Common skin lesions Flashcards
Epidermal cyst presentation
Round, yellow/flesh-coloured, slow growing, mobile, firm, fluctuant, nodule or tumour
Epidermal cyst pathophysiology
Epithelial cells displaced into dermis, epidermal lining becomes filled with keratin and lipid-rich debris
May be post-traumatic, rarely syndromic
Epidermal cyst epidermiology
most common cutaneous cyst in youth - middle age
Epidermal cyst clinical course
central punctum may rupture (foul, cheesy odour, creamy colour) and produce inflammatory reaction Can increase in size and number over time)
Epidermal cyst management
no treatment elective excision
Pilar cyst (Trichillemmal) clinical presentation
Multiple, hard, variable sized nodules under the scalp, lacks central punctum
Pilar cyst (Trichillemmal) pathophysiology
Thick-walled cyst lined with stratified squamous epithelium and filled with dense keratin Idiopathic Posttraum
Pilar cyst (Trichillemmal) epidemiology
2nd most common cutaneous cyst F>M
Pilar cyst (Trichillemmal) clinical course
rupture causes pain and inflammation
Pilar cyst (Trichillemmal) management
no tx, elective excision
dermoid cyst clinical presentation
Firm nodule most commonly found at lateral third of eyebrow or midline under nose
dermoid cyst pathophys
Rare congenital hamartomas, which arise from inclusion of epidermis along embryonal cleft closure lines, creating a thick-walled cyst filled with dense keratin
dermoid cyst epi
rare
dermoid cyst clinical course
If nasal midline, risk of extension into CNS
dermoid cyst management
no tx, elective excision
ganglion cyst clinical presentation
Usually solitary, rubbery, translucent; a clear gelatinous viscous fluid may be extruded
ganglion cyst pathophys
Cystic lesion that originates from joint or tendon sheath, called a digital mucous cyst when found on fingertip
Associated with osteoarthritis
ganglion cyst epi
older age
ganglion cyst clinical course
stable
ganglion cyst management
no treatment
incision and experession of contents
elective excision
milium clinical presentation
1-2 mm superficial, white to yellow subepidermal papules occurring on eyelids, cheeks and forehead
milium pathophys
Small epidermoid cyst, primarily arsing from pluripotential cells in epidermal or adnexal epithelium Can be secondary to blistering, ulceration, trauma, topical corticosteroid atrophy, or cosmetic procedures
milium epi
any age
40-50$ of infants
milium clinical course
in newborns spontaneously resolves in first 4 weeks of life
milium tx
no tx
incision and expression of contents
electrodessication
topical retinoid therapy
Fitzpatrick scale
I - always burns, never tans
II - always burns, little tan
III - slight burn, slow tan
IV (pale brown) - slight burn, faster tan
V - (brown) - rarely burns, dark tan
VI (dark brown or black) - never burns, dark tan
Dermatofibroma clinical presentation
button-like, firm dermal papule or nodule, skin-coloured to red-brown
- majority are asymptomatic but may be pruritic and/or tender
- site: legs > arms > trunk
- dimple sign (Fitzpatrick’s sign): lateral compression causes dimpling of the lesion
Dermatofibroma pathophy
benign tumour due to fibroblast proliferation in the dermis
Dermatofibroma etiology
- unknown; may be associated with history of minor trauma (e.g. shaving or insect bites)
- eruptive dermatofibroma can be associated with SLE
Dermatofibroma epi
adults F>M
Dermatofibroma ddx
• dermatofibrosarcoma protuberans
malignant melanoma
Kaposi’s sarcoma
blue nevus
Dermatofibroma investigations
biopsy if diagnosis uncertain
Dermatofibroma management
no tx required, excision if bothersome
skin tags clinical presentation
- small (1-10 mm), soft, skin-coloured or darker pedunculated papule, often polypoid
- sites: eyelids, neck, axillae, inframammary, and groin
skin tags pathophys
benign outgrowth of skin
skin tags epi
• middle-aged and elderly, F>M, obese, can increase in size and number during pregnancy
skin tags ddx
• pedunculated seborrheic keratosis
compound or dermal melanocytic nevus
neurofibroma
fibroepithelioma of Pinkus (rare variant of BCC)
skin tags management
excision
electrodessication
cryosurgery
skin tags are also known as
acrochordones
fibroepithelial polyps
seb keratosis clinical presentation
known as ‘wisdom spots,’ ‘age spots,’ or ‘barnacles of life’
- well-demarcated waxy papule/plaque with classic “stuck on” appearance
- rarely pruritic
- over time lesions appear more warty, greasy and pigmented
- sites: face, trunk, upper extremities (may occur at any site except palms or soles)
seb keratosis pathophys
• very common benign epithelial tumour due to proliferation of keratinocytes and melanocytes
seb keratosis epi
- unusual <30 yr old
- M>F
- autosomal dominant inheritance
- Leser-Trelat sudden appearance of SK that can be associated with malignancy, commonly gastric adenocarcinomas
seb keratosis ddx
• malignant melanoma (lentigo maligna, nodular melanoma)
melanocytic nevi
pigmented BCC
solar lentigo
spreading pigmented AK
