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Pathophysiology

• benign tumour due to fibroblast proliferation in the dermis

Etiology

• unknown; may be associated with history of minor trauma (e.g.shaving or insect bites)

• eruptive dermatofibroma can be associated with SLE

Epidemiology

• adults,F>M

Differential Diagnosis

• dermatofibrosarcoma protuberans, MM, Kaposi’

s sarcoma, blue nevus

Investigations

• biopsy if diagnosis is uncertain

Management

• no treatment required

• excision if bothersome

SKIN TAGS

Clinical Features

• small (1-10 mm),soft,skin-coloured or darker pedunculated papule,often polypoid

• sites; eyelids, neck, axillae, inframammary, and groin

Pathophysiology

• benign outgrowth of skin

Epidemiology

• middle-aged and elderly,1

;

>M,obese,can increase in size and number during pregnancy

Differential Diagnosis

• pedunculated seborrheic keratosis, compound or dermal melanocytic nevus, neurofibroma,

fibroepithelioma of Pinkus (rare variant of BCC), nevus lipomatosis superficialis

Management

• snip excision, electrodessication, cryosurgery

Hyperkeratotic Lesions

SEBORRHEIC KERATOSIS

Clinical Features

• i.e.‘wisdom spots,’‘age spots,'

or‘barnacles of life’

• well-demarcated waxy papule/plaque with classic “stuck on” appearance

• occasionally pruritic

• over time lesions appear more warty, greasy, and pigmented

• sites:face, trunk, upper extremities (may occur at any site except palms orsoles)

Pathophysiology

• very common benign epithelial tumour due to proliferation of keratinocytes and melanocytes

Epidemiology

• unusual <30 yr old

• M>1

;

• autosomal dominant inheritance

• i.eser-T relat sign:sudden appearance of seborrheic keratosis that can be associated with malignancy,

commonly gastric adenocarcinomas

Differential Diagnosis

• MM (lentigo maligna,nodular melanoma),melanocytic nevi, pigmented BCC,solar lentigo,spreading

pigmented AK

L J

Investigations

• biopsy only if diagnosis uncertain +

Management

• none required, for cosmetic purposes only

• cryotherapy, electrodessication,shave excision

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DIO Dermatology Toronto Notes 2023

ACTINIC KERATOSES (SOLAR KERATOSES)

• see Pre-Malignant Skin Conditions, D39

KERATOACANTHOMA

• see

CORNS (HELOMATA)

Clinical Features $

• 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

Pathophysiology

• localized hyperkeratosis induced by pressure on hands and feet

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

Epidemiology

• F>M, can be caused by chronic microtrauma

Differential Diagnosis

• calluses, plantar warts

Management

• relieve pressure with padding or alternate footwear, orthotics

• paring, topical salicylic acid Keloids vs. Hypertrophic Scars

• Keloids: extend beyond margins

of original injury with claw like

extensions

• Hypertrophic scars: confined to

original margins of injury

Keloids

Clinical Features

• 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 yr with

claw-like extensions

• can be pruritic and painful

• sites: earlobes,shoulders, sternum,scapular area, angle of mandible

DDx of Hyperpigmented Macules

• Purpura (e.g.solar. ASA.

anticoagulants,steroids, hemosiderin

stain)

• Post-inflammatory

• Melasma

• Melanoma

• Fixed drug eruption

Pathophysiology

• excessive deposition of randomly organized collagen fibres following trauma to skin

Epidemiology

• most common in Black patients,followed by those of Asian descent (predilection for darker skin)

• M =T, most commonly between ages 10-30

Management

• intralesional corticosteroid injections

• silicone gel sheets

Pigmented Lesions

CONGENITAL NEVOMELANOCYTIC NEVI (CNN)

Clinical Features

• i.e. congenital hairy nevi

• sharply demarcated pigmented papule or plaque with regular borders ± coarse hairs

• classified by size:small (<1.5 cm), medium (Ml: 1.5-10 cm, M2:>10-20 cm),large (LI:>20-30 cm, L2:

>30-40 cm), giant (Gl: >40-60 cm, G2:>60 cm)

• may be surrounded by smaller satellite nevi

r >

L J

Pathophysiology

• nevomelanocytes in epidermis (clusters) and dermis (strands)

Epidemiology

• 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 CNN (melanocytes in the CNS)

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Management

• take a baseline photo and observe lesion for change in shape, colour, or size out of proportion with

growth

• surgical excision if suspicious, due to increased risk of melanoma

• MR1 if suspicious for neurological involvement Other Nevi

• Halo nevus:often appears as a

typical nevus surrounded by a ring of

depigmentation: common 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 arc noted

Other Nevi

• Halo nevus: often appears as a typical nevus surrounded by a ring of depigmentation; common 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

OTHER CONGENITAL PIGMENTED LESIONS

Table 5. Comparison of Other Congenital Pigmented Lesions

Differential

Diagnosis

Clinical Feature Pathophysiology Epidemiology Clinical Course

and Management

Cafe-au-lait Macule Areas of increased Siiormoreis

melanogenesis suggestive of

neurofibromatosis

type I

Also associated with

McCune- Albright

syndrome

Brown pigmented Increased melanocyte Risk of melanoma

macular background concentration

(cald-au-lait maculelike) with dark

macular or papular

speckles

Flat light- brown

lesions with smooth

or jagged borders

Flat congenital

melanocytic nevus,

speckled lentiginous No effective

nevus

Enlarge in proportion

to the child

treatment

Speckled

Lentiginous Nevus

( i.c. nevusspilus)

Cafe-au-lait macule. Usually the light

agminated lenligines. macular background

Becker's nevus Is present at birth

and speckles develop

over time

Management is

similar tothatoICNNs

Usually ladesin early

childhood but may

persist into adulthood

similar to that of a

CNN ol the same sire

Congenital grey-blue Ectopic melanocytes

solitary or grouped in dermis

macules commonly on

lumbosacral area

Extreme sensitivity to Involves mutations

UV light,redness and in genes responsible

blistering, xerosis, for DNA repair (e g.

