treat during prodrome to prevent vesicle formation
topical antiviral (Zovirax’/Xerese* ) cream, apply 5-6 times daily for 4-7 d for facial/genital lesions
oral antivirals(e.g. acyclovir, famciclovir, valacydovir) are far more effective and have an easier
dosing schedule than topicals
Erythema Multiforme
Etiology:most often HSV or
Mycoplosmo pneumonioe. rarely drugs
Morphology:maculcs/papules with
central vesicles: classic bull'
s-eye
pattern of concentric light and dark rings
(typical target lesions)
Management:symptomatic
treatment (oral antihistamines,oral
antacids);corticosteroidsin severely
ill (controversial): prophylactic oral
acyclovir for 6-12 mo for HSV-associated
EM with frequent recurrences
. HSV-2
rupture vesicle with sterile needle if you wish to culture it
wet dressing with aluminum subacetate solution, Burow’s compression, or betadine solution
1st episode:acyclovir 200 mg PO 5x times daily x 10 d
maintenance:acyclovir 400 mg PO BID
• famciclovir and valacydovir may be substituted and have better enteric absorption and less
frequent dosing
• in case of herpes genitalis, look for and treat any other STIs
• for active lesions in pregnancy (see Obstetrics,OB31)
HERPES ZOSTER VIRUS (SHINGLES)
Clinical Features
• unilateral dermatomal eruption occurring 3-5 d after pain and paresthesia of that dermatome
• vesicles, bullae, and pustules on an erythematous, edematous base
• lesions may become eroded/ulceratcd and last days to weeks
• pain can be pre-herpetic,synchronous with rash, or post-herpetic
• severe post-herpetic neuralgia often occurs in elderly
• Ramsay Hunt syndrome (see Otolaryngology. OT'
23)
• Hutchinson’ssign:shingles on the tip of the nose signifies ocular involvement
shingles in this area involves the nasociliary branch of the ophthalmic branch of the trigeminal
nerve (VI)
• distribution:thoracic (50%), trigeminal (10-20%), cervical (10-20%); disseminated in HIV
H2V typically involves a single
dermatome; and lesions rarely cross
the midline
Etiology
• caused by reactivation of VZV
• risk factors: immunosuppression, old age, occasionally associated with hematologic malignancy
Differential Diagnosis
• before thoracic skin lesions occur,must consider other causes of chest pain
• contact dermatitis,localized bacterial infection, zosteriform HSV (more pathogenic for the eyes than
VZV)
Investigations
• none required, but can do T zanck test, direct fluorescence antibody test, or viral culture to rule out
HSV
n
Prevention
« routine vaccination in >50 yr with Shingrix* (recombinant zoster vaccine) preferred to in >60 yr
Zostavax* (live zoster vaccine)
u
Management +
• compress with normal saline, Burow'
s or betadine solution
• oral antivirals:famciclovir, valacydovir, or acyclovir for 7 d; must initiate within 72 h to be of benefit
• analgesia: NSAlDs, acetaminophen for mild-moderate pain; opioids if severe
• post-herpetic neuralgia: tricyclic antidepressants, anticonvulsants (gabapentin, pregabalin)
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D36 Dermatology Toronto Notes 2023
MOLLUSCUM CONTAGIOSUM
Clinical Features
•discrete dome-shaped and umbilicated pearly, white papules caused by DNA Pox virus (Molluscum
contagiosum virus)
•common sites: eyelids,heard (likely spread by shaving),neck, axillae, trunk,perineum,buttocks
Etiology
•virus is spread via direct contact, auto-inoculation, sexual contact
•common in children and sexually active young adults (giant molluscum and severe cases can be seen
in the setting ot'
HIV )
•virus is self-limited and can take 1 -2 yr to resolve
Investigations
•none required, however can biopsy to confirm diagnosis
Management
•topical cantharidin
•cryotherapy
•curettage
•topical retinoids
•Aldara’(imiquimod):immune modulator that produces a cytokine inflammation
WARTS (HUMAN PAPILLOMAVIRUS INFECTIONS)
Table 20. Different Manifestations of HPV Infection
Definition and Clinical Features Differential Diagnosis Distribution HPV Type
Verruca Vulgaris
(Common Warts)
Hyperkeratotic, elevated,discrete epithelial growths with papillated surface
caused by HPV
Paring of surface reveals punctale.red-brown specks (thrombosed capillaries)
Hyperkeratotic. shiny,sharply marginated growths
Paring ol surface reveals red- brown specks (capillaries),interruption ol
epidermalridges
Molluscum contagiosum. At least 80 types are known
seborrheic keratosis
Located attrauma sites:
fingers,hands, knees of
children and teens
May need lo scrape (‘pare") located alpressure sites:
lesions to differentiate wart metatarsal heads,heels.
Irom callus and corn
Verruca Plantaris Commonly HPV 1.2.4,10
(Plantar Wads)
Verruca Palmaris
(Palmar Warts)
Verruca Planae
(Flat Warts)
toes
Multiple discrete,skin coloured,flat topped papules grouped or inlinear
configuration
Common in children
Skin-coloured pinhead papules tosoft cauliflower-likemasses in clusters
Can be asymptomatic,lasting months to years
Highly contagious,transmitted sexually and non-sexually (e.g.Koebner
phenomenon via scratching,shaving),and can spreadwithout clinically apparent contagiosum
lesions
Investigations:acetowhitening (subdinical lesions seen with acetic acid 5% xS
min and handlens)
Complications:fairy-ting wails (satellite warts alperiphery of treated area ol
original warts)
Syringoma,seborrheic
keratosis,molluscum
contagiosum.lichen planus
Sites:lace, dorsa of hands,
shins,knees
Commonly HPV 3,10
Condyloma
Acuminata
(Genital Warts)
Condyloma lata (secondary Sites:genitalia and perianal
syphilitic lesion,dark field areas
strongly-ve),molluscum
Commonly HPV 6 and 11
HPV16.18.31,33 cause
cervical dysplasia,SCC. and
invasive cancer
Treatment for Warts
• first line therapies
• salicylic acid preparations (patches, solutions, creams,ointments), cryotherapy
• second line therapies
topical imiquimod, topical 5-fluorouracil, topical tretinoin,podophyllotoxin
• thirdline therapies
curettage, cautery, surgery for non plantar warts,CO’
laser,oral cimetidine (particularly
children), intralesionalbleomycin (plantar warts), trichloroacetic acid,diphenevprone
CHICKEN POX (VARICELLA)
• see Paediatrics, P63
ERYTHEMA INFECTIOSUM (FIFTH DISEASE)
• see Paediatrics. P62
HAND-FOOT-AND-MOUTH DISEASE
• see Paediatrics,P62
r T
u J
MEASLES
• see Paediatrics. P62
+
PARVOVIRUS
• see Paediatrics. P62
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D37 Dermatology TorontoXotes 2023
ROSEOLA
• see Paediatrics, P62
RUBELLA
• see Paediatrics. P63
VERRUCAE VULGARISMS
• see Table20,D36
fi Yeast Infections
CANDIDIASIS
Etiology
• many species of Candida (70-80% of infections are from Candida albicans)
• opportunistic infection in those with predisposing factors (e.g. trauma, malnutrition,
immunodeficiency)
Candidal Paronychia
• clinical features: painful red swelling of periungual skin
• management:topical agents not as effective;oral antifungals recommended
Candidal Intertrigo
• clinical features
macerated/eroded erythematous patches that may be covered with papules and pustules,located
in intertriginous areas often under breast, groin,or interdigitally
peripheral “satellite” pustules
• starts as non-infectious maceration from heat, moisture, and friction
• predisposing factors:obesity, DM,systemic antibiotics, immunosuppression,malignancy
• management:keep area dry, terbinafine,cidopirox olamine,ketoconazole/dotrimazole cream BID
until rash dears
Oral terbinafine (Lanas?-) is not effective
because it is notsecreted by sweat
glands
PITYRIASIS (TINEA) VERSICOLOR
Clinical Features
• asymptomatic superficial fungal infection with brown/white scaling macules
• affected skin darker than surrounding skin in winter,lighter in summer (does not tan)
• common sites:upper chest and back
Pathophysiology
• microbe produces azelaic acid -» inflammatory'reaction inhibiting melanin synthesis yielding variable
pigmentation
• affinity for sebaceous glands;requiresfatty acidsto survive
Etiology
• Pityrosporum ovale (Malassezia furfur)
• also associated with folliculitis and seborrheic dermatitis
• predisposing factors:summer, tropical climates, excessive sweating,Cushing’
ssyndrome, prolonged
corticosteroid use
Investigations
• clinical diagnosis hut can perform microscopic examination, KOH prep of scalesfor hyphae and
spores
Management
• ketoconazole 2% shampoo or cream daily for 3 d
• selenium sulfide 2.5% lotion applied for 10 min for 7 d
• cidopirox olamine BID
• systemic fluconazole or itraconazole for 7 d if extensive
LJ
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D38 Dermatology Toronto Notes 2023
Sexually Transmitted Infections
SYPHILIS
Clinical Features
• characterized initially by a painless ulcer (chancre)
• following inoculation,systemic infection with secondary and tertiary stages
Etiology
• Treponema pallidum
• transmitted sexually, congenitally,or rarely by transfusion
Table 21. Stages of Syphilis
Clinical Features Investigations Management Natural History of Untreated Syphilis
• Inoculation
• Primaiy syphilis (10-90 d after
infection)
• Secondary syphilis (simultaneous to
primary syphilis or up to 6 mo after
healing of primary lesion)
• Latent syphilis
• Tertiary syphilis (2-20 yr)
Single red.indurated,painless chancre,that develops into CANNOT be based on clinical features
painless ulcer with raised border and scanty serous exudate alone
Chancre develops at site of inoculation after 3 wk of VORL negative -repeat weekly for1mo single dose
incubation and heals in 4-6 wk;chancre may also develop on FTA-ABS test has greater sensitivity and
lipsor anus
Regional non-tender lymphadenopalhy appears
<1wk after onset of chancre
DOx: chancroid (painful). HSV (multiple lesions)
Penicillin G. 2.4
million units IM.
