterial infection (give antibiotics for this), osteomyelitis (rare), pneumonia (adults)
Treatment: early acyclovir in adolescents and adults, topical antipruritic lotions, oatmeal baths, keep environment cool Aspirin is contraindicated Reye’s syndrome |
Varicella (Chicken Pox)
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After natural infection or immunization, virus remain latent in the sensory dorsal root ganglion cells
Reactivation immunosupression, age Clustered small vesicles along a dermatome Pain may precede the eruption May have lesions outside the dermatome |
Varicella Zoster Virus - Herpes Zoster
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Course: 10-21 days until clear
Viral shedding the first week Pain may be severe (burning, lancinating or triggered) May recur in 5% of patients Post-herpetic neuralgia more frequent in patients over the age of 50 |
Herpes Zoster
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Diagnosis: clinical, Tzanck prep, culture? PCR, biopsy
Treatment: analgesics, thymidine kinase inhibitors (acyclovir, valacyclovir, famciclovir), antibiotics (for secondary infection) Post-herpetic neuralgia: local applications of heat, capsaicin, lidocaine 10% gel, nerve blocks, systemic steroids, tricyclic antidepressants, gabapentin (typical GABA anti-epileptic with other uses) |
Herpes Zoster
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Disease caused by mite Sarcoptes scabiei
Clinical: itchy red papules and vesicles Web spaces, body folds, genitalia, breasts, elbows, wrists, ankles Course: 2-6 weeks after exposure Diagnosis: scabies prep, response to treatment Treatment: lindane, permethrin 5%, Crotamiton, thiabendazole, sulfur 10%, ivermectin 200 microgram/kg |
Scabies
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Disease caused by mite Sarcoptes scabiei
Clinical: itchy red papules and vesicles Web spaces, body folds, genitalia, breasts, elbows, wrists, ankles Course: 2-6 weeks after exposure Diagnosis: scabies prep, response to treatment Treatment: lindane, permethrin 5%, Crotamiton, thiabendazole, sulfur 10%, ivermectin 200 microgram/kg |
Scabies
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Pompholyx
Etiologic factors: psychogenic, primary fungal, fungal id, drug reaction and idiopathic Sweat glands play a secondary role Itchy, tiny, clear vesicles on sides of digits, palms and soles Course: episodic flare, related to stress? Skin may become dry, cracked, flaky |
Dyshidrotic Eczema
Diagnosis: clinical Differential diagnosis: contact dermatitis, palmo-plantar psoriasis Treatment: topical steroids, tannic acid, tar, light treatments, methotrexate for severe disease, antibiotics for secondary infection, avoid water and stress? |
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Clinical: angular or linear distribution, history of exposure
Course: lesions develop within 1-10 days Causes: poison ivy, oak, sumac Nickel, rubber, thimerosal Neomycin (use polysporin NOT neosporin), latex preservatives Rx: remove agent, corticosteroids |
Allergic Contact Dermatitis
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Bullous Impetigo
Erythema Multiforme Pemphigus vulgaris Bullous Pemphigoid Porphyria Cutanea Tarda |
Bullous Diseases
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common, highly contagious bacterial skin infection of children
Clinical: single or few blisters, annular lesions anywhere on body (face and hands) Diagnosis: Gram stain, culture S. aureus Treatment: mupirocin 2% (Bactroban), systemic antibiotics Complications: Staphylococcal scalded skin syndrome, glomerulonephritis, scarring |
Bullous Impetigo
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Acute, self-limited, recurrent disease
Clinical: abrupt onset of symmetrical fixed red papules 1-2 cm target (Bullseye) lesions on dorsa of hands, forearms, palms, neck, face and trunk. Mucosal involvement occurs 25% Precipitating factors: Infections: herpes simplex (50%), Orf (virus), Histoplasma capsulatum, mycoplasma pneumoniae Radiation therapy Medications: (sulfa) |
Erythema Multiforme
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Autoimmune disease
Equal frequency in men and women; 5th or 6th decades Thin-walled, big flaccid, easily ruptured blisters Mouth involved (60%) then body groin, scalp, face, neck, axillae or genitals |
Pemphigus Vulgaris
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Nikolsky sign: absence of cohesion in the epidermis; lateral pressure on unblistered skin and having the epithelium shear off
Direct immunofluorescence shows intercellular IgG staining Antibodies to desmoglein 3 Elisa Treatment silver sulfadiazine 1%, systemic corticosteroids, other immune modulating agents (azathioprine, cyclophosphamide, methotrexate) |
Pemphigus Vulgaris
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Autoimmune disease, affects the elderly
Intense pruritic eruption with large tense blisters (subepidermal) Most often begins on lower extremities. Other sites: groin, axillae, flexor surfaces of forearms Associated with diabetes mellitus, rheumatoid arthritis, dermatomyositis, ulcerative colitis, lymphoproliferative disorders |
Bullous Pemphigoid
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Circulating basement membrane zone antibodies (IgG) 70%
Direct immunofluorescence shows linear deposits of IgG and C-3 along the BMZ Indirect immunofluorescence on salt-split skin Treatment: corticosteroids (lower doses than PV), immunosuppressives (azathioprine, methotrexate, mycophenolate mofetil) |
Bullous Pemphigoid
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Metabolic disease: abnormal porphyrin metabolism (Uroporphyrin decarboxylase)
Clinical: photosensitivity blisters, erosions on dorsa of hands and arms; heal with scarring, milia and dyspigmentation Hyperpigmentation of the face, neck and hands Increased facial hair Photosensitivity Triggered: ETOH, estrogens, iron overload (66%), hepatitis C, hepatitis B |
Porphyria Cutanea Tarda
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Diagnosis: pink or coral-red fluorescent urine (increased uroporphyrins) under a Wood’s UV light
Associated with diabetes mellitus, lupus Treatment: remove trigger, decrease iron (phlebotomy), alpha interferon for hepatitis C, antimalarials |
Porphyria Cutanea Tarda
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Acne vulgaris
Acne rosacea Folliculitis Candidal intertrigo |
Diseases with Pustules
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A chronic inflammatory disease of the pilosebaceous unit
True acne is a follicular process beginning with the comedon Rupture results in inflammation Papules, pustules, or cysts |
Acne Vulgaris
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Is the most common dermatologic condition treated by physicians in the U.S.
40-50 million individuals/year Can occur at any age predominately teens 85% of 12-24 year old 3% of 35-44 year old |
Acne Vulgaris
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Is the most common dermatologic condition treated by physicians in the U.S.