and changesin skin nucleotide excision

colour

Typically affects the

cyesand sun - exposed

areas; may ailed

nervoussystem

99% occurs in Asian

and Indigenous

infants

Dermal

Melanocytosis

( historically known

as Mongolian Spot)

Xeroderma

Pigmentosum

Ecchymosis

More common in

Japan. North Africa,

and Middle East

Freckles. Rothmund- Prevention by

Thomson syndrome. avoiding sun

and porphyrin disease exposure (damage is

Irreversible)

Reduce incidence

of cancer using

anlicancer drugs

(e.g. isotretinoin,

fluorouracil) in adults

repair genes)

only

ACQUIRED NEVOMELANOCYTIC NEVI (NMN)

Clinical Features

• common mole:well circumscribed, round, uniformly pigmented macules/papules <1.5 cm

• average number of moles per person: 18-40

• three stages of evolution: junctional NMN, compound NMN, and dermal NMN

Table 6. Evolution of Acquired Nevomelanocytic Nevi

Type Age of Onset Clinical Feature Histology

Childhood

Majority progress to compound

nevus

Junctional Flat, regularly bordered,

uniformly Ian-dark brown,sharply junction above basement

membrane

Melanocytes at dermal-epidermal

demarcated macule

Compound Any age Domed, regularly bordered. Melanocytes atdermal-eprdermal

smooth, lound. Ian-dark brown junction:migration into dermis

papule

Face, trunk, extremities,scalp

NOT found on palms or soles

Soft,dome-shaped,skin-coloured Melanocytes exclusively in dermis

to tan/brown papules or nodules

Sites:face, neck

ri

c j

Dermal Adults

+

Management

• new or changing pigmented lesionsshould be evaluated for atypical features which could indicate a

melanoma

• excisional biopsy should be considered if the lesion demonstrates rapid change, asymmetry, varied

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OTHER ACQUIRED PIGMENTED LESIONS

Table 7. Comparison of Other Acquired Pigmented Lesions

Clinical Feature Pathophysiology Epidemiology Differential

Diagnosis

Clinical Course and Management

Atypical Nevus

(Dysplastic

Nevus)

Variegated macule/papule with Hyperplasia and proliferation

irregular distinct melanocytes in of melanocytes extending

beyond dermal comparlmcnl

of thenevus

Often with region of adjacent

nests

Small (<5 mm) well-demarcated Increased melanin within

basal layer kcratmocytes

secondary to sun exposure

Five atypical nevi increase risk for

melanoma

Numerous dysplastic nevi may be part

of familial atypical mole andmelanoma

syndrome

Risk factor:family history

Skin phototypes IIImost commonly

Follow with baseline photographs for

changes

Excisional biopsy if lesion changing or

highly atypical

Close surveillance with whole body skin

examination

Multiply and darken with sun exposure.

fade In winter

No treatment required

Sunscreen and sun avoidance may prevent

the appearance of new freckles

Laser therapy,shave excisions,

cryotherapy

Melanoma

the basal layer

Ephclides

(i.e.Freckles)

Junctional nevi

light brown macules Juvenile lenhgines

Sites:sun-exposed skin

Solar lentigo

(i.e.liver Spot)

Well-demarcated brown/black Benign melanocytic

macules

Sites:sun-exposed skin

Most common in white individuals >40 yr Lentigo maligna,

Skin phototypes l-lll most commonly seborrheic keratosis.

pigmented AK

proliferation indermalepidermal junction duelo

chronic sun exposure

Hairy,light brown macule/patch Pigmented hamartoma with

with a papular verrucous surface increased melanin in basal

Sites:trunk and shoulders cells

Onset in teen yr

Hair growth follows onset of pigmentation

Cosmetic management (usually loo large

to remove)

Becker's Nevus M>F Hairy congenital

Often becomes noticeable at puberty melanocytic nevus

Symmetrical hyperpigmenlation Increase In number and

on sun-exposed areas of face

(forehead,upper lip.cheeks,

chin)

Post-inflammatory

Common inpregnancy and women taking hyperpigmentation

OCPorKRT

Can occur with mild endocrine

disturbances,antiepileptic medications,

and other photosensitiiingdrugs

Risk factors:sun exposure,dark skin tone

F -M Often fades over several mo alter stopping

hormone treatmentor delivering baby

Treatment:hydroguinone.aielak acid,

retinoic acid,topical steroid,combination

creams,destructive modalities (chemical

peels,laser treatment),camouflage

make-up.sunscreen,sun avoidance

Melasma

activity of melanocytes

Associated with estrogen and

progesterone

Vascular Lesions

Table 8. Vascular Tumours Compared to Vascular Malformations

Vascular Tumours Vascular Malformations Pyogenic granuloma is a misnomer:it is

neither pyogenic nor granulomatous Definition

Presence at Birth

Endothelial hyperplasia

Usually postnatal

1:3-5

Phases

Proliferating

Involuting

Involuted

Congenital malformation withnormal endothelial turnover

100% at birth (not always obvious)

M:F 1:1

Natural History Proportionate growth (can expand)

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 HEMANGIOMAS

Clinical Features

• red or blue subcutaneous mass that issoft/compressible, blanches with pressure;feels like a “bag of

worms"when palpated

Pathophysiology

• benign vascular tumour

• includes: cavernous hemangioma, capillary/infantile hemangioma, spider hemangioma

A spider angioma will blanch when the

tip of a paperclip is applied to the centre

of the lesion

r T

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Table 9. Vascular Tumours

Clinical Feature Pathophysiology Epidemiology Clinical Course Management

Appears shortly alter birth. 10% require treatment due to functional impairment

increases in size over mo.

then regresses

50% ol lesions resolve

spontaneously by 5 yr

Hemangioma ol Hot.Ilrm.red to blue plaques or

Infancy

Benign vascular

proliferation of endothelial after birth;rarely

congenilal

Appears shortly

(visual compromise,airway obstruction,high output

cardiac failure) or cosmesis

Consider treatmentilnot gone by school age; topical

timolol,propranolol:systemic corticosteroids;laser

tumours

lining

treatment;surgery

Provide early specialist referral or treatment ininfants

with high-risk hemangiomas

Spider Angioma Central red artcnolc with slender Can be associated with

(i.e.Campbell branches,blanchable

Telangiectasia)

Any age Increase in number over lime Reassurance

hyperestrogenic state(e.g.

in liver disease,pregnancy.