Primary
Syphilis
may detect disease earlier in course
Dark field examination - spirochetein
chancre fluid or lymph node
Secondary
Syphilis
Presents 2- G mo niter primary infection (patient may not
recall presence of primary chancre)
Associated with generalized lymphadenopathy,
Same as for primary
syphilis
VORL positive
FM-ASS *ve;
-ve alter 1 yr following
appearance of chancre
splenomegaly,headache,chills,fever,arthralgias,myalgias. Dark field«ve in all secondary
malaise,photophobia
Lesions heal in1-5 wk and may recur for1yr
3 types of lesions;
1. Macules and papules:flat top.scaling,non-pruritic.
sharply defined,circular/annular rash (DDx:pityriasis
rosea, tinea corporis,drugeruptions,lichen planus)
2. Condyloma lata; wart- like moist papules around genital/
perianal region
3. Mucous patches:macerated patches mainly found in
oral mucosa
Latent Syphilis
70%of untreated patients willremain in
this stage for the rest of their lives and
are immune to new primary infection
Penicillin G,2.4
million units IM
weekly x 3 wk
Tertiary
Syphilis
Extremely rare
3-7 yr after secondary
Main skin lesion:‘Gumma1
-a granulomatous non-lender
nodule
As in primary syphilis.VDRL can be
falsely negative
GONOCOCCEMIA
Clinical Features
• disseminated gonococcal infection
• hemorrhagic, tender, pustules on a purpuric/petechial background
• common sites: distal aspects of extremities
• associated with fever, arthritis, urethritis, proctitis, pharyngitis, and tenosynovitis
• neonatal conjunctivitis if infected via birth canal
Etiology
• Neisseria gonorrhoeae
Investigations
• requires high index of clinical suspicion because tests are often negative
• bacterial culture of blood, joint fluid, and skin lesions
• joint fluid cell count and Gram stain
Management
• notify public health authorities
• screen for other STIs
• cefixime 400 mg PO (drug of choice) or ceftriaxone 1 g IM
r n Herpes Simplex Virus
• see Viral Infections, 1)3-1
Human Papillomavirus
• see Viral Infections, D36 +
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D39 Dermatology Toronto Notes 2023
Pre-Malignant Skin Conditions m.
Actinic Keratoses (Solar Keratoses)
Clinical Features
• ill-defined,scaly,erythematous papules or plaques associated with sun-damaged skin (solar heliosis)
• initial lesion is a rough erythematous papule with white to yellow scale
• often easier to appreciate on palpation rather than inspection, as the lesion has a gritty,sandpaper-like
texture
• sites: areas of sun exposure (face, helices of the ears primarily in men, hairlessscalp, neck, upper
trunk, dorsal aspects of the hands and forearms)
Pathophysiology
• U V radiation damage to keratinocytes from repeated sun exposure (especially UVB)
• risk of transformation of AK to SCC (<1/1000 per yr), but higher likelihood if AK is persistent
• UV-induced p53 gene mutation
• risk factors:increased age, lightskin/eyes/hair, immunosuppression, genetic syndromessuch as
albinism or xeroderma pigmentosum
• risk factors for malignancy:immunosuppression, history ofskin cancer, persistence of AK
Epidemiology
• common with increasing age, outdoor occupation, M>1
;
• skin phototypes 1-111, rare in deeper skin tones as melanin is protective
Types of AK
• Erythematous:typical AK lesion
• Hypertrophic thicker, rough papule/
plaque
. Cutaneous horn:firm hyperkeratotic
outgrowth
• Actinic cheilitis:confluent AKs on
the lip
• Pigmented:flat, tan- brown,scaly
plaque
• Spreading pigmented
• Proliferative
• Conjunctival:pinguecula. pterygium
Differential Diagnosis
• SCC in situ,superficial BCC,seborrheic keratosis
Investigations
• biopsy refractory or suspiciouslesions (infiltrative,tender, bleeding spontaneously)
Management
• destructive:shave excision and curettage with electrodesiccation,or cryotherapy
• topical pharmacotherapy (mechanism:destruction of rapidly growing cells or immune system
modulation)
topical 5-fluorouracil cream (for 2-4 wk), imiquimod 5% (2x/wk for 16 wk), imiquimod 3.75%
(daily for 2 wk, and then daily again for 2 wk more)
• photodynamic therapy
• chemical peels (e.g. TCA, phenol)
• excision
• laser resurfacing
Leukoplakia
Clinical Features
• a morphologic term describing homogeneous orspeckled white plaques with sharply demarcated
borders
• sites:oropharynx, most often floor of the mouth,soft palate, and ventral/lateralsurfaces of the tongue
Pathophysiology
• prccancerous or pre-malignant condition
• oral variant is strongly associated with tobacco use and alcohol consumption
Epidemiology
• 1 -5% prevalence in adult population >30 yr old; peak at age >50
• M>F, fair-skinned
• most common oral mucosal pre-malignant lesion
Differential Diagnosis
• DLE,invasive SCC,candidiasis,lichen planus,oral hair)'leukoplakia, white sponge nevus
Investigations
• biopsy due to risk of malignancy
Management
• low-risk sites on buccal/labial mucosal or hard palate: eliminate carcinogenic habits,smoking
cessation, follow-up
• moderate/dysplastic lesions: excision, cryotherapy
• primary aim of treatment is to decrease the risk of oral SCC
r T
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D-iO Dermatology Toronto Notes 2023
Malignant Skin Tumours
Nonmelanoma Skin Cancers
BASAL CELL CARCINOMA
Subtypes
• nodular BCC (most common)
sldn-coloured papule/nodule with rolled, translucent (“pearly”) telangiectatic border, and
depressed/eroded/ulcerated centre
• pigmented BCC
• areas of pigment in translucent lesion with surface telangiectasia
• may mimic MM
• superficial BCC
thin, tan to red-brown plaque, often with scaly, pearly border, and fine telangiectasia at margin
• least aggressive subtype
• morpheaform BCC
• flesh/yellowish-coloured, shiny papule/plaque with indistinct borders, indurated
Pathophysiology
• malignant proliferation of basal keratinocytes of the epidermis
• low grade cutaneous malignancy, locally aggressive (primarily tangential growth), rarely
metastatic
• usually due to U VB light exposure, therefore >80% on sun exposed sites
• typical latency period of 20-50 yr between time of U V damage and onset of BCC
also associated with previous scars, radiation, trauma, arsenic exposure, or genetic predisposition
(Gorlin Syndrome)
Epidemiology
• most common malignancy in humans
• 75% of all malignant skin tumours in >40 yr old, increased prevalence in the elderly
• risk factors: M>F, skin phototypes I and 11, chronic cumulative sun exposure, ionizing radiation,
immunosuppression, arsenic exposure
Differential Diagnosis
• benign:sebaceous hyperplasia, intradermal melanocytic nevus, dermatofibroma
• malignant: nodular MM, SCC, merkel cell carcinoma (MCC)
Management
• see Table 22, Management of Nonmelanoma Skin Cancers
• follow-up for new primary disease or recurrence
• 95% cure rate if lesion <2 cm in diameter or if treated early
Workup/Investigations of Basal Cell
Carcinoma and Other Nonmelanoma
Skin Cancers
• History:duration,growth rate,
family/personal Hx of skin cancer,