40-50 million individuals/year Can occur at any age predominately teens 85% of 12-24 year old 3% of 35-44 year old |
Acne Vulgaris
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Blackhead
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Comedone/Comedo
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According to type of lesion:
Comedonal, papulopustular, cystic According to severity: Mild, moderate, severe |
Classification of Acne
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Open comedone
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Blackhead
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Closed comedone
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Whitehead
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Topicals:
Tretinoin Benzoyl peroxide Antibiotics Azelaic acid Salicylic acid Alpha-hydroxy acids Oral: Antibiotics: doxycycline, minocycline Estrogens (oral contraceptives) Retinoids (Accutane 40 mg bid x 4 months) Antiandrogens: spironolactone |
Acne Vulgaris Treatment
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Most common in fair-skin individuals
Third or Fourth decades of life Pathogenesis related to vascular hyper-reactivity Triggers: Hot drinks, red wine, spicy food, soy sauce, oral niacin, topical steroids (think hydrocortisone in trying to treat one’s self) Rol of Demodex folliculorum and Propionibacterium acnes |
Rosacea
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Vascular: flushing and facial erythema with or without telangiectasia
Papulopustular: central facial erythema with papules or pustules Ocular: foreign body sensation, burning, dryness, itching, ocular photosensitivity, blurred vision Granulomatous: firm, brown or red papules or nodules |
Clinical variants of Rosacea
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Metronidazole 1% gel qd
Tetracycline, 250 mg bid Doxycycline, 100 mg qd Minocycline 100 mg qd Sodium sulfacetamide 10% Azelaic acid 20% bid Erythromycin 2% bid Clindamycin lotion bid Metronidazol 200 mg bid |
Rosacea Treatment
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Telangiectasias treatment
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Laser treatment
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Rhinophyma treatment
Hypertrophy of the nose with follicular dilation, resulting from hyperplasia of sebaceous glands with fibrosis and increased vascularity; a form of acne rosacea |
Laser, cryosurgery, electrosurgery
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Clinical: pustules at hair follicle, especially the extremities
Diagnosis: culture, clinical Staphylococcus aureus (normal inhabitant of anterior nares in 20% adults) Complications: rupture of follicle with carbuncle or furuncle Treatment: antibacterial soap, oral antibiotics, mupirocin; rifampin (600 mg/day 10 days) |
Folliculitis
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Typically caused by C. albicans but other species can cause infection
Clinical: groin, under breasts, abdominal fat, axillae Red, moist areas with satellite papules and pustules Diagnosis: clinical, KOH, culture Treatment: topical antifungals, Silvadene, zinc oxide, oral antifungals (fluconazole, itraconazole) |
Candidal Intertrigo
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Burns
Acute fungal infections causing tinea corporis Drug Reactions (Stevens-Johnson, TEN) Friction Insect Bites Many autoimmune blistering diseases |
Other causes of blisters
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Erythema
Urticaria Erythema multiforme Erythema nodosum Vasculitis |
Spectrum of Reactive Vascular Dermatoses
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Generalized macular and papular eruptions
1. Viral exanthems 2. Drug Eruptions 3. Other Annular X 1. X annulare centrifugum 2. X migrans 3. X gyratum repens 4. X marginatum |
Erythema
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Inflammatory reaction in the superficial dermis
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Urticaria (hives)
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Reaction in the submucosa, deep dermis, and subcutaneous tissue
Recurrent large circumscribed areas of subcutaneous or mucosal edema of sudden onset, usually disappearing within 24 hours; frequently, an allergic reaction to foods or drugs. Syn: giant hives, giant urticaria |
Angioedema
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Acute urticaria
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less than 6 weeks in duration
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Chronic urticaria
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More than 6 weeks in duration
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Epidemiology of Urticaria
|
Common - up to 15-20% of college students have had
Young adults Atopic predisposition |
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Final common pathway involves mast cell degranulation and mediator release
IgE-mediated Direct efforts on mast cells Complement (eg C5A) mediated release Facilitation of release by products of lipoxygenase pathway of arachidonic acid Autoimmunity |
Pathogenesis of urticaria
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Drugs
Foods Inhalents Systemic Disease Infections Physical Agents Insect Bites Non-immunologic causes |
Causes of Urticaria
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Classify appropriately:
24-hour rule Circle lesions When to biopsy? Avoid NSAIDs Possible autoimmunity in chronic idiopathic Realistic patient counseling Combination therapy |
Urticaria
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Drugs
Infections Associated conditions – Pregnancy, Malignancy, Collagen vascular diseases, Inflammatory bowel disease Idiopathic |
Some causes of erythema multiforme/Stevens' Johnson syndrome/Toxic epidermal necrolysis
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Looks like bruising - result of inflammation of subcutaneous adipose tissue
a panniculitis marked by the sudden formation of painful nodes on the extensor surfaces of the lower extremities, with lesions that are self-limiting but tend to recur; associated with arthralgia and fever; may be the result of drug sensitivity or associated with sarcoidosis and various infections. Deep biopsies show a septal panniculitis with infiltration by lymphocytes and scattered multinucleated giant cells |
Erythema nodosum
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Griseofulvin
Nalidixic acid (An orally effective antibacterial agent used in the treatment of genitourinary tract infections.) Phenothiazines (it serves as the parent compound for synthesis of a large number of antipsychotic compounds, including chlorpromazine, thioridazine, perphenazine, and fluphenazine.) Psoralens Sulfonamides Sulfonoureas Tetracyclines Thiazides NSAIDS |
Drugs that can cause photosensitivity
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Polymorphous light eruption
Solar urticaria Lupus erythematosus |
Some photosensitivity diseases
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ABCDs of Sun Protection
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Away from midday exposure
Block with SPF 15 or greater Cover with T-shirt or hat Discuss (speak out) with family and friends |