OCP) but more oftenis not

Electrodesiccation or laser surgery if patient wishes

Cherry Angioma Bright red to deep maroon,dome- Benign vascular neoplasm »30 y« old

(i.e.Campbell Dc shaped vascular papules,1-5 mm

Morgan Spot) Site:trunk

lesions do not fade intime Usually no treatment needed

lesions bleed infrequently laser or electrocautcry for small lesions

Excision of large lesions if necessary

less friable compared to pyogenic

granulomas

Pyogenic

Granuloma

Bright red.dome-shaped sessile Rapidly developing

or pedunculated friable nodule hemangioma

Sites:fingers,lips,mouth,trunk. Proliferation of capillaries

with erosion of epidermis

DDx:glomus tumour,nodular MM. and neutrophilia

SCC,nodular BCC

'

30 yr old Surgical excision with histologic examination

Elcctrocautery:laser;cryotherapy

lesion grows rapidly over

wk -mo.then stabilizes

lesion may persist

toes indefinitely if untreated

VASCULAR MALFORMATIONS

Table 10. Vascular Malformations

Type Clinical Feature Pathophysiology Management

Nevus Flammeus

(i.e.Port-wine Stain) distribution,rarely crosses midlinc

Most common site:nape of neck

Never spontaneously regresses but grows inproportion to

the child

Nevus Simplex Pink-redirregular patches

(I.e.Salmon Patch) Midlinc macule on glabella known as “Angel Kiss."in the

nuchal regionknown as “Stork Bites"

Present in 113 of newborns

Majority regress spontaneously

Red to blue macule present at birth that follows a dermatoma! Congenital vascular malformation Laser or make- up

ol dermal capillaries:rarely

associated with Sturge-Weber

syndrome (VI.V2 distribution)

Congenital dilation of dermal

capillaries

No treatment

required

Lipoma

Clinical Features

• 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

Pathophysiology

• adipocytes enclosed in a fibrous capsule

Epidemiology

• often solitary or few in number, if multiple can be associated with rare syndromes

Differential Diagnosis

• angiolipoma, liposarcoma

Investigations

• biopsy only if atypical features (painful,rapid growth, firm)

Management

• reassurance

• excision or liposuction only if desired for cosmetic purposes r n

u j

Xanthoma

Clinical Features

• localized lipid deposits that manifest as papules, plaques, or nodules in the skin

• several variants: eruptive xanthoma (1-5 mm erythematous-to-yellow papules);tuberous xanthoma

(<3 cm vellow-to-orange or erythematous papules or nodules); tendinous xanthoma (smooth, firm,

mobile,skin-coloured nodules); plane xanthoma (soft, yellow, thin plaques)

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Pathophysiology

• xanthoma associated with hyperlipidemia:formed from macrophages due to excessive uptake and

oxidation of low density lipoprotein particles

• xanthoma not associated with hyperlipidemia (e.g. plane xanthoma):develop associated with

monoclonal gammopathy, multiple myeloma,and other hematologic diseases; immune complexes

form between antibodies and lipoproteinsleading to lipid accumulation in macrophages

• xanthoma not associated with hyperlipidemia (e.g. verruciform xanthoma): may be response to

immune reaction to local trauma or inflammation

Epidemiology

• often present in adulthood (except xanthoma associated with hypercholesterolemia, in which

xanthoma develops before 10 yr old)

• occur in both males and females, no sex predilection

Differential Diagnosis

• xanthelasma:sebaceous hyperplasia, juvenile xanthogranuloma,syringoma, nodular BCC

• plane xanthoma: necrobiotic xanthogranuloma

• eruptive xanthoma:generalized granuloma annulare, xanthoma disseminatum

• tendinous xanthoma and tuberous xanthoma:other nodular eruptions over joints and tendons (e.g.

rheumatoid nodules,gouty tophi,subcutaneous granuloma annulare, erythema elevatum diutinum)

• verrucous xanthoma: condylomata, oral papillomas, verrucous carcinoma,SCC

Investigations

• biopsy (shave, punch, or excisional)

• fasting lipid panel (except for xanthomas not associated with hyperlipidemia, e.g. verruciform

xanthomas)

Treatment of Acne Scars

. Tretinoin creams

• Glycolic acid

• Chemical peels for superficial sears

• Injectable fillers (collagen,hyaluronic

acid) for pitted scars

, Fraxellaser

• COr laser resurfacing

Management

• typically asymptomatic and therefore do not require treatment unlessfor cosmetic reasons

• options include surgical excision, cryotherapy, trichloroacetic acid 70% chemical peels, or tr:YA(» or

Nd-YAG lasers

• pharmacologic treatment of dyslipidemia usually indicated

Acneiform Eruptions topical Benzoyl Peroxide lor Acne

Cochrane DBSyst REV 2020:CD 011154

P arpose:Sestemcu I)mini t'e use of topical

benzoyl peroxide for treating acne.

Methods:RCIs comparing the use of topical benzoyl

peroxide.1«the treatment ol dentally diagnosed

acae to either placebo,or other topical medication

were eligiblelor Inclusion.Ihe primary outcome

measures that were assessed weie ‘participant

global self-assessment of acne improvement'and

‘withdrawal due to adverse eventsin Ihe whole

course of the trial’.The secondary outcome measure

that wisassessed was 'Percentage olportkipants

experiencing any adverse event in the whole course

of the trial.'