prior therapy to the lesion
• Physical:location,site,whether
circumscribed,tethering to deep
structures, full skin exam,lymph
node exam
• Biopsy:if shallow lesion,can do
shave biopsy;otherwise punch
or cxcisional biopsy may be more
appropriate
Surgical Margins
• Smaller lesions:electrodessication
and curettage with 2 3 mm margin of
normal skin
• Deep infiltrative lesions:surgical
excision with 3-5 mm margins
beyond visible and palpable tumour
border,which may require skin
graft or flap; or Mohs surgery, which
conserves tissue and does not
require margin control
Table 22. Management of Nonmelanoma Skin Cancers
Treatment Treatment Options Indications
Category
Disadvantages
Topical Imiquimod 5% cream Superficial BCCs. Bowen's Disease
(Aldara -
)
Cryotherapy
Side effects: erythema, edema, ulceration and scaling
Superficial BCCs.Bowen'
s Disease
Advantages: minimal equipment,simple to perform, cost-effective, no
restriction of activity after surgery
5-lluorouracil (Efudex | Superficial BCCs. Bowen'
s Disease
Margin around cancer may not be free,potential forscarring,minimally painful,
no skin tissue for diagnosis
Side effects: pain, burning,swelling
Procedural Photodynamic therapy Superficial BCCs Side effects: pain
Advantages:low cost, tolerable side effect profile
Radiation therapy Advanced cases of BCC.SCC
Advantages:if lesions are located in cosmetically sensitive area
Shave excision and Most types of BCCs. Bowen's Disease
electrodessication and Advantages: minimal equipment needed,simple to perforin, cost-effective,
curettage
Mohssurgery
Side effects:alopecia, pigmentary changes,fibrosis, atrophy,buccal mucositis,
gingivitis, telangiectasias
Not used for morpheaform BCC.margin around cancer may not be free,slow
healing, possible scarring
Surgical
no restriction of activity after surgery
r i
BCC and SCC lesions on the face or in areas that are difficult to reconstruct
Advantages: highest cure rate, good cosmetic results, healthy skin tissue
is preserved
Expensive, highly technical,resource intensive, activity restriction after surgery
if skin graft/flap needed L J
SCC Activity restriction alter surgery if skin graft/flap needed, healthy tissue around
cancer must be removed
Iraditional surgical
excision Advantages:margin around cancer more likely to be free than shave
excision, tissue is available for diagnosis, cosmetic satisfaction
Metastatic BCC, Gorlin Syndrome (multiple BCCs)
+
Side effects: muscle spasms, hair loss,abnormal taste,weight loss,nausea,
amenorrhea
Medical
Therapy
Vismodegib
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D ll Dermatology Toronto Notes 2023
BOWEN’S DISEASE (SQUAMOUS CELL CARCINOMA IN SITU)
Clinical Features
• sharply demarcated erythematous patch/thin plaque with scale and/or crusting
• often 1-3 cm in diameter and found on the skin and mucous membranes
• evolves to SCC in 10-20% of cutaneous lesions and >20% of mucosal lesions
Management
• see Table 22, Management of Nonmelanoma Skin Cancers, D40
SQUAMOUS CELL CARCINOMA
Clinical Features
• hyperkeratotic indurated, pink/red/skin-coloured papule/plaque/nodule with surface scale/crust ±
ulceration
• more rapid enlargement than BCC
• exophytic (grows outward), may present as a cutaneous horn
• common sites: face, ears,scalp, forearms,dorsum of hands
Pathophysiology
• malignant neoplasm of keratinocytes(primarily vertical growth)
• predisposing factors include: cumulative UV radiation, PUVA, ionizing radiation therapy/
exposure, chemical carcinogens (such as arsenic,tar, and nitrogen mustards), HPV 16 or 18,
immunosuppression
• may occur in previous scar (SCC more commonly than BCC)
Epidemiology
• second most common type of cutaneous neoplasm in less pigmented skin types
• most common cutaneous neoplasm in patients with Type 6 skin, typically in non-photoexposed sites
• primarily on sun-exposed skin in the elderly, M>F,skin phototypes I and 11, chronic sun exposure
• SCC is the most common cutaneous malignancy in immunocompromised patientssuch as in organ
transplant recipients, with increased mortality as compared to non-immunocompromised population
Differential Diagnosis
• benign:wart, psoriasis, irritated seborrheic keratosis
• pre-malignanl: AK, Bowenoid papulosis
• malignant: keratoacanthoma, Bowen'
s disease, BCC, amelanotic melanoma
Management
• see table 22, Management o/ Nonmtlanoma skin Cancers, D id
• lifelong follow-up (more aggressive treatment than BCC)
Prognosis
• good prognostic factors:early treatment, negative margins, and small size of lesion
• rate of metastasisfrom primary SCC is 2-5%
• higher risk of metastasis if diameter >2 cm,depth >2 mm,recurrent, involvement of bone/muscle/
nerve,location on scalp/ears/nose/lips, immunosuppressed,caused by arsenic ingestion,or tumour
arose from scar/chronic ulcer/burn/genital tract/sinustract
(ft KERATOACANTHOMA
Clinical Features
• rapidly growing, firm, dome-shaped, erythematous or skin-coloured volcano-like nodule with central
keratin-filled crater
• may spontaneously regress
• sites:sun-exposed skin
Pathophysiology
• epithelial neoplasm with atypical keratinocytesin epidermis
• low grade variant of SCC
Interventionsfor IK
Cochrane D8 Syst Rev 2012:2:C004415
Purport:la assess thetffiucy of trejirrentsfor AK.
Methods:Systematic rev eve ot KCIs.
Results: A total of 83 RCTs (10036 patients)were
Included evaluating 24 treatments.Cryotherapy,
diclofenac. 5-fluorouracil. imiqiimd.ingenol
mebutate. photodynamic therapy,resurfacing and
trichloroacetic acid peel mere all effective at treating
AK and generally comparahte with one another.Skin
irritation was more common with diclofenac and
S-fluorouracil.Photodynamic therapy andimiqoimod
treatment resulted in better cosmetic appearance.
Conclusion:for individual lesions,photodynamic
therapy is more effective than cryotherapy,for
field-directed treatments. S-Duorouracrl.diclofenac
imiquimod and ingenol mebutate had comparable
efficacy.
Etiology
• HPV, U V radiation, chemical carcinogens(tar,mineral oil)
Epidemiology
• most common in >50 yr old, rare in <20 yr old
Differential Diagnosis
• treat as SCC until proven otherwise
• nodular BCC, MCC, hypertrophic solar keratosis, verruca vulgaris
n
L J
+
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D12 Dermatology Toronto Notes 2023
Management
• surgical excision or saucerization (shave biopsy) followed by electrodesiccation of the base,treated
similarly to SCC
• intralesional methotrexate or 5-fluorouracil injection
Malignant Melanoma
Clinical Features
• malignant characteristics of a mole: “ABCDE” mnemonic
• sites:skin, mucous membranes, eyes, CNS
•
—2/3 arise de novo without an associated nevus
• abnormal dermoscopic features
Does this Patient have a Mole or
Metanoma?
ABCDE checklist
Asymmetry
Border (irregular and/or indistinct)
Colour (varied)
Diameter (increasing or >6 mm)
Enlargement, elevation, evolution(i.e.