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Eukaryotic organisms with nucleus, nuclear membrane, ER, & mitochondria
~80,000 species of which <400 (<0.5%) are medically important <50 species cause >90% of human infections X infections = Mycoses Superficial Cutaneous Subcutaneous Invasive or disseminated Endemic (primary or systemic) Opportunistic |
Fungi
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Infections that involve internal organs (skin +/- involved)
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Invasive fungal infections (deep fungal infections or deep mycoses)
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Grow as multinucleate, branching hyphae, forming a mycelium; undergo asexual reproduction
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Filamentous fungi (moulds)
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Grow as ovoid or spherical single cells that multiply by budding & division
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Yeast
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Form hyphae at environmental temperatures but grow as yeast in the body
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Dimorphic fungi
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Many of the fungi that cause human disease are free-living organisms in the environment (e.g. Aspergillus) that may be acquired by inhalation (most common route of entry), ingestion, or inoculation thru the skin; certain of these fungi have a very restricted geographic endemicity (e.g. Coccidioides)
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Exogenous in origin - fungi
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Some fungal pathogens are part of the normal human flora (e.g. Candida) & invade when host defenses become impaired
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Endogenous in origin
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Aggressive chemoRx of malignancies
Increasing #’s of transplants Expanding usage of immunosuppressive Rxs HIV epidemic Increasing encroachment of humans into sylvan habitats |
Population of pts at risk for IFIs has expanded dramatically over past 20 yrs
As a consequence, incidence of and mortality due to IFIs has significantly increased |
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Epidemiology
Clinical features Radiographic findings Histopathology: Potassium hydroxide (KOH) Gomori methenamine silver (GMS) Periodic acid-Schiff (PAS) Culture: Sabouraud’s agar Brain heart infusion agar Serology or antigen detection |
Diagnosis of Invasive Fungal Infection
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Blastomycosis
Histoplasmosis Coccidioidomycosis Sporotrichosis Paracoccidioidomycosis |
IFIs: Endemic Mycoses
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Endemic mycoses =
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Dimorphic fungi
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Endemic to southeastern/south central US, the Great Lakes region, & near St. Lawrence River
Acquired via inhalation during outdoor activities near decaying vegetation, moist soil, or body of water |
Blastomycosis
Epidemiology |
|
|
Majority of infected pts manifest symptomatic clinical disease (≥ 90%)
Causes an acute or chronic pneumonia May disseminate to skin, bone, GU tract, or liver Mimics malignancy (esp. lung and skin) |
Blastomycosis
Clinical Features |
|
|
Smears & histopath
Broad-based budding yeasts with thick refractile walls (KOH, GMS, PAS) Culture Sabouraud dextrose agar→Grow as a mould Serology Not reliable Antigen detection Emerging utility as diagnostic test; serum & urine |
Blastomycosis
Diagnosis |
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Blastomycosis
Treatment |
Severe disease
Amphotericin B Mild to moderate disease Itraconazole (fluconazole) |
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Dimorphic fungus
SE & south central US & Great Lakes area <10% asymptomatic : >90% symptomatic Chronic pneumonia; skin Broad-based budding yeast No useful serology (? serum antigen) Amphotericin (serious) or itraconazole (mild or moderate) |
Blastomycosis
Key Teaching Points |
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Endemic to Ohio & Mississippi River valleys, Mexico, & Central America
Acquired via inhalation of conidia during dust storms or building renovation or near large quantities of bird or bat guano in caves |
Histoplasmosis
Epidemiology |
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|
Majority of infections asymptomatic; 10% of patients have clinical disease
Chronic pneumonia; mucosal ulcers Disseminated infection +/- CNS involvement in the compromised host |
Histoplasmosis
Clinical Features |
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|
Smears & histopath→Ovoid 3-5 µm yeasts with narrow-based budding; often within macrophages; seen best with GMS
Culture→Sab; grows as mould Serology→Comp fix Antigen detection→Mainstay of dx; urine > blood; sensitivity 75+% Skin testing→Useful for epi not clinincal dx |
Histoplasmosis
Diagnosis |
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Histoplasmosis
Treatment |
Majority of pts require no Rx
Severe disease Amphotericin B Mild to moderate disease Itraconazole or fluconazole |
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Dimorphic fungus
Mississippi & Ohio River valleys 90+% asymptomatic : <10% symptomatic Pneumonia; disseminated infection Small yeast often within macrophages Serum and urine antigen assays Amphotericin or itraconazole |
Histoplasmosis
Key Teaching Points |
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Endemic to southwestern US (epicenter in south central Arizona), Mexico, & S. America→Travel hx
Inhalation of arthrospores when arid, sandy desert soil is disturbed→Military maneuvers in the desert; archaeological digs; off-road riding, etc |
Coccidioidomycosis
Epidemiology |
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|
60% of infxns asymptomatic
Acute or chronic pneumonia Disseminated disease→Skin, bones and joints, CNS (most feared site – cure rate is about nil) Erythema nodosum |
Coccidioidomycosis
Clinical Features |
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Smears & histopath→Spherules & endospores
Culture→Grows on routine media as well as Sab→Mould Serology→Comp fix useful in predicting dissemination (1:16) Antigen detection→Under developement Skin testing→Useful as epidemiologic tool |
Coccidioidomycosis
Diagnosis |
|
|
“Uncomplicated” pneumonia:
“Watchful waiting” (predictors of progression) or itraconazole Progressive pneumonia or disseminated infection: Amphotericin B or itraconazole CNS infection: Amphotericin B or fluconazole |
Coccidiomycosis
Treatment |
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Dimorphic fungus
Southwestern US 60% asymptomatic : 40% symptomatic Pneumonia; CNS infection Spherules and endospores Complement fixation serology Amphotericin or itraconazole (fluconazole) |
Coccidiomycosis
Key Teaching Points |
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Yeasts:
Candida species Cryptococcus Trichosporon Moulds (Invasive filamentous fungi): Aspergillus The zygomycetes Pseudallescheria/Scedosporium Fusarium Others |
IFI: Opportunistic Mycoses