Results:A total of 120 studiesincluding 25592

people were included in thisreview. For‘participant

global self -assessment of acoe improvement'

benzoyl peroiide was moie effective than placebo

or no treatment (visit ratio (RH)127,95% confidence

interval (Cl) 1.12-1.45:3 RCIs: 2234 participants;

treatment for 10-12 wit:low-certainty evidence),

little lo nodrfference existed between benzoyl

peroiide and adapalene (RR 0.99,95% Cl 0.9CM.10:

5 RCTs;1472 participants;treatmenf for11-12 wt)

and chiidamycm (RR 0.95.95% Cl 0.68- 1.34:1

SCI:240 participants:treatmentfor 10 weeks|.

Withdrawal due loadvttse effects was higher with

benzoyl peroiide than with no treatment or placebo

and the most common cited adverse effectsincluded

erythema, pruritus, aod skin homing.

Low quality evidence suggestslittle to nodrfference

in withdrawal due to adverse events between benzoyl

peroxide and adapalene.clindamycin, erythromycin,

ov salicylic acid.Very low quality evidence exists

comparing the incidence ol any adverse events

between benzoyl peroiide and other treatments,

however most reported adverse events weremild.

Acne Vulgaris/Common Acne

Clinical Features

• a common inflammatory pilosebaceous disease categorized with respect according to severity

• Type 1: comedonal,sparse, no scarring

Type 11: comedonal, papular, moderate ± little scarring

• Type III: comedonal, papular, and pustular, with scarring

Type IV: nodulocystic acne, risk ofsevere scarring

• sites of predilection:face, neck, upper chest, and back

Pathophysiology

• hyperkeratinization at the follicular ostia (opening) blocks the secretion ofsebum leading to the

formation of microcomedones

• androgens promote excess sebum production

• Culibacterium acnes acnes) metabolizes sebum to free fatty acids and produces pro-inflammatory

mediators

Epidemiology

• age of onset typically 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- ofsevere

acne ri

LJ

Differential Diagnosis

• folliculitis, keratosis pilaris (upper arms,face, thighs), perioral dermatitis,rosacea

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Table 11. Management of Acne

Compound/Drug Class Product Names Notes

Acne Myths Debunked

• Eating greasy food and chocolate

does not cause or worsen acne

t Blackheads (comedones) are black

because of oxidized fatty acids,

not dirt

• Acne is not caused by poor hygiene:

on the contrary,excessive washing of

face can be an aggravator

MILO ACNE:OTC

TopicalTherapies

Benzoyl peroxide (8P0) Solugel '

. Beniac .Ocsquam '

,

fostex '

.Ceralfe Acne Foaming

Cleanser 1

Helps prevent Propionibaclenum ernes|P. ocnes) resistance,is a

bactericidal agentftargets P. ocnes), and is comedolytic

Salicylic acid Akurza '

cream,Oermaione '

Used when patients cannot tolerate a topical retinoid due to skin

irritation

MUD ACHE:Prescription

Topical Therapies

Antimicrobials

Retinoids

clindamycin (Dalacin T’

•).erythromycin High rate of resistance when used as monotherapy

vitamin A acid (tretinoin.Stieva- A

'

. Backbone of topical acne therapy

Retin A Micro*),adapalene (Differin:

). All regimens should include a retinoid unless patient cannot tolerate

ARAZlO '

(tazarotene) Lotion 0.045%,

AKLIEF -

(Infarolene) Cream

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)

Allows for greater adherence and efficacy

Combines different mechanisms of action to increase efficacy and

maximize tolerability

Combination products clindamycin and CPO (Clindoxyl ’

)

clindamycin and 8P0 (Benzaclm )

TactuPump* (adapalene and BPO)

clindamycin and tretinoin (Biacna '

)

erythromycin and BPO (Bcntainycin '

)

MODERATEACNE

Tetracyclinc/Minocydinc/ Sumycin iMinocin'

fVibramycin '

Doxycydine

Use caution with regard to drug interactions:do not use with isotretinoin

Sun sensitivity

Antibiotics require 3 mo of use before assessing efficacy

After 35 yr of age.estrogenfprogesterone should only be considered in

exceptional circumstances,carefully weighing the risk/benefit ratio with

physician guidance

May causehyperkalemia if concurrent renal dx

Black box warning for breast cancer

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 os leaning face on hands

• Emotional stress

Cyproterone acetate 0iane-35

ethinyl estradiol

Spironolactone Aldactone *

SEVERE ACHE

Isotretinoin Accutane -

. Clarus:

.Epuris - See Table 29.D53 for full side effect profile

Most adverse effects are temporary and will resolve when the drug is

discontinued

Baseline lipidprofile (riskof hypertriglyceridemia).LFTsand p-hCG

before treatment

May transiently exacerbate acne beforepatient sees improvement

Refractory cases may require multiple courses of isotretinoin

A combination of topical retinoids and

topical erythromycin or clindamycin is

more effective than either agent used

alone

Perioral Dermatitis

Clinical Features

• discrete erythematous papulopustular eruptions that often become confluent, forming inflammatory

plaques on perioral, perinasal, and /or periorbital skin

• commonly symmetrical, rim of sparing around Vermillion border of lips

Intralesional Injections

Intralesional corticosteroid injections are

effective in the treatment of individual

acne nodules

Epidemiology

• 15-40 yr old, occasionally in younger children

• predominantly females

Differential Diagnosis

• contact dermatitis, rosacea, acne vulgaris

Management

• avoid all topical steroids, avoid ointment/oil-based products,stop all cosmetic products

• topical: metronidazole 0.75% gel or 0.75- 1% cream to affected area B11)

• systemic: tetracycline family antibiotic (utilized for its anti-inflammatory properties)

• occasional use of a topical calcineurin inhibitor cream (i.e. pimecrolimus)

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

t Patients should use two forms of

contraception while on isotretinoin

Rosacea Important Controversies Associated with

Isotretinoin Therapy tor Acne

An J Clin Dermatol 2013;14JI-76

MainPoints:

1. The evidence on whether isotretinoin causes

depression and suicide is inconsistent:however,

numerous controlled studies haw shown an

improvement in anxiety and depression scores in

those taking isotretinoin.