seb keratosis investigations
biopsy if unsure
seb keratosis management
none req, cosmetic only
cryotherapy, electrodessication, excision
Corns (helomata) clinical presentation
- firm papule with a central, translucent, cone-shaped, hard keratin core
- painful with direct pressure
- sites: most commonly on dorsolateral fifth toe and dorsal aspects of other toes
Corns (helomata) pathophys
• localized hyperkeratosis induced by pressure on hands and feet
Corns (helomata) epi
• F>M, can be caused by chronic microtrauma
Corns (helomata) ddx
callus
plantar wart
Corns (helomata) management
- relieve pressure with padding or alternate footwear, orthotics
- paring, topical salicylic acid
corns vs warts vs calluses
- Corns have a whitish yellow central translucent keratinous core; painful with direct pressure; interruption of dermatoglyphics
- Warts bleed with paring and have a black speckled central appearance due to thrombosed capillaries; plantar warts destroy dermatoglyphics (epidermal ridges)
- Calluses have layers of yellowish keratin revealed with paring; there are no thrombosed capillaries or interruption of epidermal ridges
keloids clinical presentation
- firm, shiny, skin-coloured or red-bluish papules/nodules that most often arise from cutaneous injury (e.g. piercing, surgical scar, acne), but may appear spontaneously
- extends beyond the margins of the original injury, and may continue to expand in size for years with claw-like extensions
- can be pruritic and painful
- sites: earlobes, shoulders, sternum, scapular area, angle of mandible
keloids pathophy
• excessive deposition of randomly organized collagen fibres following trauma to skin
keloids epi
- most common in black patients, followed by those of Asian descent (predilection for darker skin)
- M=F, all age groups
keloids managemetn
- intralesional corticosteroid injections
* silicone compression
keloids vs hypertrophic scars
keloids extend beyond margins of original injury with claw-like extensions
hypertrophic scars are confined to original margins of injury
congenital nevomelanocytic nevi (CNMN) clinical presentation
sharply demarcated pigmented papule or plaque with regular borders ± coarse hairs
• classified by size: small (<1.5 cm),
medium M1: 1.5-10 cm, M2: >10-20 cm),
large (L1: >20-30 cm, L2 >30-40 cm),
giant (G1: >40-60 cm, G2: >60 cm)
• may be surrounded by smaller satellite nevi
congenital nevomelanocytic nevi (CNMN) pathophy
• nevomelanocytes in epidermis (clusters) and dermis (strands)
congenital nevomelanocytic nevi (CNMN) epi
- present at birth or develops in early infancy to childhood
- malignant transformation is rare (1-5%) and more correlated with size of the lesion
- neurocutaneous melanosis can occur in giant CNMN (melanocytes in the central nervous system)
congenital nevomelanocytic nevi (CNMN) management
- take a baseline photo and observe lesion for change in shape, colour, or size out of proportion of growth
- surgical excision if suspicious, due to increased risk of melanoma
- MRI if suspicious for neurological involvement
ddx of hyperpigmented macules
- Purpura (e.g. solar, ASA, anti-coagulants, steroids, hemosiderin stain)
- Post-inflammatory
- Melasma
- Melanoma
- Fixed drug eruption
cafe-au-lait macule clinical presentation
Flat light brown lesions with smooth or jagged borders
cafe-au-lait macule patohophys
Areas of increased melanogenesis
cafe-au-lait macule epi
6 or more is suggestive of neurofibromatosis type I
Also associated with McCune Albright syndrome
cafe-au-lait macule ddx
Flat congenital melanocytic nevus, speckled lentiginous nevus
cafe-au-lait macule clinical course and management
enlarge in proportion to the child
No effective treatment
speckled lentiginous nevus (nevus spilus) clinical presentation
Brown pigmented macular background (caféau-lait macule-like) with dark macular or papular speckles
speckled lentiginous nevus (nevus spilus) pathophys
Increased melanocyte concentration
speckled lentiginous nevus (nevus spilus) epi
Risk of melanoma similar to that of a CNMN of the same size
speckled lentiginous nevus (nevus spilus) ddx
Café-au-lait macule, agminated lentigines, Becker’s nevus
speckled lentiginous nevus (nevus spilus) clinical course and management
usually the light macular background is present at birth and speckles develop over time. Management is similar to that of CNMNs
Dermal melanocytosis (historically known as Mongolian Spot) clinical presentation
Congenital greyblue solitary or grouped macules commonly on lumbosacral area
Dermal melanocytosis (historically known as Mongolian Spot) pathophys
Ectopic melanocytes in dermis
Dermal melanocytosis (historically known as Mongolian Spot) epi
99% occurs in Asian and Indigenous infants
Dermal melanocytosis (historically known as Mongolian Spot) ddx
Ecchymosis
Dermal melanocytosis (historically known as Mongolian Spot) clinical course and management
usually fades, may persist
halo nevus