change in colour, size,or shape)
Sensitivity 92% (Cl 82-96%)
Specificity 100% (Cl 54-100%)
JUU199l;2tt:WS-W1
Clinical Subtypes of Malignant Melanoma
Listed from most to least common subtype
• superficialspreading melanoma (60-70% of all melanomas)
• atypical melanocytes initially spread laterally In epidermis then invade the dermis
• irregular, indurated, enlarging plaques with red/white/blue discolouration, focal papules or nodules
• ulcerate and bleed with growth
• subtype most likely associated with pre-existing nevus
• nodular melanoma (15-30% of all melanomas)
• atypical melanocytes that initially grow vertically with little lateral spread
• uniformly ulcerated, blue-black, and sharply delineated plaque or nodule
• rapidly fatal
• may be pink or have no colour at all, this is called an amelanotic melanoma
• EFG = elevated,firm, growing
• lentigo maligna
• MM in situ (normal and malignant melanocytes confined to the epidermis)
2-6 cm, tan/brown/black uniformly flat macule or patch with irregular borders
lesion grows radially and produces complex colours
often seen in the elderly
10% evolve to lentigo maligna melanoma
• lentigo maligna melanoma (5-15% of all melanomas)
• older individuals, ~7th decade
• malignant melanocytes invading into the dermis
• associated with pre-existing solar lentigo, not pre-existing nevi
• flat, brown,stain-like, gradually enlarging witn loss of skin surface markings
with time, colour changesfrom uniform brown to dark brown with black and blue
• found on all skin surfaces,especially those often exposed to sun,such as the face and hands
• acral lentiginous melanoma (5-10% of all melanomas)
ill-defined dark brown, blue-black macule
• palmar, plantar,subungualskin
melanomas on mucous membranes have poor prognosis
most common subtype found in patients with Type 6 skin
• amelanotic melanoma (2-8% of all melanomas)
little to no pigment
• pink or red macules, papules, or nodules,some may present with light-brown pigmentation
delay in diagnosis may contribute to its poor prognosis
MM in young children is more commonly amelanotic variant
<§)
Risk Factors for Melanoma
no SPF is a SIN
Sun exposure
Pigment traits (blue eyes, fair/red hair,
pale complexion)
Freckling
Skin reaction to sunlight (increased
incidence of sunburn)
Immunosuppressive states(e.g.renal
transplantation)
Nevi (dysplastic nevi:increased
number of benign melanocytic nevi)
$
Node Dissection for Lesions
. >1mm thick OR <1mm and ulcerated
OR >1 mitoses/mm2(Stage IB or
higher melanoma patients should
be offered a sentinel lymph node
biopsy)
• Assess sentinel node at time of wide
excision
Pathophysiology
• malignant neoplasm of pigment-forming cells (melanocytes and nevus cells)
Epidemiology
• I in 75 (Canada), I in 50 (US)
• risk factors: increasing age, fair skin, red hair, positive pcrsonal/family history, familial dysplastic
nevussyndrome, large congenital nevi (>2() cm), any dysplastic nevi, >50 common nevi,
immunosuppression,sun exposure with sunburns, tanning beds
• most common sites: back (M), calves (F)
• worse prognosis if: male, on scalp, hands,feet, late lesion, no pre-existing nevus present
Differential Diagnosis
• benign: nevi,solar lentigo,seborrheic keratosis, dermatofibroma,spitz nevus
• malignant:pigmented BCC, dermatofibrosarcoma protuberans
Set Landmark Dermatology trialstabic lot nott
reformation on the Inal by Hodi elal.2010. which
d Claris improved survival with Iprlimmnab in patterns
vnth metastatic melanoma .
Management
• excisional biopsy preferable (margin determined by Breslow depth), otherwise incisional biopsy,
sentinel lymph node dissection controversial
• remove full depth of dermis and extend beyond edges of lesion only after histologic diagnosis
• beware of lesions that regress-tumour is usually deeper than anticipated
• high dose ll-
'
N for stage 11 (regional), chemotherapy (cis-platinum, BCG) and high dose ll-
'
N forstage
Ill (distant) disease
• newer chemotherapeutic regimens, immunotherapy, and vaccines in metastatic melanoma
• radiotherapy may be used as adjunctive treatment
+
See Landmark Dermatology Trials table for more
information on the DDIH-3 trial comparing the efficacy
ofBRJkf kinase inhibitor vemurafemb(PlX4032)to
dacubaiine in patients with metastatic melanoma.
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D43 Dermatology Toronto Notes 2023
Table 23. American Joint Committee on Cancer Staging System Based on Breslow’s Thickness of
Invasion
Tumour Depth Stage Approximate 5 Yr Survival
II<1.0 mm
121.01-2.0 mm
T32.01-4.0 mm
M»4.0mm
Stage IT1a - T2a
Stage II T2b - T4b
StageIII any nodes
Stage IV any mets
5-yr survival 90%
5-yr survival 70%
S-yr survival45%
5-yr survival10%
a •no ulceration:b - ulceration
Other Cutaneous Cancers
CUTANEOUS T-CELL LYMPHOMA
Clinical Features
• Mycosis fungoides (limited superficial type)
characterized by slightly atrophic scaling, erythematous patches/plaques/nodules/tumours,
which may be pruritic and poikilodermic (atrophy, telangiectasia, hyperpigmentation,
hypopigmentation)
• common sites include: trunk, buttocks, proximal limbs
• mildly symptomatic, usually excellent prognosis for early disease
• hypopigmented subtype most commonly seen in children with deeperskin tones
• Sezary syndrome (widespread systemic type)
rare variant characterized by erythroderma,lymphadenopathy, WBC >20 x 109/L with Sezary
cells
» can be considered to have evolved from mycosis fungoides (not initially meeting diagnostic
criteria), but more commonly arises de novo
associated with intense pruritus,alopecia, palmoplantar hyperkeratosis,and systemic symptoms
(fatigue, fever)
• high mortality
Pathophysiology
• clonal proliferation ofskin-homing CD4 T-cells
Epidemiology
• seen in >50 yr, M:T ratio is 2:1
Differential Diagnosis
• tinea corporis, nummular dermatitis, psoriasis, DLL, Bowen'
s disease, adult T-Cell leukemialymphoma (ATL)
Investigations
• skin biopsy (histology, “lymphocyte antigen cell” markers,TcR gene arrangement)
• blood smear looking for Sezary cells or flow cytometry (e.g. CD4:CD8 >10 is characteristic but not
diagnostic of Sezary)
• imaging (forsystemic involvement)
Management
• Mycosis fungoides
depends on stage of disease
early stage:topicalsteroids, topical chemotherapy, topical retinoids, topical imiquimod, local
radiation, and/or PUVA, NB-UVB (311-313 mm)
advanced stage: biologies, low-dose methotrexate,systemic retinoids, PUVA
• Sezary syndrome
» oral retinoids and Il-
'
N
extra-corporeal photopheresis
• may need radiotherapy for total skin electron beam radiation
• may maintain on U V therapy
other chemotherapy agents
KAPOSI SARCOMA r-I
L J
Definition
• an angioproliferative neoplasm that requires infection with human herpesvirus 8 (HHV-8)
• 4 types based on the clinical circumstance at which it develops
• classical:develops in middle or old age in individuals of Mediterranean descent
• endemic:seen in sub-Saharan indigenous Africans
» iatrogenic:associated with immunosuppressive drug therapy and renal allograft recipients
AIDS associated
+
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Dll Dermatology Toronto Xotes 2023
Clinical Features
• purplish, reddish blue, or dark brown/black macules, plaques, and nodules on the skin
• skin nodules can range in size from very small to several centimeters in diameter, and lesions may
ulcerate and bleed
• lesions typically present on the distal extremities
• also atfects the gastrointestinal tract and lymphatics leading to secondary lymphoedema
Epidemiology
• incidence is 0.02% to 0.06% of all malignant tumours, M>F
Differential Diagnosis
• well-differentiated angiosarcoma, benign lymphangiomatosis, hypertrophic lichen planus
Investigations
• biopsy
• PCR - can identify HHV-8 DNA sequences
Treatment
• surgery', cryotherapy, lasersurgery, photodynamic therapy,topical retinoids, immunomodulators for
superficial macules and plaques
• radiation therapy,systemic chemotherapy
Diseases of Hair Density
Hair Growth
Hair Regrowth Potential
Ability to regrow hair depends on
location of inflammatory infiltrates on
hair follicle asstem cells are located
at the upper part (bulge region) of the
hair follicle
• Scarring alopecia:Inflammatory
infiltratesfound in upper part of hair
follicles, destroying stem cells
• Non-scarring alopecia:Hair follicle
is not permanently damaged, and
therefore spontaneous or treatmentinduced regrowth is possible
• hair grows in a cyclic pattern that is defined in 3stages(mostscalp hairs are in anagen phase)
growth stage = anagen phase
2.transitional stage = catagen stage
3.resting stage = telogcn phase
• total duration of the growth stage reflects the type and location of hair: eyebrow, eyelash, and axillary
hairs have a short growth stage in relation to the resting stage
• growth of the hair follicles is also based on the hormonal response to testosterone and
dihydrotestosterone (DHT); this response is genetically controlled
1.
Non-Scarring (Non-Cicatricial) Alopecia
ANDROGENETIC ALOPECIA
ODx of Non-Scarring (Non-Cicatricial)
Alopecia Clinical Features
• male- or female-pattern alopecia
• males:fronto-temporal areas progressing to vertex, entire scalp may be bald
• females:widening of central part, “Christmas tree” pattern
Pathophysiology
• action of DHT on hair follicles
Autoimmune
• Alopecia areata
Endocrine
• Hypothyroidism
• Androgens
Micronutrient deficiencies
• Iron
. Zinc
Toxins
• Heavy metals
• Anticoagulants
• Chemotherapy
. Vitamin A
Trauma to the hair follicle
• Trichotillomania
• Tight ponytail or braiding styles
Other
• Syphilis
. Severe illness
. Childbirth
Epidemiology
• males:early 20s-30s
• females: 40s-50s
Management
• camouflage techniques(i.e. wigs, hair extensions, powders, concealing lotions orsprays)
• topical minoxidil (Rogaine*) solution or foam to reduce rate of loss/partial restoration
• females:spironolactone (anti-androgenic effects), cyproterone acetate (Diane-35*)
• males:finasteride (Propecia*) (5-a-reductase inhibitor) 1 mg/d
• oral minoxidil
• procedural (hair transplant, platelet-rich plasma)
TELOGEN EFFLUVIUM
Clinical Features <§>
• uniform decrease in hair density secondary to hairsleaving the growth (anagen) stage and entering
the resting (telogen)stage of the cycle
Precipitant!of Telogen Effluvium
"SEND" hair follicles out of anagen and
into telogen
St ress and Scalp disease (surgery)
Endocrine (hypothyroidism, post
-
partum)
Nutritional (iron and protein deficiency)
Drugs (acitretin, heparin, lithium. IFN.