2. There isnoassociation between ISO and

isotietinoin use.Only one study showed

a sgr hcantly increased riskof UC.When

cor sidenng using isotretinoin ina patient with

IBDorwith a stiongfacnily history,consider

Clinical Features

• 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,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

r

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•phyma: a distinctswelling caused by lymphedema and hypertrophy ofsubcutaneous tissue,

particularly affecting the nose (rhinophyma)

•ocular manifestations:blepharoconjunctivitis, keratitis, iritis

Pathophysiology

•unknown

Epidemiology

•although found in all skin types, highest prevalence in fair-skinned people

•30-50 yr old; T>M

Differential Diagnosis

•acne vulgaris,seborrheic dermatitis, perioral dermatitis, contact dermatitis Figure 7. Rosacea distribution

Management

•trigger avoidance and daily sunscreen use for long-term management

•avoid topical corticosteroids

•telangiectasia:treated by physical ablation;electrical hvfrecators, vascular lasers, and intense pulsed

light therapies

•phymas: treated by physical ablation or removal; paring, electrosurgery, cryotherapy, laser therapy

(CO2, argon, Nd:YAG)

Rosacea

ocan be differentiated from

acne by the absence of comedones,a

predilection for the central face , and

symptoms of flushing

First

Table

Line

12. Specific Rosacea Treatments

Second Line Third Line

$

Guidelines for the Diagnosis of

Rosacea

J Drugs Dermatol 2012:11(6):725-730

• Presence of one or more of the

following primary features:

• Flushing (transient 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

Oral tetracyclines

Topical metronidarole

Oral erythromycin (2S0-500 mg PO BIO)

Topical acelaic acid

Topical ivermectin

Topical clindamycin

Topical erythromycin 2% solution

Oral melronldaiole

Oral retinoids

Dermatitis (Eczema)

Definition

• inflammation of the skin

Clinical Features

• poorly demarcated erythematous patches or plaques

• symptoms include pruritus and pain

• acute dermatitis:papules, vesicles

• subacute dermatitis:scaling, crusting, excoriations

• chronic dermatitis:lichenihcation, xerosis, Assuring Emollients and Moisturiscrs for Eczema

Cochrane OB Syst Rev 2017:00012119

P urpose:To review the effects of mosturirersfor

eczema.

Methods:This review irC.ded RCTs published prior

toOetember 2015 on the elf eels of modtontei on

ecrema.

Results:77studies with a total of 6603 participants

were included m tlw renew. Mootunzeisshowed

beneficial effects on ecrena symptoms and seventy.

Key benefitsincluded prolonging tune to flares,

reducing Ihe number of dares, and reducing the

amount of corticosteroids needed.When active

treatmentwascombmedwith moisturizer, greater

benefits were seen. Evidence does not e»1st to

support the use ol one moisturizer ovei another.

Asteatotic Dermatitis

Clinical Features

• 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"

Management

• skin rehydration with moisturizing routine ± corticosteroid creams

Atopic Dermatitis

Clinical Features

• subacute and chronic eczematous reaction associated with prolonged severe pruritus

• distribution depends on age

• inflammation,lichenification, and excoriations are secondary to relentless scratching

• atopic palms:hyperlinearity of the palms (associated with ichthyosis vulgaris)

• associated with: keratosis pilaris (hyperkeratosis of hair follicles, “chicken skin"), xerosis,

occupational hand dryness

• associated with severe or poorly controlled psychosocial distress and psychiatric comorbidities

Epidemiology

• frequently affects infants, children, and young adults

• 10-20% of children in developed countries <5 yr old are affected

• associated with personal or family history of atopy (asthma, hay fever), anaphylaxis, eosinophllia

• polygenic inheritance:one parent >6096 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

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

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Pathophysiology

• a T-cell driven inflammatory process with epidermal barrier dysfunction

Investigations

• clinical diagnosis

• consider:skin biopsy,serum lgE levels, patch testing if allergic contact dermatitisis suspected

Management

• goal:reduce signs and symptoms, prevent or reduce recurrences/flares

• better outcomes (e.g. less flare-ups, modified course of disease) if diagnosis made early

• avoid triggers of AD (e.g. wool,scented products, heat, etc.)

• be vigilant for depressive symptoms and the possible need for psychiatric referral,especially among

those with severe disease

• 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

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 ofsteroid potency depends on age, body site,short vs.long-term use

apply one adult fingertip unit (0.5 g) to an area the size of two 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% (lilidel*)

can be used as acute treatments and assteroid-sparing agents in the long-term

advantages over long-term corticosteroid use: no skin atrophy;safe for sensitive areas such as

the face and neck

apply BID for acute flares, and 2-3x/wk to recurrentsites to prevent relapses

local side effects:stinging, burning, cost

U.S. black box warning of malignancy risk: rare cases of skin cancer and lymphoma reported;

no causal relationship established, warning is discounted by both the Canadian Dermatology

Association and the American Academy of Dermatology

biologies

dupilumab (anti>Il 4/13)

upadacitinib ()AK Inhibitor)

topical PDE-4 inhibitor

crisaborole (Eucrisa)

Figure 8. AD distribution

The typical distribution of AD in

infants <6 mo (top), children >18 mo

(middle), and adults >18 yr (bottom)

Complications

• infections

• treatment of infections:

topical mupirocin, ozenoxarin, or fusidic acid (Canada only, not available in US)

oral antibiotics (e.g. cloxadllin, cephalexin) for widespread S.aureus infections

^

Initial assessment of disease history, extent, and severity (impact on family, psychological distress)

)

i

Patient education, daily emollient use

J

Disease

remission (no

signs or

symptoms)

Adjunctive therapy

• Avoidance of

triggers

• Treat bacterial

superinfections

(topical or oral

antibiotics)