often a typical appearing nevus surrounded by a ring of depigmentation; not rare in children; uncommonly associated with vitiligo; no treatment required unless irregular colour or borders
blue nevus
round to oval macule/papule with homogenous blue to blue-black colour; often appears in childhood and late adolescence; no treatment required unless atypical features are noted
acquired nevomelanocytic nevi clinical presentation
- common mole: well circumscribed, round, uniformly pigmented macules/papules <1.5 cm
- average number of moles per person: 18-40
- 3 stages of evolution: junctional NMN, compound NMN, and dermal NMN
acquired nevomelanocytic nevi management
- new or changing pigmented lesions should be evaluated for aypical features which could indicate a melanoma
- excisiona biopsy should be considered if the lesion demonstrates asymmetry, varied colours, irregular borders, pruritus or persistent bleeding
junctional acquired nevomelanocytic nevi onset, clinical presentation and histology
childhoood, majority progress to compound
Flat, regularly bordered, uniformly tan-dark brown, sharply demarcated macul
Melanocytes at dermal-epidermal junction above basement membrane
compound acquired nevomelanocytic nevi onset, clinical presentation and histology
Any age
Domed, regularly bordered, smooth, round, tan-dark brown papule Face, trunk, extremities, scalp NOT found on palms or soles
Melanocytes at dermal-epidermal junction; migration into dermis
dermal acquired nevomelanocytic nevi onset, clinical presentation and histology
Adults
Soft, dome-shaped, skin-coloured to tan/brown papules or nodules Sites: face, neck
Melanocytes exclusively in dermis
Atypical nevus (dysplastic nevus) clinical presentation
Variegated macule/ papule with irregular distinct melanocytes in the basal layer Risk factors: family history
Atypical nevus (dysplastic nevus) pathophys
Hyperplasia and proliferation of melanocytes extending beyond dermal compartment of the nevus Often with region of adjacent nests
Atypical nevus (dysplastic nevus) epi
> 5 atypical nevi increases risk for melanoma Numerous dysplastic nevi may be part of familial atypical mole and melanoma syndrome
Atypical nevus (dysplastic nevus) ddx
melanoma
Atypical nevus (dysplastic nevus) clinical course and management
Follow with baseline photographs for changes Excisional biopsy if lesion changing or highly atypica
ephelides (freckles) presentation
Small (<5 mm) welldemarcated light brown macules Sites: sun-exposed skin
ephelides (freckles) pathophys
Increased melanin within basal layer keratinocytes secondary to sun exposure
ephelides (freckles) epi
Skin phototypes I-II most commonly
ephelides (freckles) ddx
Junctional nevi
Juvenile lentigines
ephelides (freckles) clinical course and management
Multiply and darken with sun exposure, fade in winter
No treatment required
Sunscreen and sun avoidance may prevent the appearance of new freckles
Solar lentigo (liver spot) clinical presentation
Well-demarcated brown/black macules Sites: sun-exposed skin
Solar lentigo (liver spot) pathophys
Benign melanocytic proliferation in dermal- epidermal junction due to chronic sun exposure
Solar lentigo (liver spot) epid
Most common in Caucasians >40 yr Skin phototypes I-III most commonly
Solar lentigo (liver spot) ddx
Lentigo maligna, seborrheic keratosis, pigmented actinic keratosis
Solar lentigo (liver spot) clinical course and management
Laser therapy, shave excisions, cryotherapy
Becker’s Nevus presentation
Hairy, light brown macule/patch with a papular verrucous surface Sites: trunk and shoulders onset in teen years
Becker’s Nevus pathophys
Pigmented hamartoma with increased melanin in basal cells
Becker’s Nevusepi
M>F Often becomes noticeable at puberty
Becker’s Nevus ddx
Hairy congenital melanocytic nevus
Becker’s Nevus clinical course and managemetn
hair growth follows onset of pigmentation
Cosmetic management (usually too large to remove
melasma clinical presentation
Dark, usually symmetrical, skin discolouration on sunexposed areas of face (forehead, upper lip, cheeks, chin)
melasma pathophys
Increase in number and activity of melanocytes Associated with estrogen and progesterone
melasma epi
F>M Common in pregnancy and women taking OCP or HRT Risk factors: sun exposure, dark skin tone Can occur with mild endocrine disturbances, antiepileptic medications and other photosensitizing drug
melasma ddx
Post-inflammatory hyperpigmentation
melasma course and tx
often fades over several months after stopping hormone treatment or delivering baby
Treatment: hydroquinone, azelaic acid, retinoic acid, topical steroid, combination creams, destructive modalities (chemical peels, laser treatment), camouflage make-up, sunscreen, sun avoidance
Hmangiomas of infancy clinical presentation
Hot, firm red to blue plaques or tumours
Hmangiomas of infancy pathophys
benign vascular proliferation of endothelial lining
Hmangiomas of infancy epi
Appears shortly after birth; rarely may be congenital
Hmangiomas of infancy clinical course