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Spectrum of infections that encompasses cutaneous, mucosal, and deeply invasive disease→Endogenous in origin
Deeply invasive infections may manifest as fungemia, disseminated disease with multiorgan involvement, or single organ disease Candida species are most frequent cause of IFI in neutropenic hosts & surgical ICU pts Candida species are the 4th most common cause of blood stream infections in US (7.6%) with an associated crude mortality rate of 40% |
Candidiasis
Overview |
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|
25-50% of Candida infections occur in pts in ICUs
C. albicans is the most common species causing infection but the non-albicans species are increasing in frequency: ? Greater risk for invasion→dissemination Higher incidence of antifungal drug resistance: C. glabrata→30% resistant to fluconazole C. krusei→91% resistant to fluconazole |
Candidiasis
Overview |
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|
Central venous catheters
Exposure to the ICU Hemodialysis (renal failure) Documented mucosal colonization Parenteral hyperalimentation Systemic antibiotics Abdominal surgery Neutropenia >1 wk Immunosuppressive therapy |
Candidiasis
Risk Factors for Invasive Infection |
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|
Identification of “typical” clinical features
Biopsies of involved tissues that reveal yeast and/or pseudohyphae Cultures of blood or involved tissues NO useful serologies or antigen detection techniques |
Candidiasis
Diagnosis |
|
|
Amphotericin B (or lipid formulations), azoles (fluconazole, itraconazole, voriconazole), or echinocandins (caspofungin, micafungin, anidulafungin)
Choice of agent and duration of Rx dependent upon type disease, severity, & causative species |
Candidiasis
Treatment |
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Yeast
Normal human flora (GI, skin) Colonizer or pathogen Associated with ↓PMNs, ↓CMI, or ICU stay Mucosal disease; fungemia; visceral abscesses Yeast &/or pseudohyphae No useful serologies; culture of blood or tissue Amphotericin, azoles, echinocandins |
Candidiasis
Key Teaching Points |
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Aspergillosis is the most common form of invasive filamentous fungal disease (IFFD) in humans, with A. fumigatus the most common causative agent (Property of angioinvasion)
Inhalation of airborne spores is the usual route of infection (exogenous in origin)→Pneumonia is most common type of invasive aspergillosis (IA) (>50% of pts) Almost all pts with IA have an underlying immunocompromising condition (98%); < 5% of disease occurs in “normal hosts” |
Aspergillosis
Overview |
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Allergic bronchopulmonary aspergillosis
Aspergilloma (fungus ball) Semi-invasive (chronic necrotizing) aspergillosis Invasive pulmonary aspergillosis |
Pulmonary Aspergillosis
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Rapidly progressive disease, often disseminated, occurring in markedly immunocompromised pts, esp those with prolonged & severe neutropenia
Classic radiographic findings include a pleural based infiltrate, the “halo” sign (90%), or the “air-crescent” sign (~60%) Organisms may or may not be demonstrable in sputum or bronchoalveolar lavage fluid specimens |
Pulmonary Aspergillosis
Invasive Pulmonary Aspergillosis (IPA) |
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|
Clinical features and radiographs may suggest diagnosis but are not definitive
Whenever possible, dx should be based on compatible tissue histo + positive cx Remember that tissue histology alone is not specific for Aspergillus Serum antigen detection (galactomannan – part of cell wall) is an evolving diagnostic test |
Invasive Aspergillosis
Diagnosis |
|
|
Septated, acute branching hyphae - looks like an "A"
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Aspergillosis
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Primary Rx of proven or probable dz
Voriconazole Salvage Rx for non-responders Lipid formulation of Amphotericin B Caspofungin (Micafungin) Itraconazole Combination therapies Role of surgery w/pulmonary & sinus dz |
Invasive Aspergillosis
Treatment |
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Mould
Ubiquitous in the environment→Spore Opportunistic pathogen→↓PMNs>↓CMI Pneumonia>sinusitis>other Septated hyphae w/ acute angle branching Galactomannan antigen assay Rx: Voriconazole>Ampho>Caspo or Itra |
Aspergillosis
Key Teaching Points |
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|
Absence of primary skin lesions
Usually extensive and symmetric Insidious onset, progressive |
Pruritis with Systemic Disorder
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1. Endocrine
Diabetes mellitus - 5%, though vaginal itching common 20 Candida Hyperthyroid > hypo - 10% Hypoparathyroidism - 15% have Candida 2. Hepatobiliary disease Obstructive biliary disease of any cause Primary biliary cirrhosis Pruritus of pregnancy 3. Chronic renal disease - 50% 4. Lymphoproliferative Hodgkin's Disease - 25% Chronic lymphocytic leukemia Mycosis fungoides (cutaneous lymphoma) 5. Lots of others |
Systemic causes of Pruritis
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|
Collagen vascular disease (lupus, dermatomyositis, scleroderma)
|
Nail fold telangiectasia
|
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apparent leukonychia with white bands parallel to lunula of the nails, seen in hypoalbuminemia.
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Muehrcke Bands
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horizontal white bands of the nails seen in chronic arsenical poisoning, and occasionally in leprosy.
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Mees lines
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|
Growth occurs from matrix
Growth 0.1 mm per day (3 mm/month) Calcium content low Gelatin does not - nail growth or strength |
Nail growth
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Genetic, especially in pts. with Medit. background
Porphyria Cutanea Tarda Cushing's Disease or Syndrome Acromegaly Virilizing Syndrome - ovarian, adrenal tumors Polycystic ovary syndrome Anorexia nervosa Drugs |
Hirsutism and Hypertrichosis causes
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Red Skin
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Erythema
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Scaly skin
|
Hyperkeratosis
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|
1) Primary epidermal process- Proliferation (rapid epidermal growth) e.g. psoriasis
2) Secondary epidermal repair - after any "bright red rash" e.g. peeling after sunburn or drug eruption |
SCALE - epidermis is involved in the pathologic process
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|
This is a common, inherited problem often in association with other related allergic diseases such as asthma and hayfever
All patients have itchy skin Dry skin Minor irritants can cause significant itch, starting an itch-scratch cycle Prone to Staphylococcal overgrowth |
Atopic Dermatitis
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|
Number one symptom in dermatology
|
Itch
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|
Prevalence of increased in the last 40 years reaches 10-17% of population (especially in Western world).