• Antihistamines

• Psychological

interventions

Acute control of flare

• Topical corticosteroids or topical calcineurin inhibitor

FLARE

1

Maintenance therapy il disease is persistent

and/or frequent recurrences

• Use topical corticosteroid or calcineurin inhibitor

at earliest sign of flare

* Long-term maintenance use of calcineurin inhibitors r t

I

u

Severe refractory disease

• Phototherapy

• Potent topicalsteroids

• Psychotherapeutics

• Azathioprine

• Dupilumab

• Methotrexate

• Oral cyclosporin

• Oral steroids

+

Figure 9. Atopic dermatitistreatment algorithm

Adapted lr urn:Hid C.et al.ICCA0IIFaculty.International Consensus Conference on Atopic DermatitisII(ICCADII):clinical update andcurrent

treatment strategies.Br JDermatol 2003:148(Suppl 63}:3-10 Activate Windows

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Dl8 Dermatology Toronto Xotes 2023

Contact Dermatitis NS

Clinical Features

• cutaneous inflammation caused by an external agent(s)

Table 13. Contact Dermatitis

Irritant Contact Dermatitis Allergic Contact Dermatitis

Mechanism olReaction Toxic injury to skin;ron immnne mechanism Cell-mediated delayed (Type IV) hypersensitivity

reaction (see Rheumatology,RH2)

Erythema with a papulovesicular eruption.swelling.

pruritus

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

Majority;will occur in anyone given sufficient

concentration of irritants

Hands are the most common site

Soaps,weak alkali,detergents,organic solvents,

alcohol,oils

Frequency Minority;patient acquires susceptibility to allergen that

persists indefinitely

Areas exposed to allergen

Many allergens are irritants,so may coincide with

irritant dermatitis

Nickel

Tattoos

Patch testing to determine specific allergen

Avoid allergen and its cross-reactants

Wet compresses soaked in Burow's solution

Topical steroids BID PRN

Systemic steroids PRN if extensive

Distribution

Examples

Avoidance of irritants

Wet compresses with Burow's solution (drying agent)

Barrier moisturiters

Topical/oral steroids

Management

Dyshidrotic Dermatitis

Clinical Features

• “tapioca pudding"

papulovesicular or bullous dermatitis of hands and feet that coalesce into plaques,

followed by painful Assuring

• 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

Pathophysiology

• unknown

• NO T caused by hyperhidrosis (excessive sweating)

• emotional stress may precipitate Hares

Management

• topical:high potency corticosteroid with plastic cling wrap occlusion to Increase penetration

• systemic

• prednisone in severe cases

• alitretinoin (Toctino*) for all types of chronic hand dermatitis, including dyshidrotic dermatitis

• antibiotics for secondary S. aureus infection

Nummular Dermatitis

Clinical Features

• nummular (coin-shaped), pruritic, dry,scaly, erythematous plaques

• often associated with atopic and dyshidrotic dermatitis

• secondary infection common

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

Management r T

• moisturization

• mid- to high-potency corticosteroid ointment BID

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Seborrheic Dermatitis

Clinical Features

• greasy, erythematous, yellow,scaling, papules and plaques in areasrich 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 ofscalp margin with yellow to white flakes, pruritus, and underlying

erythema

• sites:scalp, nasolabial folds, eyebrows, eyelashes, beard, glabella, post-auricular, oversternum,trunk,

body folds, genitalia

Pathophysiology

• possible etiologic association with Malassezia spp.(yeast)

Epidemiology

• common in infants, adolescents, and males

• increased incidence and severity in immunocompromised patients and Parkinson’s disease

• in adults can cause dandruff (pityriasissicca)

Management

• face: keratolytic creams ketoconazole (Nizoral*) cream daily or BID and/or mild steroid cream dailv

or BID

• scalp:Derma-Smoothe FS* lotion (peanut oil, mineral oil,fluocinolone acetonide 0.01%) to remove

dense scales, ketoconazole 2% 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 Features

• erythematous,scaly, pruritic plaques on lower legs, particularly the medial ankle

• brown hemosiderin deposition,woody fibrosis, atrophy blanche,and lipodermatosderosis in late

stages

• usually bilateral, accompanied by swelling,oozing,crusting,may have accompanying varicosities

Pathophysiology

• chronic venousinsufficiency leadsto venousstasis

• surrounding soft tissue inflammation and fibrosis results

Investigations

• Doppler ifsuspicious for DVT,other vascularstudies (e.g. venous duplex,ankle-brachial index)

• swab for bacterial culture if there is crusting

Management

• compression stockings

• rest and elevate legs (above the level of the heart)

• moisturizer daily aftershower to treat xerosis

• mid-high potency topical corticosteroidsto control inflammation

Complications

• ulceration (common at medial malleolus),secondary bacterial infections

Lichen Simplex Chronicus

Clinical Features

• well-defined plaque(s) of lichenified skin with increased pruritic skin markings ± excoriations

• common sites:neck,scalp, extremities,urogenital area

• often seen in patients with atopy, anxiety'disorders, nonspecific emotionalstress, among other

conditions

Pathophysiology

• skin hyperexcitable to itch, resulting in continued rubbing/scratching ofskin

• eventually lichenification occurs

Investigations

• histopathology/biopsy confirms diagnosisif clinical diagnosis uncertain

• if patient has generalized pruritus,rule outsystemic cause:CBC with differential count,

transaminases, bilirubin,ferritin,renal and thyroid function tests,TSH,glucose, SPEP

• CXR if lymphoma suspected

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Management

• antipruritics(e.g. antihistamines,topical or intralesional glucocorticoids)

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D20 Dermatology Toronto Xotes 2023

Papulosquamous Diseases

Lichen Planus

The 6 Ps of Lichen Planus

Purple

Pruritic

Polygonal

Peripheral

Papules

Penis (i.e.mucosa)

Clinical Features

• acute or chronic inflammation of skin or mucous membranes

• morphology:pruritic, well-demarcated, violaceous, polygonal,flat-topped papules and plaques

• common sites:wrists, nails, scalp, mucous membranes in 60% (mouth, vulva, glans)

• distribution:symmetrical and bilateral

• Wickhamsstriae:reticulate white-grey lines over surface; pathognomonic but may not be present