Appears shortly after birth, increases in size over months, then regresses 50% of lesions resolve spontaneously by 5 yr
Hmangiomas of infancy management
10% require treatment due to functional impairment (visual compromise, airway obstruction, high output cardiac failure) or cosmesis Consider treatment if not gone by school age; topical timolol, propranolol; systemic corticosteroids; laser treatment; surgery
spider angioma (Campbell telengiectasia) clinical presentation
Central red arteriole with slender branches, blanchable
spider angioma will blanch when the tip of a paperclip is applied to the centre of the lesion
spider angioma (Campbell telengiectasia) pathophys
Can be associated with hyperestrogenic state (e.g. in hepatocellular disease, pregnancy, OCP) but often is not
spider angioma (Campbell telengiectasia) epi
any age
spider angioma (Campbell telengiectasia) clinical course
Increase in number over tim
spider angioma (Campbell telengiectasia) management
reassurance
electrodessication or laser if patient wishes
cherry angioma (Campbell De Morgan Spot) clinical presentation
Bright red to deep maroon, domeshaped vascular papules, 1-5 mm Site: trunk Less friable compared to pyogenic granulomas
cherry angioma (Campbell De Morgan Spot) pathophys
Benign vascular neoplasm
cherry angioma (Campbell De Morgan Spot) epi
> 30 years old
cherry angioma (Campbell De Morgan Spot) clinical course
Lesions do not fade in time Lesions bleed infrequently
cherry angioma (Campbell De Morgan Spot) management
usually no tx
Laser or elect ocautery for small lesions Excision of large lesions if necessary
pyogenic granuloma clinical presentation
Bright red, dome-shaped sessile or pedunculated friable nodule Sites: fingers, lips, mouth, trunk, toes DDx: glomus tumour, nodular MM, SCC, nodular BCC
pyogenic granuloma pathophys
Rapidly developing hemangioma Proliferation of capillaries with erosion of epidermis and neutrophilia
pyogenic granuloma epi
<30 yo
pyogenic granuloma clinical course
Lesion grows rapidly over weeks to months, then stabilizes Lesion may persist indefinitely if untreated
pyogenic granuloma management
surgical excision with histologic examination Electrocautery; laser; cryotherapy
what is a venous lake
benign blue or violaceous papular lesion occurring on the face, lips, and ears due to dilation of a venule. Distinguished from malignant pigmented lesions through diascopy, as compression blanches the lesion
nevus flammeus (port-wine stain) clinical presentation
Red to blue macule present at birth that follows a dermatomal distribution, rarely crosses midline Most common site: nape of neck Never spontaneously regresses but grows in proportion to the child
nevus flammeus (port-wine stain) pathophys
congenital vascular malformation of dermal capillaries; rarely associated with Sturge-Weber syndrome (V1, V2 distribution)
nevus flammeus (port-wine stain) management
laser or make up
nevus simplex (salmon patch) clinical presentation
Pink-red irregular patches Midline macule on glabella known as “Angel Kiss”; on nuchal region known as “Stork Bites Present in 1/3 of newborns Majority regress spontaneously
nevus simplex (salmon patch) pathophys
Congenital dilation of dermal capillaries
nevus simplex (salmon patch) management
none req
lipoma clinical presentation
- single or multiple non-tender subcutaneous tumours that are soft and mobile
- occurs most frequently on the trunk, and extremities but can be anywhere on the body
lipoma pathophys
• adipocytes enclosed in a fibrous capsule
lipoma epi
often solitary or few in number, if multiple can be associated with rare syndromes
lipoma ddx
angiolipoma, liposarcoma
lipoma investigations
biopsy if atypical features (painful, rapid growth, firm)
lipoma management
reassurance
excision or liposuction only if desired for cosmetic purposes
Acne vulgaris/common acne clinical presentation
a common inflammatory pilosebaceous disease categorized with respect to severity
■ Type I: comedonal, sparse, no scarring
■ Type II: comedonal, papular, moderate ± little scarring
■ Type III: comedonal, papular, and pustular, with scarring
■ Type IV: nodulocystic acne, risk of severe scarring
• sites of predilection: face, neck, upper chest, and back
Acne vulgaris/common acne pathophysiology
- hyperkeratinization at the follicular ostia (opening) blocks the secretion of sebum leading to the formation of microcomedones
- androgens promote excess sebum production
- Propionibacterium acnes metabolize sebum to free fatty acids and produces pro-inflammatory mediators
Acne vulgaris/common acne epi
- age of onset in puberty (10-17 yr in females, 14 19 yr in males)
- in prepubertal children consider underlying hormonal abnormality (e.g. late onset congenital adrenal hyperplasia)
- incidence decreases in adulthood
- genetic predisposition: majority of individuals with cystic acne have parent(s) with history of severe acne
Acne vulgaris/common acne ddx
• folliculitis
keratosis pilaris (upper arms, face, thighs)