Much variation in different countries; western industrialized countries have higher rates. |
Epidemiology of Atopic Dermatitis
|
|
|
Distribution of lesions varies with age
Early infancy: Scalp involvement face and chins and extensor areas. Childhood; Prominent flexural areas; antecubital fossa and popliteal fossa, neck wrists. Adolescents: similar to childhood Adults: nummular (discoid or coin-shaped) eczema, Lichen simplex chronicus (a thickened area of itching skin resulting from rubbing and scratching) |
Clinical presentation of Atopic Dermatitis
|
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|
thickening of the skin due to repeated scratching
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Lichenification
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Generalized erythroderma; All body involvement requires occasionally hospitalization and aggressive systemic therapy
|
Severe form of Atopic Dermatitis
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|
Is defined clinically as generalized redness and scaling of the skin
Systemic manifestations include peripheral edema, tachycardia, loss of fluid and proteins, and disturbances in thermoregulation Has multiple etiologies; the most common causes are atopic dermatitis, psoriasis, cutaneous T-cell lymphoma (CTCL), and drug reactions |
Erythroderma
|
|
|
Genetic disease with multiple genes involved
Mutation in Fillagrin protein gene part of the skin barrier function Increased IgE Environmental factors: Improved hygiene in infancy and the protection by early use of antibiotics promote the development Endogenous antimicrobial peptides are low in condition (definsin, cathelicidins) |
Advances in Pathophysiology – Atopic Dermatitis
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Moisture the Skin
Avoid irritants and harsh soaps Topical mild to moderate corticosteroid treatments Topical immunomodulators: Ascomycins; tacrolimus pimecrolimus Oral antibiotics for acute flare ups Oral sedating anti-histamines – better sleep- less itch |
Mainstay of treatment for atopic dermatitis
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|
Atrophy: thinning of the skin
Striae: stretch marks Telangiectasis: prominent fine blood vessels Systemic effects are unusual but can occur with large quantities applied for long periods |
Side effects: topical corticosteroids
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|
|
90% clear over 15 years
Most have manifestations of "sensitive skin" |
Prognosis
|
|
|
Prescribing the right quantity helps with patient compliance
In general, patients prefer to use creams For dry, scaly rashes, ointments are beneficial Patient education may improve compliance |
Patient compliance required for optimal treatment of AD
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|
Common 2-3% of population
Proliferative epidermal immune disorder Scalp, Extensor body surfaces: knees, elbows 10% may develop arthritis |
Psoriasis
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|
|
Psoriasis type:
erythematous scaly plaques: most common type |
Plaquae
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|
Psoriasis type:
small scaly papules, abrupt onset after Strep infections |
Guttate
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|
Psoriasis type:
sterile pustules on red scaly plaques |
Pustular
|
|
|
Psoriasis type:
Involvment of all body (like a burn) - this can be life threatening |
Erythrodermic
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|
refers to skin lesions appearing on lines of trauma.
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Koebner phenomenon
|
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|
patients tend to have pitting in the nails
|
Psoriatic arthritis
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|
Pathophysiology: immune mediated disease: T cells involved
Hyperproliferation of keratinocytes: 10 times faster than normal→scales Massive invasion by neutrophils |
Psoriasis
|
|
|
Anti inflammatory and anti-proliferative topicals:
Topical Corticosteroids Vitamin D Tar & Anthralin Salicylic acid Phototherapy: UV-B Psoralen + UVA Systemic therapy: Methotrexate Oral Retinoids (vitamin A Analogues) Biologic Therapies: 2 major targets T cells and TNF- alpha |
Psoriasis treatment
|
|
|
Red scaly rash on face around perinasal areas and eyebrows, scalp and ears
Common Aggravated by stress Common in atopic eczema |
Seborrheic Dermatitis
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|
"Cradle cap" in infants
Worse with mental/physical stress Neuropsych patients Maybe severe in HIV infection |
Seborrheic Dermatitis variants
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|
|
Reactive epidermal proliferation to a normal skin organism (Pityrosporum yeast)
Antiproliferative treatment: Tar Topical steroids Antifungal: Selenium Zinc pyrithrione Ketoconazole |
Seborrheic Dermatitis
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|
Clinical:
red scaling ring or serpiginous more scale at edge |
Dermatophyte fungus
tinea, ringworm |
|
|
Scalp- tinea capitis
Feet- tinea pedis Hands- tinea manum Groin- tinea cruris Whole body- tinea corporis Nails- Onychomycosis |
Variants of Dermatophyte infections by body sites
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|
In kids
Patchy hair loss with itch Mild scale to severe inflammation Severe forms: kerion with pustules crusting and oozing Systemic oral medication: griseofulvin USA- Tr. Tonsurans |
Tinea capitis
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|
Rings: annular - circinate
Asymmetric Edge more distinct than the rest Scaling more obvious at the edge Itch |
Tinea corporis
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|
“Jock itch”- inner thighs spares the scrotum and genitals
Bilateral M>>F Common in adults rare in children Common in obese |
Tinea Cruris
Dermatophyte won’t grow in scrotum/genitals due to lower temperature. Remember, though, candida can grow on genitals. |
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|
Chronic - powdery scale of web spaces and toes
Acute - red, vesicular itchy in arch and webs if weepy, painful, smelly - may have bacterial mixed infection *uncommon in kids |
Feet - tinea pedis, athlete's foot, jungle rot
more prone on third and fourth toe webs |
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|
nails
many patterns hard to treat |
Onychomycosis
|
|
|
Fungus thrives on keratin protein of skin, hair, nails
Evokes mild inflammatory (red, itchy) and proliferative (scaly) response Variable immune response to infection |
Tinea/dermatophyte fungus
Pathophysiology |
|
|
Clinical diagnosis
Scrape for KOH (potasium hydroxide) Look for Hyphae |
Tinea/Dermatophyte identification
|
|
|
Topicals:
Azoles (miconazole, ketoconazole) Terbinafine (Lamisil) Orals: Griseofulvin (Best for scalp, not effective for nails) Terbinafine (best for nails and body) Azoles |
Treatment of tinea/dermatophyte infection
|
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Red+ scaly+ satellite pustules
|
Candidal intertrigo
|
|
|
Slightly red+ slightly scaly + hyperpigmentation or hypopigmentation
|
Tinea versicolor
|
|
|
Spaghetti and meatballs on microscopy
|
Hyphae and spores of tinea versicolor
|
|
|
Sun exposed areas: face, chest
Plaques with central atrophy and scarring Scalp involvement: with scarring hair loss+ alopecia Treatment; Sun protection Antiinflammatories: Topical Corticosteroids Hydroxychloroquine : Plaquanil |
Chronic Cutaneous Lupus: Discoid lupus erythematosus (DLE)
Very common in African Americans |
|
|
Slip
Slop Slap |
Slip - on a shirt
Slop - on some sunscreen Slap - on a hat |
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|
315 to 400 nm
|
UVA range
|
|
|
280 to 315 nm
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UVB range
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Wavelength of Light:
Longer wavelengths penetrate deeper Peak DNA absorption in UVB range Number of photons: Each photon hit is a probabilistic event No good epidemiologic evidence causally links burns with cancer |
Influences the DNA damage probability
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In the U.S., sunscreens are measured with Sun Protection Factor (SPF)
Assumptions include: Solar simulator Product applied at 2.0 mg/cm2 (Europe 1.5 mg/cm2) Measurements without sweating, water exposure, rubbing of clothing |
SPF assumptions
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SPF
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[Solar Simulator Dose to Burn With Sunscreen]/
[Solar Simulator Dose to Burn Without Sunscreen] |
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refer to UVB only and not UVA
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For practical purposes, SPF measures
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Addition of UVA blockade, 0 to 4 stars
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Proposed FDA regulations
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are an adaptive mechanism that allows for cellular auto-destruction in the event of high intensity UV exposure
The epidermis kills itself – dead cells don’t reproduce Suberythemogenic doses (UV doses insufficient to cause cellular death) cause damage DNA of cells |
Burns Are Painful, But Not Likely Harmful
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All of the cellular damage and DNA seen in sunburns occurs with either suberythemogenic UVA or UVB
Suberythemogenic doses of UVA and UVB induce cancer in all animals studied The DNA does not know whether sufficient photons have been absorbed to cause vasodilation |
Damage Occurs Before You Are Red
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215 subjects ages 18 to 83 years with a wide range of sunscreen experience
Sunscreen given with fluorescent dye, subjects told to apply it normally Photographic interpretation by 4 physicians: Most misapplied sunscreen Neck, temples, and ears had poorest coverage |
People Don't Adequately Cover Skin
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SPF 50 applied at at 0.5 mg/cm2 =
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SPF 2.7
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Products require 15 to 30 min to soak into the skin
I have personally observed numerous MDs and PhDs apply product to themselves (or kids) and then immediately jump into the pool Excellent way to remove unwanted product |
People don't let it soak in
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8 patients with xeroderma pigmentosum who practiced intensive sun protection (motivated!)