• mucous membrane lesions:lacy, whitish reticular network, milky-white plaques/papules; increased

risk of SCC in erosions and ulcers

• nails:longitudinal ridging; pterygium formation, complete dystrophy

• scalp: known aslichen planopilaris,scarring alopecia with perifollicular hyperkeratosis and erythema

• usually resolves spontaneously but may last for wk, mo, or yr

• rarely associated with hepatitis C

• Koebner phenomenon

Pathophysiology

• immune-mediated, antigen unknown

• lymphocyte activation leads to keratinocyte apoptosis

Epidemiology

• 1%,30-60 yr, F>M

Investigations

• consider a skin biopsy

• hepatitis C serology if patient has risk factors

Management

• topical or intralesional corticosteroids

• short courses of oral prednisone (rarely)

• phototherapy,oral retinoids, or systemic immunosuppressants (e.g. azathioprine, methotrexate,

cyclosporine) for extensive or recalcitrant cases

Pityriasis Rosea

Clinical Features

• acute,self-limiting eruption characterized by red, oval plaques/patches with central scale that does

not extend to edge of lesion

• long axis of lesions follows skin tension lines (i.e. Langer lines) parallel to ribs producing “Christmas

tree"

pattern on back

• varied degree of pruritus

• most start with a “herald"

patch which precedes other lesions by 1-2 wk

• common sites: trunk, proximal aspects of arms and legs

Pathophysiology

• suspected HHV-7 or HHV-6 reactivation

Investigations

• none required

Management

• none required; clears spontaneously in 6-12 wk

• symptomatic: topical corticosteroids if pruritic, cool compresses, emollients

Skin Treatments lor Chronic Plaque Psoriasis

Cochrane 08Syst Rev 2013:00005028

P urpose:lo renew the eflectneness. tolqribility.

and safety of topical treatmentsfor chronic plaque

psoriasis.

Methods:This renew identified RCls comparing

active topical treatments to either placebo or litemm

0 analogues(used alone or m combination) in people

with chronic plaque psoriasis.

Results:1)0 studiesincluding a total ol 34808

participantswere included in this review.

Conclusion : Both topical coticosteroids and vitar -

0 analogues were effective in treating throne plaque

psoriasis ol the body.Corticosteroidsshowed benefits

over vitamin 0 analoguesin treating chronic plaque

psoriasis of the scalp,treatments combining vitamin

0 analogues and topical corticosteroids were mote

eHective than using eithervitamm D analogues

or corticosteroids alone. Vitamin D analogues did

result in more local adverse eventsthan topical

corticosteroids, the most common event being skin

irritation or burning.People were moeelikely to

discontinue using vitamin Oanalogues than topical Psoriasis corticosteroids.

Classification

1. plaque psoriasis 2. guttate psoriasis 3. erythrodermlc psoriasis

•4. pustular psoriasis 5.inverse psoriasis Calcipotriol is a Vitamin D Derivative

Dovobet '

calcipotriene combined with

betamethasone dipropionate and is

considered to be one of the most potent

topical psoriatic therapies

Pathophysiology

• not fully understood, genetic and immunologic factors

• shortened keratinocyte cell cycle correlates with lit I - and '

1 hi7- mediated inflammatory response +

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D21 Dermatology Toronto Notes 2023

Epidemiology

• 1.5-2%,M=F

• all ages:peaks of onset:20-39 yr and 50-60 yr

• polygenic inheritance:8% with one affected parent, 41% with both parents affected

• risk factors:smoking, obesity, alcohol,drugs,infections, physical trauma (Koebner phenomenon)

See landmark OematologyTriaIsiab'e far mote

informationon the BE VIVID trialcompilingthe

efficacy andsafety a!a 52 wk treatment irith

bimekicomah vs.p'acebo vs.usteknemab in patiects

with mpderate to severe Dlaqne psp-asis.

Differential Diagnosis

• mycosis fungoides (cutaneous T-cell lymphoma),seborrheic dermatitis,tinea, nummular dermatitis,

lichen planus

Investigations

• none required;biopsy if atypical presentation

PLAQUE PSORIASIS

Clinical Features

• chronic and recurrent disease characterized by well-circumscribed erythematous papules/plaques

with silvery-white scales

• often worse in winter (lack of sun)

• Auspitz sign: bleeds from minute points when scale is removed

• common sites:scalp, extensorsurfaces of elbows and knees, trunk (especially buttocks), nails,

pressure areas

Management

• depends on severity of disease, as defined bv BSA affected or less commonly PASI

• mild (<3% BSA)

• first line treatment includes topical steroids ± topical vitamin D analogue combination

topical retinoid ± topical steroid combination,anthralin.and tar are also effective but tend to be

less tolerated than first line therapies

emollients

phototherapy orsystemic treatment may be necessary if the lesions are scattered or in difficult-totreat areas (e.g. palms,soles,scalp,and genitals)

• moderate (3-10% BSA) to severe (>10% BSA)

goal of treatment is to attain symptom control that is adequate from patient’s perspective

• phototherapy if accessible

systemic or biological therapy based on patient’

streatment history and comorbidities

topical steroid ± topical vitamin D3analogue as adjunct therapy

Table 14. Topical Treatment of Psoriasis

Treatment Mechanism Comments

Emollients Reduce fissure formation

Salicylic acid1-12%

Tar (LCD:liquor carbonis detergens)

Topical corticosteroids

Removescales

inhibits OKA synthesis,increases celt turnover Messy,poor long term compliance

Reduce scaling,redness and thickness Use appropriate potency steroid in different

areas for degree of psoriasis

Vitamin D analogues:calcipotriene/

calcipotriol (Dovonex .Silkis )