8-blockers, valproic acid.SSRIs)
Pathophysiology
• variety of precipitating factors (i.e. post-partum, psychological stress, major illness)
• hair loss typically occurs 2-4 mo after exposure to precipitant
• regrowth occurs within a few mo but may not be complete
+
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D45 Dermatology Toronto Notes 2023
ANAGEN EFFLUVIUM
Clinical Features
• hair loss due to insult of hair follicle impairing its mitotic activity (growth stage)
Pathophysiology
• precipitated by chemotherapeutic agents (most common), other medications(bismuth, levodopa,
colchicine, cyclosporine), exposure to chemicals(thallium, boron, arsenic)
• dose-dependent effect
• hair loss 7-14 d aftersingle pulse of chemotherapy;most clinically apparent after 1-2 mo
• reversible effect;follicles resume normal mitotic activity few wk after agent stopped
(§)
Hair Loss
TOP HAT
Telogen effluvium, Tinea capitis
Out of iron,zinc
Physical:trichotillomania,tight ponytail
or braiding styles
Hormonal: hypothyroidism, androgenic
Autoimmune: SLE. alopecia areata
Toxins: heavy metals, anticoagulants,
chemotherapy, vitamin A,SSRIs
ALOPECIA AREATA
Clinical Features
• autoimmune disorder characterized by patches of complete hair loss often localized to scalp, but can
affect eyebrows, beard, eyelashes, etc.
• may be associated with dystrophic nail changes-fine stippling, pitting
• “exclamation mark” pattern (hairsfractured and have tapered shafts, i.e.looks like “!”)
• may be associated with autoimmune conditions: pernicious anemia, vitiligo, thyroid disease,
Addisons disease
• spontaneous regrowth may occur within mo of first attack (worse prognosis if young at age of onset
and extensive loss)
• frequent recurrence often precipitated by emotional distress
• alopecia totalis:complete loss of hair on scalp
• alopecia universalis: complete loss of scalp hair, eyelashes, eyebrows, and body hair
Non-scarring alopecia:intact hair
follicles on exam * biopsy not required
(but may be helpful)
Scarring alopecia: absent hair follicles Management on exam •*biopsy required
• excellent prognosis for localized disease
• topical corticosteroids and intralesional triamcinolone acetonide (corticosteroids) can be used for
isolated patches
• topical immunotherapy (diphencyprone, anthralin)
• systemic immunosuppressants for refractory or extensive disease
• immunomodulatory (diphencyprone, anthralin)
• newer treatments:janus kinase inhibitors
Alopecia Areata Subtypes
Alopecia totalis:loss of allscalp hair and
eyebrows
Alopecia universalis: loss of all body hair
OTHER
• trichotillomania: impulse-control disorder characterized by compulsive hair pulling with irregular
patches of hair loss, and with remaining hairs broken at varying lengths
• traumatic (e.g. tight braiding styles, wearing tight ponytails, tight tying of hair coverings)
Scarring (Cicatricial) Alopecia
Clinical Features
• irreversible loss of hair follicles with fibrosis
Etiology
• physical: radiation, burns
• infections:fungal, bacterial, I B, leprosy, viral (HSV )
• primary inflammatory -subdivided into lymphocytic, neutrophilic, and mixed
lymphocytic:
lichen planus(lichen planopilaris) - white scale around hair follicles, up to 50% have lichen
planus at other body sites
DLL (note that SIL can cause an alopecia unrelated to DLL lesions which are non-scarring)
central centrifugal cicatricial alopecia (CCCA):seen in up to 40% of Black women,starting
at centralscalp;one of the most commonly diagnosed scarring alopecias, may be associated
with hair care practices
keratosis follicularisspinulosa decalvans (autosomal dominant, X-linked)
* neutrophilic:
folliculitis decalvans - discharge of pus and blood, tufting of hair follicles
dissecting cellulitis of the scalp -follicular papules, pustules, nodules, and abscesses develop
on the scalp
• mixed
acne keloidalis nuchae - dome-shaped papules, pustules, and plaques on the occipital scalp
• morphea: “coup de sabre” with involvement of centre of scalp
ri
Investigations
• biopsy from active border
Management
• infections: treat underlying infection
• inflammatory: topical/intralesionalsteroids, anti-inflammatory antibiotics, antimalarials,
immunosuppressants(e.g. cyclosporine)
+
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D-16 Dermatology Toronto Notes 2023
Postmenopausal Hair Changes
• estrogen regulates the growth and cycling of hair follicles
• hormonal changes (e.g. reduced estrogen) during menopause leads to decreased hair diameter, growth
rate, and percentage of hairs in the anagen phase; moreover, chronological age affects hair density
• these compounded effects of the two factors above (hormone changes and aging) may lead to a
perception of decreased scalp hairsin middle-aged women
Nails and Disorders of the Nail Apparatus
Table 24. Nail Changes in Systemic and Dermatological Conditions
Nail Abnormality Definition/Etiology Associated Disease
NAIL PLATECHAN6ES
Clubbing Proximal nail platehas greater than180" angle to Cyanotic heart disease,bacterial endocarditis,
nail fold,watch-glass nails,bulbous digits pulmonary disorders.Gl disorders,etc.
Iron deficiency,malnutrition.DM
Psoriasis,dermatophytes,thyroid disease,repetitive
trauma
Hypertrophy ol the nail plate producing a curved, Poor circulation,chronic inflammation,tinea
daw like delormity
Subungual hematoma
Fungal infection of nail (e.g.dermatophyte,yeast. HIV. DM. peripheral arterial disease
mould)
Hail plate detachment fromproximal nail fold due Manicures,ecrema,chronic paronychia,severe or
to severe trauma that produces a complete arrest febrile illness,erythroderma
of nailmatrix activity
Koilonychia
Onycholysis
Spoon shaped nails
Separation of nail plale from nail bed
Onychogryphosis
Onychohemia
Onychomycosis
Trauma to nail bed
Onychomadesis
SURFACE CHANGES
V-Shaped Nicking
Pterygium Inversum Unguis
Distal margin has Y-shaped loss of the nail plate Darier's disease (keralosisfollicularis)
Distal nail plale docs not separate from underlying Scleroderma
nail bed
Punctate depressions that migrate distally with
growth
Transverse depressions,often more in central
portion of nail plate
Pitting Psoriasis (random pattern),alopecia areata
(geometric,grid-shaped arrangement),eczema
Serious acute illness slows nail growth (when present
in all nails - Beau's lines),eczema,chronic paronychia,
trauma
Poisons, hypoalbuminemia (Muchtcke’s lines)
Lichen planus,psoriasis,normal aging,fungal
infection
Transverse Ridging
Transverse White lines
Onychorrhexis
8ands of while discolouration
Brittle nails leading to longitudinal ridging
COLOUR CHANGES
Yellow Tinea,(aundice.tetracycline,pityriasis rubra pilaris,
yellow nail syndrome,psoiiasis.tobacco use
Pseudomonas
Melanoma,hematoma
Nicotine use,psoriasis,poisons,longitudinal
melanonychia (more common in FitzpalrickV and VI)
Extravasation of blood from longitudinal vessels of ftauma,bacterial endocarditis, blood dyscrasias.
nail bed.blood attaches to overlying nail plate and psoriasis
moves distally as it grows
8rown-yellow discolouration
White nails
White proximal nail,darker distal nail with ground liver cirrhosis
glass appearance,no lunula
Green
Black
Brown
Splinter Hemorrhages
Oil Spots
Leukonychia
Terry's Nails
Psoriasis
Hypoalbuminemia,chronic renal failure
NAIL FOLD CHANGES
Herpetic Whitlow
Paronychia
HSV infection of distal phalanx
Local inflammation of thenail fold around the
nail bed
HSV infection
Acute:painful infection
Chronic:constant welting (e.g.dishwashing.