Patients all wore protective clothing & sunscreens Results Mean values of serum 25-OH D were low normal 1,25-(OH)2D, calcium, ionized calcium and PTH levels were normal |
Vitamin D and sunscreen
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10 sunscreen (SPF 15) users compared with 18 controls over 2 years
Bone mass evaluated each season Findings: no significant differences between groups throughout the study |
Sunscreen and bone mass
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Wrinkling, lentigenes, and skin cancers occur overwhelmingly on exposed skin
Skin cancers are uncommon in covered areas - average weight T-shirt provides SPF of about 5 Wang J Am Acad Dermatol 2001 Skin cancers are rare in double-covered areas (e.g., bra and underwear areas) People who consistently wear hats decrease their chance of getting skin malignancies |
Physical blockade works
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A study assessed efficacy of products to a variety of natural sunlight spectra
The products tested always provides less protection in natural sunlight, and the deviation from labeled value is greatest when the sun is low in the sky The maximum deviation from labeled value is a factor of 2 |
Solar Simulators don't Mimic Natural Sunshine
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There is ample evidence that nonmelanoma skin cancer is prevented by solar protection
There is no evidence that melanoma is prevented by solar protection: Melanoma is multifactorial, and UV exposure only plays an important but limited role |
Protection from sunshine has an effect on NMSC
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Randomized controlled trial of a sunscreen (SPF 17) in Australia for one summer
Mean number of AKs increased by 1.0 per subject in the control group and decreased by 0.6 in the sunscreen group There was a significant dose-response relationship between sunscreen use and AK prevention |
Sunscreens reduce actinic keratoses
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Contact or photocontact allergy in a study was found to be most likely due to
Oxybenzone Isopropyl debenzoylmethane |
Sunscreens: Cause Allergic Contact Disease
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I have removed over 6,000 skin cancers in those with European ancestry, and 7 in those of African ancestry
Patients with African ancestry look young Most people with African skin maintain an SPF of about 5 for life That is, the skin gets as much ultraviolet in 350 yrs as a person of Celtic ancestry gets in 70 yrs Lesson: a real SPF=5 is a lot ! Look under a farmer’s t-shirt |
African skin and sun protection
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Three triathletes in the 1999 Ironman Triathlon World Championships (3.9 km swim + 180 km bike + 42 km run) in Hawaii studied with UV dosimeters
Mean personal UV dose was 8.3 MED, corresponding to 0.8 to 1.3 MED/hr Athletes were sunburned despite use of water-resistant sunscreen (SPF 25+) |
Athletes and sun exposure risk
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Windburn was invented by doctors in an era prior to the recognition that UV was responsible
What we tell patients today, right or wrong, will persist for decades |
Windburn Does Not Exist & Never Has
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Tans do confer some solar protection
Tans documented to provide a mean SPF of 4 Those who tan easily & darkly are most protected People who minimally tan or freckle: big trouble Many stop all solar protection approaches when tan, yet damage continues – myth of base tan |
Myth of tan protection
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Unlike sunshine, tanning units operate 365 days/yr
People can increase skin cancer risk by 2 Most people display reasonable modesty in sunshine, but expose all in tanning units Will we need to check under bra & panty areas in the future? |
Risks of tanning beds
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Hats and protective clothing work !
Sunscreens For prolonged exposure (>30 min), use a broad spectrum sunscreen with SPF ≥ 30 Use a lot & use it often For daily use for indoor workers, SPF ≥ 15 Avoid exposure 10:00 am to 2:00 pm whenever possible |
Sun protection recommendations
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This is nonpalpable. Causes include: quantitative platelet defects (e.g. chemotherapy, idiopathic thrombocytopenic purpura, etc.), qualitative platelet defects (e.g. aspirin therapy), or reduced connective tissue support (e.g. solar purpura, corticosteroid therapy, Ehlers Danlos syndrome)
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Non-inflammatory purpura
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inflammation of dermal blood vessels with histopathologic “leukocytoclastic vasculitis”. This is a combination of fibrinoid necrosis of blood vessel walls, extravasation of erythrocytes, and breakdown of neutrophils. This can be divided into small vessel (target is a post capillary venule) and larger vessel (target is a muscular artery). The mechanism probably involves circulating immune complexes.
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Inflammatory purpura (vasculitis)
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Palpable purpura on dependent sites
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Small vessel vasculitis
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Loss of significant "wedges" of tissue
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Larger vessel vasculitis
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The extent of the process should be assessed by thorough history and physical examination and screening laboratory assessment such as urinalysis, complete blood count, and erythrocyte sedimentation rate.
The underlying cause (i.e. the antigen in the circulating immune complexes) is identified in only 50% of patients. Causes include infection (bacterial - e.g. streptococcal antigens, viral - e.g. hepatitis B or hepatitis C, fungal, rickettsial); drugs; diseases associated with immune complexes (e.g. systemic lupus erythematosus, lymphoma, inflammatory bowel disease, chronic active hepatitis, etc.). |
Evaluation of inflammatory purpura
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If cutaneous only then no therapy required. Systemic corticosteroid therapy, immuno-suppressive therapy (e.g. azathioprine, cyclophosphamide), and plasmapheresis have been used in severe systemic cases.