perioral dermatitis
rosacea
Treatment of acne scars
- Tretinoin creams
- Glycolic acid
- Chemical peels for superficial scars
- Injectable fillers (collagen, hyaluronic acid) for pitted scars
- Fraxel laser
- CO2 laser resurfacing
Does eating greasy food and chocolate cause or worsen acne?
no
Why are blackheads black?
Blackheads (comedones) are black because of oxidized fatty acids, not dirt
Is acne caused by poor hygiene?
Acne is not caused by poor hygiene; on the contrary, excessive washing of face can be an aggravator
Role of antibiotics in acne
Antibiotics are used in inflammatory skin conditions since they also have antiinflammatory properties (e.g. macrolides in acne).
Topical antibiotics may also be used to treat secondary bacterial superinfections (e.g. impetigo)
Acne exacerbating factors
- Systemic medications: lithium, phenytoin, steroids, halogens, androgens, iodides, bromides, danazol
- Topical agents: steroids, tars, ointments, oily cosmetics
- Mechanical pressure or occlusion, such as leaning face on hands
- Emotional stress
Management of mild acne
Mild acne - topical therapies OTC
Benzoyl peroxide (BPO) - solugel, benzac, desquam, fostex
Salicylic acid - Akurza Cream, dermalzone
- prescription topical therapies
Antimicrobials - Clindamycin (Dalacin T), Erythromycin
Retinoids - Vit A Acid (tretinoin, Stieva-A, Retin A) Adapalene (Differin)
Combination products - Clindoxyl (Clindamycin and BPO), Benzaclin (Clindamycin and BPO), Tactuo (Adapalene and bpo), biacna (clindamycin and tretinoin), benzamycine (bpo and erythromycin)
A combination of topical retinoids and topical erythromycin or clindamycin is more effective than either agent used alone
Indication for intralesional corticosteroid injections for acne
Intralesional corticosteroid injections are effective in the treatment of individual acne nodules
Salicylic acid indication in acne therapy
Used when patients cannot tolerate a topical retinoid due to skin irritation
why not use antimicrobials as monotherapy for acne
high rate of resistance when used as monotherapy
retinoids indication in acne therapy
Backbone of topical acne therapy
All regimens should include a retinoid unless patient cannot tolerate
Benefit of combination acne products
greater adherence and efficacy by combining different MOAs to increase efficacy and maximize tolerability
Benefit of combination acne products
greater adherence and efficacy by combining different MOAs to increase efficacy and maximize tolerability
moderate acne therapy
tetracycline/minocycline/doxycycline (sumycin/minocin/vibramycin)
Cyproterone acetate-ethinyl estradiol (Diane 35)
Spironolactone (Aldactone)
caution and duration before assessing efficacy for tetracycline/minocycline/doxycycline (sumycin/minocin/vibramycin)
Use caution with regard to drug interactions: do not use with isotretinoin
Sun sensitivity
Antibiotics require 3 mo of use before assessing efficacy
age limit for cyproterone acetate ethinyl estradiol
After 35 yr of age, estrogen/progesterone should only be considered in exceptional circumstances arefully weighing the risk/benefit ratio with physician guidance
spironolactone adverse effects/black box warning
May cause hyperkalemia at higher doses
Black box warning for breast cancer
Isotretinoin and pregnancy
- Use of Isotretinoin during pregnancy is associated with spontaneous abortion and major birth defects such as facial dysmorphism and cognitive impairment
- Pregnancy should be ruled out before starting isotretinoin
- Patients should use 2 forms of contraception while on isotretinoin
Severe acne treatment
isotretinoin (accutane, clarus, epuris)
isotretinion adverse effects
Most adverse effects are temporary and will resolve when the drug is discontinued
Baseline lipid profile (risk of hypertriglyceridemia), LFTs and β-hCG before treatment
May transiently exacerbate acne before patient sees improvement
Refractory cases may require multiple courses of isotretinoin
Clinical presentation perioral dermatitis
discrete erythematous micropapules that often become confluent, forming inflammatory plaques on perioral, perinasal, and periorbital skin commonly symmetrical, rim of sparing around vermillion border of lips
perioral dermatitis epi
- 15-40 yr old, occasionally in younger children
* predominantly females
perioral dermatitis ddx
• contact dermatitis, rosacea, acne vulgaris
perioral dermatitis mx
- avoid all topical steroids
- topical: metronidazole 0.75% gel or 0.75-1% cream to affected area bid
- systemic: tetracycline family antibiotic (utilized for its anti-inflammatory properties)
- occasional use of a non-steroidal anti-inflammatory cream (i.e. tacrolimus or pimecrolimus)
Important controversies associate with isotretinoin therapy for acne
- The evidence on whether isotretinoin causes depression and suicide is inconsistent; however, numerous controlled studies have shown an improvement in anxiety and depression scores in those taking isotretinoin.