thumbsucking)
Nail Fold Telangicctasias Cuticular hemorrhages,roughness,capillary Scleroderma,SIE.dermalomyosltrs
changes r T
L J
LOSS OF HAILS
Occurs without scarring Trauma (especially toenails or fingernails after large
subungual hematoma).Beau's lines after severe
illness
Lichen planus (pterygium),genetic abnormalities
(rare)
Temporary Loss
Permanent Loss Occurs with scarring +
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D47 Dermatology Toronto Notes 2023
Adnexal Disorders
HIDRADENITIS SUPPURATIVA
Definition
• a chronic inflammatory skin condition that is a result of poor occlusion of the pilosebaceous units
within intertriginous zones
Clinical Features
• primary lesions are inflammatory nodules
• presence ofsinusformation,clusters of open comedones (double tombstone comedones), and
hypertrophic scarring of intertriginous areas
• sites: occurs primarily in the intertriginous areas of the axillae (most common site), inguinal area,
inner thighs, perianal and perineal areas, mammary and inframammary regions, buttocks, pubic
region,scrotum, vulva, trunk, and occasionally the scalp and retroauricular areas
• additionally significant hyperpigmentation and keloid formation can be seen in more pigmented skin
types
Pathophysiology
• follicular occlusion, follicular rupture, and an immune response
Epidemiology
• affects 1-4% of the population,1
;
>M
• onset ofsymptoms occur between puberty and age 40, typically in 2nd or 3rd decade
• increased incidence in people of African descent
• associated with smoking and excess weight
Differential Diagnosis
• folliculitis,furuncles, carbuncles, acne vulgaris,Crohn’s disease, granuloma inguinale, pyoderma
gangrenosum
Investigations
• clinical diagnosis
Treatment
« behavioural: patientself-management including avoidance ofskin trauma,smoking cessation, and
weight management
• pain management with NSAIDs
• mild disease:local therapy with topical clindamycin, intralesional corticosteroid injections, topical
resorcinol
• moderate to severe disease: antibiotic therapy (oral tetracyclines, clindamycin and rifampin
combination, dapsone), oral retinoids, hormonal therapy,surgery (punch debridement),laser and
light-based therapies(C02laser and Nd:YAG)
• refractory moderate to severe disease:TNF-a inhibitorssuch as adalimumab and infliximab,systemic
glucocorticoids, and cyclosporine
PRIMARY HYPERHIDROSIS
Definition
• secretion of sweat in amounts greater than physiologically needed for thermoregulation
Clinical Features
• focal, visible, excessive sweating of at least 6 mo without apparent cause
• symptoms typically develop during childhood or adolescence and persist throughout life
• symptoms occur only during waking hours(diurnal)
• focal symptomstypically localized to the palms, soles, and axillae, and less commonly the scalp and
face
Pathophysiology
• abnormal or exaggerated central response of the eccrine sweat glands to normal emotional stress
n
Epidemiology L J
• affects 1-5% of the population
• most patients have a family history of hyperhidrosis
Differential Diagnosis
• excessive heat, medications (e.g.antidepressants, antipyretics,cholinergic agonists, hormonal agents),
menopause, and spinal cord injuries (autonomic dysreflexia,orthostatic hypotension, posttraumatic
syringomyelia)
+
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D48 Dermatology Toronto Notes 2023
Investigations
• clinical diagnosis,iodine starch test
Treatment
• antiperspirants, botulinum toxin, microwave thermolysis, topical glycopyrronium bromide,suction
curettage,systemic agents(oral glycopyrrolate, oral oxybutynin), iontophoresis, or endoscopic
thoracic sympathectomy
Oral Diseases
LEUKOPLAKIA
• see Laikoplukiii, D39
RECURRENT APHTHOUS STOMATITIS
Clinical Features
• also known as “cankersores”
• painful,shallow, typically less than 5 mm in diameter,round to oval shaped,covered by a creamvwhitc pseudomembrane with an erythematous halo
• sites:labial and buccal mucosa,floor of the mouth, ventralsurface of the tongue,soft palate, and
oropharyngeal mucosa
Pathophysiology
• dysfunction in the immune system resulting in immunologically mediated damage to epithelial cells
• triggered by trauma, infectious agents,genetic factors, HIV infection, and hormonal fluctuations
• early lesions can show a neutrophilic vessel-based submucosal infiltrate
Epidemiology
• women more commonly affected than men
• peak prevalence in ages 20-30
Differential Diagnosis
• Behcet syndrome, SLE, gluten-sensitive enteropathy, HSV
Investigations
• diagnosis is made clinically
Treatment
• oral hygiene:soft toothbrush,waxed tape-style dental floss,soft-tipped gum stimulator for plaque
removal, and nonalcoholic mouthwash
• reduce traumatic factors inside the mouth such as biting cheeks or lips, and sharp/rough dental
restorations
• pain control:lidocaine viscous 2%, diphenhydramine liquid (12.5 mg/5 mL),dyclonine lozenges
• severe refractory’cases: colchicine
e.J
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DllJ Dermatology Toronto Notes 2023
Skin Manifestations of Systemic Disease
Table 25. Skin Manifestations of Internal Conditions
Disease Related Dermatoses
Raynaud's Phenomenon DDx AUTOIMMUNE DISORDERS
COLD HAND
Cryoglobulins/Cryofibrinogens
Obstruction/Occupational
Lupus erythematosus,other connective
tissue disease
DM/Drugs
Hematologic problems (polycythemia,
leukemia,etc.)
Arterial problems (atherosclerosis)
Neurologic problems (vascular tone)
Disease of unknown origin (idiopathic)
Behcet's Disease
Buerger's Disease
Dermatomyositis
Painful aphthous ulcers in oral cavity t genital mucousmembranes,erythema nodosum,acneiform papules
Superficial migratory thrombophlebitis, pallor,cyanosis, gangrene,ulcerations,digital resorptions
Periorbital and extensor violaceouserythema,heliotrope withedema.Gottron's papules (violaceousflattopped papules with atrophy),periungual erythema,telangiectasia,calcinosis culis
Subcutaneous nodules, stellate purpura,erythema,gangrene, splinter hemorrhages, livedo reticularis,
ulceration
Keratoderma blennorrhagica (on leet),balanitis circinata (on male penis)
Petechiae,urticaria,erythema nodosum,rheumatoidnodules,evanescent rash
Raynaud's,non-pitting edema,waxy/shiny/tense atrophic skin (morphea),ulcers,cutaneous calcification,
periungual telangiectasia,acrosderosis.salt-and- pepper pigmentation
Malar erythema,discoid rash (erythematous papules or plaques with keratotic scale, follicular plugging,
atrophic scarring on lace,hands,and arms),hemorrhagic bullae,palpable purpura, urticarial purpura,
patchy/diffuse alopecia,mucosal ulcers,photosensitivity
Pyoderma gangrenosum,erythema nodosum.Sweet's syndrome
Polyarteritis Nodosa
Reactive Arthritis
Rheumatic Fever
Scleroderma
SLE
Crohn's Disease/UC
ENDOCRINE DISORDERS
Addison's Oiscasc
Cushing's Syndrome
Generalired hyperpigmcntalion or limited to skin folds,buccal mucosa,and scars
Moon lades,purple striae,acne,hyperpigmcntalion,hirsutism,atrophic skin with telangiectasia
Infections (e.g.boils,carbuncles, candidiasis. S.aureus,dermatophytoses,tinea pedis and cruris,
infectious ecrematoid dermatitis),pruritus,eruptive xanthomas,necrobiosis lipoidica diabeticorum,
granuloma annulare,diabetic foot,diabetic bullae,acanthosis nigricans,calciphylaxis
Moist,warm skin,seborrhea,acne,nailatrophy,hyperpigmentation,toxic alopecia,pretibial myxedema,
acropachy.onycholysis
Cool,dry,scaly,thickened,hyperpigrncnled skin;toxic alopecia with dry.coarse hair, brittle nails,
myxedema, loss of lateral 113 eyebrows
DM
Acanthosis Nigricans
An asymptomatic dark thickened
velvety hyperpigmentation of flexural
skin most commonly around the neck.
Associated with DM. obesity,and other
endocrine disorders,and malignancy.It
is a cutaneous marker of tissue Insulin
resistance
Hyperthyroidism
Hypothyroidism
HIV- RELATED
Infections Viral (e.g. HSV. H2V,HPV.CMV.Molluscum contagiosum,oralhairy leukoplakia),bacterial (impetigo,
acneiform folliculitis,dental caries,cellulitis,bacillary epithelioid angiomatosis, syphilis),fungal
(candidiasis, histoplasmosis,cryptococcus, blastomycosis)
Seborrhea,psoriasis,pityriasis rosea,vasculitis
Kaposi's sarcoma,lymphoma,BCC,SCC,MM
Inflammatory Dermatoses
Malignancies
MALIGNANCY
Adenocarcinoma
Gastrointestinal
Ccrvix /anus/rcctum
Peutz- Jeghers:pigmentedmacules on lips/oralmucosa
Paget's disease:eroding scaling plaques ol perineum
Carcinoma
Breast
Paget's disease:eczematous and crusting lesions ol the skin ol the nipple and usually areola ol thebreast
Palmoplanlar keratoderma:thickened skin of palms/soles
Sipple's syndrome:multiple mucosal neuromas
Dermatomyositis:heliotrope erythema of eyelids and violaceous plaques over knuckles
G!