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Therapy for inflammatory purpura
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1.Etiology - Unknown. 1) Primary vascular disorder, 2) abnormality of connective tissue formation, 3) autoimmune disease
2. Incidence -F:M= 3:1, 2.7 new patients per 1 million population. Onset often 30-50 years of age. 3. Clinical Features - Skin involvement almost always present. High incidence of Raynaud’s phenomenon. Characteristic facies with shiny bound skin on forehead, pinched nose, mouth with constricting radial furrows. Telangiectatic mats. Sclerodactyly of hands. Calcinosis of fingers, elbows. Periungual telangiectasia, “Salt and Pepper” hypo and hyperpigmentation. CREST - calcinosis, Raynaud’s, esophageal dysmotility, sclerodactyly and telangiectasia - less fulminant course often than rapidly progressive, truncal pattern: Esophagus - dysmotility leads to reflux and stricture; also intestinal involvement Lung - restrictive disease and impaired diffusion capacity Cardiac - pericarditis, arrhythmias Renal - malignant hypertension 4. Laboratory: CREST Patients - anticentromere antibody |
Progressive Systemic Sclerosis (Scleroderma)
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No specific treatment. Emollients to skin. Physical therapy to prevent disuss atrophy. Minipress 1 mg b.i.d. orally (or Nifedipine or Captopril) for Raynaud’s. Penicillamine under investigation.
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Therapy for Scleroderma
Death can occur from cardiac or renal disease |
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Definition - ARA criteria - primarily guidelines, cannot be absolute. Do not include many newer tests. Four or more criteria required:
1. Malar rash 2. Discoid lupus 3. Photosensitivity 4. Oral ulcers 5. Arthritis 6. Proteinuria > 0.5 g/day, or cellular casts 7. Seizures or psychosis 8. Pleuritis or pericarditis 9. Hemolytic anemia or leukopenia or lymphopenia or thrombocytopenia 10. Antibody to DNA or Sm antigen or the presence of LE cells or a biologically false positive VDRL 11. Positive FANA (fluorescent antinuclear antibody) |
Systemic Lupus Erythrematosus
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Etiology - Immune complex role in pathogenesis of many systemic and cutaneous (i.e. vasculitis) manifestations is well studied. UV light - DNA produced in epidermis - Possible cytotoxic T-cell effect on the epidermis. Genetic factors including complement deficient families. Drug induced especially hydralazine and procainamide, INH, dilantin, penicillamine. Sun exposure is a provoker.
Incidence - 27.5/million for white females, 75.4/million for black females. F:M=8:1 (peak at third decade). Higher male percentage in children and elderly |
SLE etiology and incidence
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Skin - Butterfly erythema - heals without scarring, more persistent than sunburn. Common presenting manifestation of SLE.
Poikiloderma - hyper and hypopigmentation, telangiectasia, and epidermal atrophy Maculopapular rash - may be purpuric, but can be identical to “drug rash” Discoid lesions (see above) Alopecia - diffuse, bifrontal or scarring; Periungual telangiectasia; vasculitis lesions - palpable purpura, ulcers, gangrene; palmar erythema, livedo reticularis, rare bullous lesions, Raynaud’s phenomenon, urticaria, oral ulceration and nasal septal ulcerations, erythema multiforme, panniculitis lupus profundus |
Clinical features of SLE
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Assess all systems involved. Systemic corticosteroids. Azathioprine (Imuran) or cyclophosphamide (Cytoxan) may have steroid sparing effects. Antimalarials benefit skin and joints, but do not help vasculitis. Non steroidal anti-inflammatory agents.
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SLE treatment
five year survival approaching 95% in some trials. Five year survival in early days of corticosteroids was only 70%. |
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A multisystem granulomatous (Term applied to nodular inflammatory lesions, usually small or granular, firm, persistent, and containing compactly grouped modified phagocytes (e.g., epithelioid cells, giant cells, and other macrophages)) disease with prominent cutaneous features including lesion characterized by dermal granulomas. The dermatologist can confirm the diagnosis by skin biopsy.
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Sarcoidosis
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These dermal nodules often occur over pressure sites and correlate with more severe, erosive form of this autoimmune condition
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Rheumatoid nodules
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These yellowish plaques classically occur on the lower extremities in diabetics. They may ulcerate. Recognition and histologic confirmation of this diagnosis by the dermatologist may occur in patients with previously unsuspected diabetes mellitus.
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Necrobiosis lipoidica dibeticorum
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Xanthelasmas, tuberous and tendinous types are associated with deposition of cholesterol in the dermis. They may be a marker for Type II or other cholesterol related hyperlipemias and increased risk for cardiovascular disease. Eruptive xanthomas occur due to triglyceride deposition. They occur in types I, IV and V hyperlipidermisas especially in diabetic patients
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Xanthomas
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These plaques which usually occur on the skin are associated with hyperthyroidism. The dermatologist can confirm their clinical suspicion histologically. This condition may be induced by long acting thyroid stimulator (LATS).
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Pretibial myxedema
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This disease is characterized by hypertrichosis on the face and by bullae in a photodistribution. It occurs due to uroporphyrinogen decarboxylase deficiency. Alcohol induced liver disease the most common precipitant. The ringed molecules (uro and copro porphyrinogen) which cause the photosensitivity are detectable in the urine.
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Porphyria cutanea tarda
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This condition is characterized by rapidly progressive cutaneous ulcers with typical undermined borders. Vasculitis, granulomatous infection and squamous carcinoma must be excluded histologically and by culture before this diagnosis can be made. Inflammatory bowel disease, chronic active hepatitis, leukemia and erosive arthritis have been associated with condition.
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Pyoderma gangrenosum
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A variegated hyperpigmentation and telangiectasia of the skin, followed by atrophy
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Poikiloderma
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Patients with this collagen vascular disease have condition with proximal extensor muscle weakness and a characteristic cutaneous eruption. The heliotrope sign (periorbital violaceous poikiloderma - see lupus) and Gottron’s sign (poikilodermatous papules or plaques over the extensors) are typical. Up to 25-30% of adults with condition have an associated malignancy.
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Dermatomyositis
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This distinctive velvety, hyperpigmented thickening occurs classically in the axillae and flexures. It may be a marker for occult malignancy or for insulin resistance. Insulin - like growth factors may account for the epidermal proliferation in the second setting and tumor associated similar factors in the first setting.