- There is no association between IBD and isotretinoin use. Only one study showed a significantly increased risk of UC. When considering using isotretinoin in a patient with IBD or with a strong family history, consider involving a gastroenterologist.
Rosacea clinical presentation
- dome-shaped inflammatory papules ± pustules
- flushing, non-transient erythema, and telangiectasia
- distribution: typically on central face including forehead, nose, cheeks, and chin; rarely on scalp, neck, and upper body
- characterized by remissions and exacerbations
- exacerbating factors: heat, cold, wind, sun, stress, drinking hot liquids, alcohol, caffeine, spices
- all forms of rosacea can progress from mild to moderate to severe
- rarely in longstanding rosacea, signs of thickening, induration and lymphedema in the skin can develop
- phyma: a distinct swelling caused by lymphedema and hypertrophy of subcutaneous tissue, particularly affecting the nose (rhinophyma)
- ocular manifestations: blepharoconjunctivitis, keratitis, iritis
Rosacea pathophysiology
unknown
Rosacea epi
all skin types, highest prevalence in fair-skinned people
30-50 year old; F>M
Rosacea ddx
acne vulgaris, seborrheic dermatitis, perioral dermatitis, contact dermatitis
Rosacea mx
- trigger avoidance and daily sunscreen use for long-term management
- avoid topical corticosteroids
- telangiectasia: treated by physical ablation; electrical hyfrecators, vascular lasers, and intense pulsed light therapies
- phymas: treated by physical ablation or removal; paring, electrosurgery, cryotherapy, laser therapy (CO2, argon, Nd:YAG)
1st line - Oral tetracyclines Topical metronidazole Oral erythromycin (250-500 mg PO bid) Topical azelaic acid Topical Ivermectin
2nd line Topical clindamycin Topical erythromycin 2% solution Topical benzoyl peroxide Oral metronidazole
3rd line
oral retinoids
How can rosacea be differentiated from acne
Rosacea can be differentiated from acne by the absence of comedones,
a predilection for the central face
and symptoms of flushing
Guidelines for the diagnosis of rosacea
Presence of one or more of the following primary features: • Flushing (tansient erythema) • Nontransient erythema • Papules and pustules • Telangiectasia
May include one or more of the following secondary features: • Burning or stinging • Dry appearance • Edema • Phymatous changes • Ocular manifestations • Peripheral location
Dermatitis (eczema) definition
inflammation of the skin
Dermatitis (eczema) clinical presentation
- poorly demarcated erythematous patches or plaques
- symptoms include pruritus and pain
- acute dermatitis: papules, vesicles
- subacute dermatitis: scaling, crusting, excoriations
- chronic dermatitis: lichenification, xerosis, fissuring
Asteatotic dermatitis clinical presentation
- diffuse, mild pruritic dermatitis secondary to dry skin
- very common in elderly, especially in the winter (i.e. “winter itch”) but starts in the fall
- shins predominate, looks like a “dried river bed”
Asteatotic dermatitis management
• skin rehydration with moisturizing routine ± corticosteroid creams
Atopic dermatitis clinical presentation
- subacute and chronic eczematous reaction associated with prolonged severe pruritus
- distribution depends on age
- inflammation, lichenification excoriations are secondary to relentless scratchng
- atopic palms: hyperlinearity of the palms (associated with ichthyosis vulgaris)
- associated with: keratosis pilaris (hyperkeratosis of hair follicles, “chicken skin”), xerosis, occupational hand dryness
Atopic dermatitis epi
- frequently affects infants, children, and young adults
- 10-20% of children in developed countries under the age of 5 are affected
- associated with personal or family history of atopy (asthma, hay fever), anaphylaxis, eosinophilia
- polygenic inheritance: one parent >60% chance for child; two parents >80% chance for child
- long-term condition with 1/3 of patients continuing to show signs of AD into adulthood
Atopic dermatitis pathophysiolgoy
• a T-cell driven inflammatory process with epidermal barrier dysfunction
Atopic dermatitis investigations
- clinical diagnosis
* consider: skin biopsy, patch testing if allergic contact dermatitis is suspected
Atopic dermatitis mx
- goal: reduce signs and symptoms, prevent or reduce recurrences/flares