Thyroid
Breast/lung/ovary
Lymphoma/leukcmia
Hodgkin's
Acute leukemia
Multiple Myeloma
Ataxia telangiectasia:telangiectasia on pinna,bulbar conjunctiva
Ichthyosis:generalized scaling especially on extremities.Sweet's syndrome
Bloom's syndrome:butterfly erythema on face,associated with short stature
Amyloidosis:large,smooth tongue with facial petechiae and waxy papules on eyelids,nasolabial folds,
and lips
OTHERS
Liver Disease Pruritus,hyperpigmcntalion. spider nevi. palmar erythema,white nails (ferry's nails),porphyria culanea
tarda, xanthomas,hair loss,jaundice
Pruritus,pigmentation,half and hall nails,perforating dermatosis,calciphylaxis
Erythematous papules or urticarial plaques in distribution of striae distensae:buttocks,thighs,upper inner
arms,and lower back
Palpable purpura in cold exposed areas. Raynaud's,cold urticaria,acral hemorrhagic necrosis,bleeding
disorders,associated with hepatitis C inlection
Renal Disease
Pruritic Urticarial Papules and
Plaques of Pregnancy
Cryoglobulinemia
r “i
L J
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D50 Dermatology Toronto Notes 2023
Paediatric Exanthems
• see Paediatrics. P62
Miscellaneous Lesions
Angioedema and Urticaria
Angioedema
• deeper swelling of the skin involving subcutaneous tissues; often involves the eyes, lips, and tongue
• may or may not accompany urticaria
• hereditary or acquired forms
• hereditary angioedema (does not occur with urticaria)
onset in childhood; 80% have positive family history
• recurrent attacks; 25% die from laryngeal edema
• triggers: minor trauma, emotional upset, temperature changes
• types of acquired angioedema
acute allergic angioedema (allergens include food, drugs, contrast media, insect venom, latex)
non-allergic drug reaction (drugs include ACEI)
• acquired Cl inhibitor deficiency
• treatment
• prophylaxis with danazol or stanozolol for hereditary angioedema
• epinephrine pen to temporize until patient reaches hospital in acute attack
DDx for Urticaria
MAD HIVES
Malign ancy
Allergic
Drugs and foods
Hereditary
Infection
Vasculitis
Emotions
Stings
Urticaria
• also known as “hives”
• transient, red, pruritic well-demarcated wheals
• each individual lesion lasts less than 24 h
• second most common type of drug reaction
• results from release of histamine from mast cells in dermis
• can also result after physical contact with allergen Approach to Urticaria
• Thorough Hx and physical exam
• Acute:no immediate investigations
needed;consider referral for allergy
testing
. Chronic:further investigations
required:CBC and differential,
urinalysis,ESR,TSH,LFTs to help
identify underlying cause
• Vasculitic:biopsy of lesion and
referral to dermatology
Table 26. Classification of Urticaria
Type Etiology
Acute Urticaria
>213 of cases
Attacks last <6 wk
Individual lesions last <24 h
Drugs:especially ASA.NSAIDs
Foods:nuts,shellfish,eggs,fruit
Idiopathic
Infection
Drugs (antibiotics,hormones,local anesthetics)
Foods
Parasitic infections
Insect stings (bees,wasps,hornets)
Physical contact (animal saliva,plant resins,lalei.metals,lotions, soap)
Direct mast cell release
Opiates,muscle relaxanls,radio-contrast agents
Complement-mediated
Serum sickness,transfusion reactions
Infections,virat/bacterial (>80% of urticaria in paediatric patients)
Idiopathic (90% of chronic urticaria patients)
lg£-dependenl:trigger associated
Aeroallergens
Urlicarial vasculitis
Arachldonlc acid metabolism
ASA. NSAIDs
Physical
Oermatographism (Inchon,rubbing skin),cold (ice cube,cold water),cholinergic(hot shower,exercise),solar,
pressure (shoulder strap,buttocks),aquagenic (exposure to watei),adrenergic (stress),heat
Other
Mastocytosis,urticaria pigmentosa
Parasitic infections
Systemic diseases:SLE.endocrinopathy,neoplasm
Stress
Idiopathic
Infections
Hepatitis
Autoimmune diseases
Wheal
• Typically erythematous flat-topped,
palpable lesions varying insize with
circumscribed dermal edema
• Individual lesion lasts <24 h
• Associated with mast cell release of
histamine
• May be pruritic
Chronic Urticaria
<1/3 of cases
Attacks last >6 wk
Individual lesion lasts <24 h
Mastocytosis (Urticaria Pigmentosa)
Rare disease due to excessive infiltration
of the skin by mast cells.It manifests as
many reddish-brown elevated plaques
and macules.Friction to a lesion
produces a wheal surrounded by intense
erythema (Darier's sign),due to mast
cell degranulation:this occurs within
minutes of rubbing
r
Urticarial Vasculitis
Individual lesions last >24 h
Often painful,less likely
pruritic,wheals with bruise
type lesions
Biopsy indicated
SLE
Drug hypersensitivity
Cimetidine and dilliazem +
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D51 Dermatology Toronto Notes 2023
Erythema Nodosum B
Clinical Features
• acute or chronic inflammation of subcutaneous fat (panniculitis)
• round, red, tender, poorly demarcated nodules
• sites:asymmetrically arranged on extensor lower legs (typically shins), knees,arms
• associated with arthralgia, fever, malaise
Etiology
• 40% are idiopathic
• drugs:sulfonamides, OCPs (also pregnancy), analgesics, all-trans retinoic acid
• infections: GAS, I B, histoplasmosis, Yersinia
• inflammation:sarcoidosis, Crohn’
s > UC
• malignancy: acute leukemia, Hodgkin'
s lymphoma
Epidemiology
• 15-30 vr old, 1:M=3:1
• lesionslast for days and spontaneously resolve in 6 wk
DDx of Erythema Nodosum
NODOSUMM
NO cause (idiopathic)in 40%
Drugs (sulfonamides. OCP. etc.)