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Acanthosis nigricans
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This is a not uncommon dominantly inherited genodermatosis (genetically-inherited skin condition). Cafe-au-lait macules and cutaneous neurofibromas are diagnostic. The dermatologist can confirm the diagnosis histologically.
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Neurofibromatosis
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This autosomal dominant disorder is also characterized by numerous cutaneous markers. These include angiofibromas which present as the classic adenoma sebaceum, and periungual fibromas. The chagrin patch is actually a connective tissue hamartoma which occurs on the back. Most defining and first appearance - the ash leaf macules are areas of hypopigmentation which may be the first sign of the disease detectable by the dermatologist.
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Tuberous sclerosis
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Dark brown to black macules which develop in sun-exposed areas.
Lesions may increase in size over the years. Increase with age. a variably pigmented benign lentigo occurring on exposed skin of older white people |
Solar Lentigo
The essential histologic feature of the lentigo is linear (non-nested) melanocytic hyperplasia (hyperplasia restricted to the cell layer immediately above the basement membrane) that produces a hyperpigmented basal cell layer. |
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Common, often multiple, benign tumors which usually first appear in middle life.
Affect any part of the body, except plams and soles. Eruptive form is associated with internal malignancies (Lesser-Trelat sign). A well-demarcated coinlike pigmented lesion containing dark keratin-filled surface plugs is composed histologically of proliferations of basaloid cells with formation of prominent keratin-filled "horn" cysts (B), some of which communicate with the surface (pseudo-horn cysts) and correlate with the plugs observed clinically. |
Seborrheic Keratosis
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The most common cutaneous malignant neoplasm
Affects mostly sun-exposed areas of the skin. May develop in organoid nevi (20%), basal cell nevus syndrome and Bazex syndrome. Pearly, telangiectatic nodules (A) are composed of nests of basaloid cells within the dermis (B) that are often separated from the adjacent stroma by thin clefts (C). |
Basal Cell Carcinoma
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Nodular
Fibroepithelioma of Pinkus Superficial Infundibulocystic |
Types of Basal Cell Carcinomas
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A, Excessive scale formation in this lesion has produced a "cutaneous horn." B, Basal cell layer atypia is associated with marked hyperkeratosis and parakeratosis. C, Progression to full-thickness nuclear atypia, with or without the presence of superficial epidermal maturation, heralds the development of early squamous cell carcinoma in situ.
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Actinic Keratosis
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histologic term used to describe epithelial lesions in which the cytologic changes of malignancy are confined to the epithelium, with no evidence of local invasion or distant metastases. It is considered a precancerous condition because of its potential to evolve into invasive cancer
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Carcinoma in-situ (Bowen's disease)
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Retention of nuclei in the cells of the stratum corneum of the epidermis, observed in many scaling dermatoses such as psoriasis and subacute or chronic dermatitis
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Parakeratosis
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have not invaded through the basement membrane of the dermoepidermal junction (termed in situ carcinoma) appear as sharply defined, red, scaling plaques. More advanced, invasive lesions are nodular, show variable keratin production appreciated clinically as hyperkeratosis, and may ulcerate ( Fig. 25-14A ). Well-differentiated lesions may be indistinguishable from keratoacanthoma. When the oral mucosa is involved, a zone of white thickening may be seen, an appearance caused by a variety of disorders and referred to clinically as leukoplakia.
Lesions are often nodular and ulcerated. B, Tongues of atypical squamous epithelium have transgressed the basement membrane, invading deeply into the dermis. C, Invasive tumor cells exhibit enlarged nuclei with angulated contours and prominent nucleoli. |
Squamous cell carcinoma
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rapidly developing neoplasm that clinically and histologically may mimic well-differentiated squamous cell carcinoma. Often it will heal spontaneously, without treatment! Men are more often affected than women, and lesions most frequently affect sun-exposed skin of whites older than age 50 years
appear clinically as flesh-colored, dome-shaped nodules with a central, keratin-filled plug, imparting a crater-like topography. Lesions range in size from 1 cm to several centimeters across and have a predilection for facial skin, including the cheeks, nose, and ears, and the dorsa of the hands. characterized histologically by a central, keratin-filled crater surrounded by proliferating epithelial cells that extend upward in a liplike fashion over the sides of the crater and downward into the dermis as irregular tongues. This epithelium is composed of enlarged cells showing evidence of reactive cytologic atypia. These cells have a characteristically "glassy" eosinophilic cytoplasm and produce keratin abruptly (without the development of an intervening granular cell layer). This mode of keratinization is analogous to that of the normal hair follicle and is similar to that seen in the pilar cyst described earlier, giving rise to speculation that it is a neoplasm of follicular epithelium. The early tumor infiltrates into the collagen and elastic fibers and entraps them. Little, if any, host inflammatory response is present during this rapidly proliferative phase, but as the lesion evolves, there is some stromal response that is fibrotic and contains numerous inflammatory cells. |
Keratoacanthoma
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In clinical appearance, lesions are small, relatively flat, symmetric, and uniform. B, On histologic examination, junctional nevi are characterized by rounded nests of nevus cells originating at the tips of rete ridges along the dermoepidermal junction.
the compound nevus (A) is more raised and dome shaped. The symmetry and uniform pigment distribution suggest a benign process. Histologically (B), compound nevi combine the features of junctional nevi (intraepidermal nevus cell nests) with nests and cords of nevus cells in the underlying dermis. |
Melanocytic lesions/nevus/moles
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a melanocytic nevus that is visible at birth, is often larger than an acquired nevus, and more frequently involves deeper structures. Congenital nevus larger than 20.0 cm in diameter have a 6–12% lifetime risk of developing
melanoma Also show fatty neoplasia on biopsy |
Congenital nevus
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Malignant counterpart of nevi – contained in epidermis. Younger the patient the higher the likelihood for metastasis. Favorable prognosis when contained in epidermis.
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Melanoma
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Flat lesions with irregular borders and color variegation.
Most commonly on the face and neck but they can affect any area of the body |
Clinical features of melanoma
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Asymmetrical lesions.
Variation in the size and shape of the nests. Poor circumscription. Predominance of single melanocytes and presence of pagetoid melanocytes above the dermal-epidermal junction. |
Histological features of melanoma
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White, black, brown and red nests
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Nodular melanoma
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mitosis in melanocytic lesion
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Poor prognostic factor in melanoma
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Small, dark nests all over the body
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Metastatic melanoma
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