- better outcome (e.g. less flare-ups, modified course of disease) if diagnosis made early
Initial assessment ->
patient education, daily emollient use ->
acute control of flare (topical corticosteroids or topical calcineurin inhibitor) ->
maintenance therapy if disease is persistent and/or frequent recurrences (topical corticosteroid or calcineurin inhibitor at earliest sign of flare, long-term maintenance use of calcineurin inhibitors) ->
Severe refractory disease
- azathioprine
- methotrexate
- oral cyclosporin
- oral steroids, potent topical steroids
- phototherapy
- psychotherapeutics
Adjunctive therapy • avoid triggers of AD - treat bacterial superinfections (topical or oral abx) - antihistamines - psychological interventions
• non-pharmacologic therapy
■ moisturizers
◆ apply liberally and reapply at least twice a day with goal of minimizing xerosis
◆ include in treatment of mild to severe disease as well as in maintenance therapy
■ bathing practices
◆ bathe in plain warm water for a short period of time once daily followed by lightly but not completely drying the skin with a towel; immediately apply topical agents or moisturizers after this
◆ use fragrance-free hypoallergenic non-soap cleansers
• pharmacologic therapy
■ topical corticosteroids
◆ effective in reducing acute and chronic symptoms as well as prevention of flares
◆ choice of steroid potency depends on age, body site, short vs. long-term use
◆ apply 1 adult fingertip unit (0.5 g) to an area the size of 2 adult palms bid for acute flares
◆ local side effects: skin atrophy, purpura, telangiectasia, striae, hypertrichosis, and acneiform eruption are all very rarely seen
■ topical calcineurin inhibitors
◆ tacrolimus 0.03%, 0.1% (Protopic®) and pimecrolimus 1% (Elidel®)
◆ use as steroid-sparing agents in the long-term
◆ advantages over long-term corticosteroid use: sustained effect in controlling pruritus; no skin atrophy; safe for the face and neck
◆ apply 2x/d for acute flares, and 2-3x/wk to recurrent sites to prevent relapses
◆ local side effects: stinging, burning, allergic contact dermatitis
◆ U.S. black box warning of malignancy risk: rare cases of skin cancer and lymphoma reported; no causal relationship established
Atopic dermatitis complications
• infections
■ treatment of infections
◆ topical mupirocin or fusidic acid (Canada only, not available in US)
◆ oral antibiotics (e.g. cloxacillin, cephalexin) for widespread S. aureus infections
Triggers for atopic dermatitis
- Irritants (detergents, solvents, clothing, water hardness)
- Contact allergens
- Environmental aeroallergens (e.g. dust mites)
- Inappropriate bathing habits (e.g. long hot showers)
- Sweating
- Microbes (e.g. S. aureus)
- Stress
Atopic dermatitis distribution in infants <6 months
Scalp
Extensor elbow
Atopic dermatitis distribution in children >18 months
Neck
Flexor elbow
Flexor knee
Atopic dermatitis distribution in adults
Scalp, neck
Hands, feet
Contact dermatitis clinical presentation
cutaneous inflammation caused by an external agent(s)
irritant contact dermatitis
mechanism of reaction
type of reaction
frequency
distribution
examples
management
mechanism of reaction - Toxic injury to skin; non-immune mechanism
type of reaction - Erythema, dryness, fine scale, burning
Acute: quick reaction, sharp margins (e.g. from acid/alkali exposure)
Cumulative insult: slow to appear, poorly defined margins (e.g. from soap), more common
frequency - Majority; will occur in anyone given sufficient concentration of irritants
distribution - hands most common site
examples - soaps, oils, detergents, weak alkali, organic solvents, alcohol
management - avoidance of irritants, wet compresses with Burrow’s solution, barrier moisturizers, topical/oral steroids
allergic contact dermatitis
mechanism of reaction
type of reaction
frequency
distribution
examples
management
mechanism of reaction - cell mediated delayed (Type IV) hypersensitivity reaction
type of reaction - erythema with a papulovesicular eruption, swelling, pruritus
frequency - Minority; patient acquires susceptibility to allergen that persists indefinitely
distribution - areas exposed
examples - many are same as irritants
management - Patch testing to determine specific allergen
Avoid allergen and its cross-reactants
Wet compresses soaked in Burrow’s solution (drying agent)