Other infections (Group A Strep)
Sarcoidosis
UC and Crohn's
Malignancy (leukemia,Hodgkin
lymphoma)
Many Infections
Investigations
• CXU (to rule out chest infection and sarcoidosis)
• throat culture, ASO titre, PPD skin test
Management
• symptomatic: bed rest, compressive bandages, wet dressings
• NSAIDs, intralesional steroids,oral potassium iodide
• treat underlying cause
Pruritus B
Clinical Features
• a sensation provoking a desire to scratch, with or without skin lesions
• lesions may arise from the underlying disease, or from excoriation causing crusts, lichenified plaques,
or wheals DDx of Pruritus
Etiology
• dermatologic - generalized
asteatotic dermatitis(“winter itch"due to dry skin)
• pruritus of senescent skin (may not have dry skin, any time of year)
infestations:scabies, lice
• immunoglobulins disease (bullous pemphigoid)
• drug eruptions: ASA, antidepressants, opiates
psychogenic states
• dermatologic -local
• atopic and contact dermatitis, lichen planus, urticaria, insect bites, dermatitis herpetiformis
• infection: varicella, candidiasis
lichen simplex chronicus
• prurigo nodularis
• systemic disease - usually generalized
hepatic:obstructive biliary disease, cholestatic liver disease of pregnancy
renal:chronic renal failure, uremia secondary'to hemodialysis
hematologic:Hodgkin’
s lymphoma, multiple myeloma,leukemia, polycythemia vera,
hemochromatosis, iron deficiency anemia, cutaneousT-cell lymphoma
neoplastic:lung, breast, gastric (internal solid tumours), non-Hodgkin'
slymphoma
endocrine:carcinoid, DM, hypothyroid/thyrotoxicosis
infectious:HIV,trichinosis,echinococcosis,hepatitis C
psychiatric:depression, psychosis
neurologic: post-herpetic neuralgia, multiple sclerosis
SCRATCHED
Scabies
Cholestasis
Renal
Autoimmune
Tumours
Crazies (psychiatric)
Hematology (polycythemia, lymphoma)
Endocrine (thyroid, parathyroid, iron)
Drugs, Dry skin
Consider biopsy of any non-healing
wound to rule out cancer
Investigations
• blood work:CBC, ESR, Cr/BUN,LIT, TSH, fasting blood sugar,stool culture, and serology'for
parasites
• biopsy
ri
LJ
Management
• treat underlying cause
• cool water compresses to relieve pruritus
• bath oil and emollient ointment (especially if xerosis is present)
• topical corticosteroid and antipruritics (e.g. menthol, camphor, phenol, mirtazapine, capsaicin)
• systemic antihistamines: H1 blockers are most effective, most useful for urticaria
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D52 Dermatology Toronto Notes 2023
• phototherapy with UVB or PUVA
• doxepin, amitriptyline
• immunosuppressive agents if severe:steroids and steroid-sparing Skin Phototypes (Fitzpatrick)
Phototype Colour of Skin's Response
to Sun Exposure
(without SPF
protection)
Skin Wounds and Ulcers
• see Plastic Surgery, PL8, PL17 l White Always bums,
never tans
White Always burns,
little tan
White Slight burn,
slow tan
Pale brown Slight burn,
faster tan
Brown Rarely burns,
dark tan
Never burns,
brown or dark tan
black
II Sunscreens and Preventative Therapy
Sunburn (Solar Erythema)
• erythema 2-6 h post U V exposure often associated with edema, pain and blistering with subsequent
desquamation of the dermis, and hyperpigmentation
• chronic UVA and UVB exposure leads to photoaging, immunosuppression, photocarcinogenesis
• prevention: avoid peak U VR (10 am-4 pm), wear appropriate clothing, wide-brimmed hat,sunglasses,
and broad-spectrum sunscreen
• clothing with UV protection expressed as UV protection factor ( UPP) is analogous to SP1
;
of sunscreen
IV
V
VI Bulk
Sunscreens
• under ideal conditions an SP1
;
of 10 means that a person who normally burnsin 20 min will burn in
200 min following the application of the sunscreen
• topical chemical: absorbs UV light
requires application at least 15-30 min prior to exposure,should be reapplied every 2 h (more
often ifsweating,swimming)
• UVB absorbers: PABA,salicylates, cinnamates, benzylidene camphor derivatives
• UVA absorbers:benzophenones, anthranilates, dibenzoylmethanes, benzylidene camphor
derivatives
• topical physical: reflects and scatters U V light
titanium dioxide, zinc oxide, kaolin, talc, ferric chloride, and melanin
• all are effective against the UVA and U VB spectrum
less risk of sensitization than chemical sunscreens and waterproof, but may cause folliculitis or
miliaria
• some sunscreen ingredients may cause contact or photocontact allergic reactions, but are uncommon
Management
• sunburn: if significant blistering present, consider treatment in hospital; otherwise,symptomatic
treatment (cool wet compresses, oral anti-inflammatory, topical corticosteroids)
• antioxidants, both oral and topical are being studied for their abilities to protect the skin; topical
agents are limited by their ability to penetrate the skin
SPF - burn time with cream/burn time
without cream
UV Radiation
UVA (320-400 nm):Aging
• Penetratesskin more effectively than
UVB or UVC
• Responsible for tanning, burning,
wrinkling, photoallergy, and
premature skin aging
• Penetrates clouds, glass and is
reflected off water,snow, and
cement
UVB (290-320 nm):Burning
• Absorbed by the outer dermis
• Is mainly responsible for burning and
premature skin aging
• Primarily responsible for BCC, SCO
• Does not penetrate glass and is
substantially absorbed by ozone
UVC (200-290 nm)
• Is filtered by ozone layer
Topical Steroids
Table 27. Potency Ranking of Topical Steroids
Relative Potency Relative Strength Generic Names Trade Names Usage
x1 hydrocortisone - 2.5% (1% available Emo Cort ’ Intcrlriginous areas,
children,lace,thin skin
Arm, leg. trunk
Weak Body Site:
Relative Percutaneous Absorption
Forearm 1.0
Plantar foot 0.14
Palm
Back
Scalp
Forehead 6.0
Cheeks 13.0
Scrotum 42.0
Calculation of strength of steroid
compared to hydrocortisone on forearm:
relative strength of steroid x relative
percutaneous absorption
QIC)
hydrocortisone 17-valerale - 0.2%
dcsonide
mometasone luroate
Moderate >3 Westcort’5
Tridesilon- 0.83
Elocom 5
Betnovale "
Celestoderm - V :
CydocorU
Oiprosone '
Lidex. fopsyngeL
lyderm!
Halog '
Dermovate!
1.7
3.7 betamethasone - 0.1%
17-valerale - 0.1%
amcinonide
betamethasone
dipropionate - 0.05%
fluocinonide -0.05%
halcinonide
dobetaso! propionate - 0.05% (most
potent)
betamethasone
dipropionale ointment
halobetasol propionate - 0.05%
Potent 16 Body
Very Potent x9 Palms and soles
Extremely Potent x12 Palms and soles
Oipiolene
Side Effects of Topical Steroids
• Local:atrophy, perioral dermatitis,
steroid acne,rosacea, contact
dermatitis, tachyphylaxis (tolerance),
telangiectasia,striae, hypertrichosis,
hypopigmentation
• Systemic:suppression ol HPA
axis,mood changes, nervousness,
insomnia, hyperglycemia, fluidf
sodium retention.Increased appetite,
weight gain, muscular weakness
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D53 Dermatology TorontoNotes 2023
Dermatologic Therapies
Topical Vehicles
. Ointment (water in oil):hydrate,
greasy
• Cream (oil in water):hydrate,
variable
• Lotion (powder in water):drying,
cosmesis
• Solutions (water,alcohol,propylene
glycol)
• Gel (solution that melts on contact
with skin,alcohol):drying
• Foam is a newer vehicle and several
agents are now available in foam
vehicles.Examples include Olux E*
(dobetasol).Verdeso'
(desonide).
Luxiq'(betamethasone), and
Enstilar '
(betamethasone propionate
and cakipotriol))
• Sprays:lamlsir (terbinafine) spray.
Clobex" spray (dobetasol)
• Lacquers:Penlac- (ddopirox),
Jublia '
(efinaconazole)
Table 28. Common Topical Therapies
Drug Name Dosing Schedule Indications Comments
Cakipotriol
(Oovonex |
0.005% cream,ointment,scalp Psoriasis
solution,apply BID
for maintenancetherapy.apply
once daily
Burning,itching,skinirritalion, worsening olpsoriasis
Avoid face,mucous membranes,eyes:wash hands after
application
Manimum weekly dosage of cream by age:
2-5»r - 25 g/wk
6-10 yr - 50 g/wk
11-14 yr - 75 g/wk
»14 y> -100 g/wk
Inactivated by light (do not apply before phototherapy)
Avoid natural/arlificral UV exposure
Local skin and application site reactions
Erythema, ulceration,edema,flu-like symptoms
Works best for warts on mucosal surfaces
May induce inflammation and erosion
Do not use in children*2 yr
Hypersensitivity to drug,or known sensitivity to
chrysanthemums
localreactions only (resolve rapidly):including burning,
pruritus
Low toxicity, excellent results
Consider second application after 7 d
Burning
Lacks adverse effects ol steroids
May be used on all skinsurfaces including head.neck,and
interlriginous areas
Expensive
Burning
Lacks adverse effects of steroids
May be used on allskinsurfaces including head.neck,and
interlriginous areas
Expensive
5% crearn applied 3x/wk
Apply at bedtime,leave on
8-10 h,then wash off with mild AK
soap and waler
Max duration 16 wk
Genital warts
Cutaneous warts
Imiqulmod
(Aldara )
Superficial BCC
Permethrin
(Kwellada - P
lotion and Nix
Dermal Cream)
1% or 5% cream,applied once Scabies (Kwellada-P
overnight to allskin areas from Lotion.Nix - Oermal
neck down,repeated one wk later Cream)
Pediculosis IKwellada P
Crime Rinse . Nix Crime
Rinse - )
Deciding on the Amount of Steroid
to Use
. 1palm -1% BSA
• 1fingertip unit (FTU)'Amount of
topical medication (from 5 mm
nozzle) placed on pad of Index finger
from distal tiplo DIP*500 mg *
2% BSA
• Therefore give 30 g for every 2 palms
of area to cover (if applying steroid
BID.1mo supply)
1% cream BID
Use for as long as lesions persist
and discontinue upon resolution
of symptoms
Pimccrollmus
(Elidcl )
AD (mild to moderate)
Tacrolimus
Topical
(Protopic )
0.03% (children) or 0.1% (adults) A0 (mild lo moderate)
ointment BID
Continue for duration of disease
plus1wk after clearing
Table 29. Common Oral Therapies
Drug Name Dosing Schedule Indications Comments
Acitrclin
(Soriatane -
)
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