Topical Steroids BID prn Systemic steroids prn if extensive
Dyshidrotic dermatitis clinical presentation
- “tapioca pudding” papulovesicular dermatitis of hands and feet that coalesce into plaques, followed by panful fissuring
- acute stage often very pruritic
- secondary infections common
- lesions heal with desquamation and may lead to chronic lichenification
- sites: palms and soles ± dorsal surfaces of hands and feet
Dyshidrotic dermatitis pathophysiology
- NOT caused by hyperhidrosis (excessive sweating)
* emotional stress may precipitate flares
Dyshidrotic dermatitis management
- topical: high potency corticosteroid with plastic cling wrap occlusion to increase penetration
- intralesional triamcnolone injection
• systemic
■ prednisone in severe cases
■ antibiotics for secondary S. aureus infection
Nummular dermatitis clinical presentation
- nummular (coin-shaped), pruritic, dry, scaly, erythematous plaques
- often associated with atopic and dyshidrotic dermatitis
- secondary infection common
Nummular dermatitis pathophysiology
• little is known, but it is often accompanied by xerosis, which results from a dysfunction of the epidermal lipid barrier; this in turn can allow permeation of environmental agents, which can induce an allergic or irritant response
Nummular dermatitis management
- moisturization
* mid to high potency corticosteroid ointment bid
Seborrheic dermatitis clinical presentation
- greasy, erythematous, yellow, scaling, minimally elevated papules and plaques in areas rich in sebaceous glands, can look moist and superficially eroded in flexural regions
- infants: “cradle cap”
- children: may be generalized with flexural and scalp involvement • adults: diffuse involvement of scalp margin with yellow to white flakes, pruritus and underlying erythema
- sites: scalp, eyebrows, eyelashes, beard, glabella, post-auricular, over sternum, trunk, body folds, genitalia
Seborrheic dermatitis pathophysiology
possible etiologic association with Malassezia spp. (yeast)
Seborrheic dermatitis epi
- common in infants and adolescents
- increased incidence and severity in immunocompromised patients
- in adults, can cause dandruff (pityriasis sicca)
Seborrheic dermatitis management
- face: ketoconazole (Nizoral®) cream daily or bid + mild steroid cream daily or bid
- scalp: salicylic acid in olive oil or Derma-Smoothe FS® lotion (peanut oil, mineral oil, fluocinolone acetonide 0.01%) to remove dense scales, 2% ketoconazole shampoo (Nizoral®), ciclopirox (Stieprox®) shampoo, selenium sulfide (e.g Selsun®) or zinc pyrithione (e.g. Head and Shoulders®) shampoo, steroid lotion (e.g. betamethasone valerate 0.1% lotion bid)
Stasis dermatitis clinical presentation
- erythematous, scaly, pruritic plaques in lower legs, particularly the medial ankle
- brown hemosiderin deposition, woody fibrosis, atrophy blanche, and lipodermatosclerosis in late stages usually bilateral, accompanied by swelling, oozing, crusting, may have accompanying varicosities
Stasis dermatitis pathophysiology
- chronic venous insufficiency leads to venous stasis
* surrounding soft tissue inflammation and fibrosis results
Stasis dermatitis investigations
- Doppler and colour-coded Duplex sonography if suspicious for DVT
- swab for bacterial culture if there is crusting
Stasis dermatitis management
- compression stockings
- rest and elevate legs (above the level of the heart)
- moisturizer to treat xerosis
- mid-high potency topical corticosteroids to control inflammation
Stasis dermatitis complications
• ulceration (common at medial malleolus)
secondary bacterial infections
Lichen simplex chronicus clinical presentation
- well-defined plaque(s) of lichenified skin with increased skin markings ± excoriations
- common sites: neck, scalp, lower extremities, urogenital area
- often seen in patients with atopy
Lichen simplex chronicus pathophys
- skin hyperexcitable to itch, continued rubbing/scratching of skin results
- eventually lichenification occurs
Lichen simplex chronicus investigations
- if patient has generalized pruritus, rule out systemic cause: CBC with differential count, transaminases, bilirubin, renal and thyroid function tests, TSH, glucose, SPEP
- CXR if lymphoma suspected
Lichen simplex chronicus mx
• antipruritics (e.g. antihistamines, topical or intralesional glucocorticoids, Unna boot)