Betamethasone - calcipotriene (Dovobei ) Combined corticosteroid andvitamin 0

analogue.See above mechanisms

Retinoid derivative,reducescaling

Reduceskeratmocyte hyperproliferation

Not to be used on face or folds

Tazarotene (Tazorac I(gel/cream) Irritating

Table 15. Systemic Treatment of Psoriasis

Treatment Considerations Adverse Effects

Acitretin More effective when used in combination with

phototherapy

Used for intermittent controlrather than continuously

Avoid using for >1yr

Has been used for over 50 yr

Alopecia,cheilitis,teratogenicity,hepatotoxicity,

photosensitivity,epistaxis. xerosis,hypertriglyceridemia

Renal toxicity,hypertension,hypertriglyceridemia,

immunosuppression,lymphoma

Bone marrow toxicity,hepatic cirrhosis,teratogenicity

6Iupset headache,loose stool,weight loss

Pruritus,burning,skin cancer

Figure 10.Psoriasis distribution Cyclosporine

Methotrexate

Apremilast (Otezla:

) Extremely safe

PUVA Highly effective in achieving remission

Avoid >200 sessions in lifetime

Broadband UVB and UVB is muchless carcinogenic thanPUVA.N8-UVB has not Rare burning

NB- UVB (311-312 nm) been shown toincrease therisk of skin cancer

r T

Mechanism of Biologies

“-mab"- monoclonal antibody

u

*cept"-receptor

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D22 Dermatology Toronto Notes 2023

Table 16. Biologies Approved in Canada

Treatment Route Dosing Schedule Effectiveness Action

EtanercepfEnbrel - }* SC

Adalimumab|Huniira '

}* SC

InfliximablAemicade '

)* IV

Uslckinumab (Slelara '

)* SC

SecukinumablCosentyi')* SC

Ixekizumab (Taltz :

)* SC

50 mg twice per wk for 3 mo, then 50 mg every wk

80 mg »1.then 40 mg at wk 1 and every 2 wk thereafter

5 mg/kg al wk 0.2, 6.and every 8 wk the reader

45 mg or 90 mg at wk 0.4, and every 12 wk Iherealter

300 mg al wk 0,1, 2, 3.4, and every month Iherealter

160 mg at wk 0, then 80 mg at wk 2, 4,6,8.10,12, then

80 mg every 4 wk thereafter

100 mgatwkO, 4. and every 8 wk thereafter

210 mg at wk 0.1,2 and every 2 wk thereafter

Anti-INF

Anti-INF

+ +

Anti- INF

Anli I112/23

Anti IL 1 /A

Anti-IL 17A

+

+ +4++

Guselkumab|Tremfya:

) SC

Brodalumab (Siliq - ) SC

Anti-IL 23

mAb IL-17R (brodalumabis

a monoclonal antibody that

targets the IL-17 receptor

Anti INF

+*+++

Ccrtolixumab pcgol SC

(ClmiiaT

Risankiiomab (Skyriu '

) SC

Tildrakizumab (IIUMYA ) SC

Bimekizumab (BIM2ELX [

) SC

400 mg every 2 wk

150 mg al wk 0, 4.and every 12 wk Iherealter

100 mg at wk 0.4. and every 12 wk thereafter

320 mg at wk 0.4.8.12.16, and every 8 wk thereafter

Aziti- IL 23

Anti-1123

++* Anti-IL 17A/IL 17F •+

'Can also be used to treat psoriatic arthritis

GUTTATE PSORIASIS (“RAIN DROP-LIKE”)

Clinical Features

• discrete,scattered salmon- pink small scaling papules

• sites:diffuse, usually on trunk and legs,sparing palms and soles

• often antecedent streptococcal pharyngitis

Management

• UVB phototherapy,sunlight, lubricants, topical steroids

• penicillin V, erythromycin, or azithromycin ifCiAS on throat culture

ERYTHRODERMIC PSORIASIS

Clinical Features

• generalized erythema (>90% of BSA) with fine desquamative scale on surface

• associated signs and symptoms:arthralgia, pruritus, dehydration, electrolyte imbalance

• aggravating factors:lithium, p-blockers, NSAlDs, antimalarials, phototoxic reaction, infection

Management

• potentially life-threatening, requires immediate medical care

• IV fluids, monitor fluids and electrolytes, may require hospitalization

• treat underlying aggravating condition

• cyclosporine, acitretin, methotrexate, UV, biologies

PUSTULAR PSORIASIS

Clinical Features

• sudden onset of erythematous macules and papules which evolve rapidly into pustules, can be painful

• may be generalized or localized

• patient usually has a history of psoriasis; may occur with sudden withdrawal from steroid therapy

Management

• methotrexate, cyclosporine, acitretin, UV, biologies

INVERSE PSORIASIS

Clinical Features

• erythematous plaques on flexural surfaces such as axillae, inframammary folds, gluteal fold, inguinal

folds

• lesions may be macerated

Management

• low potency topical corticosteroids

• topical vitamin D analogues (e.g. calcipotriene, calcitriol)

• topical calcineurin inhibitors (e.g. tacrolimus, pimecrolimus)

• phototherapy

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D23 Dermatology Toronto Notes 2023

PSORIATIC ARTHRITIS

• 20-30% of patients with psoriasis also suffer from psoriatic arthritis

• psoriatic patients with nail orscalp involvement are at a higher risk for developing psoriatic arthritis

• see Rheumatology. RH25

Vesiculobullous Diseases

Bullous Pemphigoid s

Clinical Features

• chronic autoimmune bullous eruption characterized by pruritic, tense,subepidermal bullae on an

erythematous or normal skin base

• can present as urticarial plaques without bullae

• common sites:flexor aspect of forearms, axillae, medial thighs, groin, abdomen, mouth in 33%

Pathophysiology

• IgG produced against dermal-epidermal basement membrane proteins (hemidesmosomes) leading to

subepidermal bullae

Epidemiology

• mean age of onset: 60-80 yr, l

'

=M

Investigations

• immunofluorescence shows linear deposition of lgCi and C3 along the basement membrane

• anti-basement membrane antibody (IgG) (pemphigoid antibody detectable in serum)

Prognosis

• heals withoutscarring, usually chronic

• rarely fatal

Management

• prednisone 0.5- 1 mg/kg/d until clear, then taper ± steroid-sparing agents (e.g. azathiopri ne,

cyclosporine, mycophenolate mofetil)

• topical potent steroids (dobetasol) may be as effective assystemic steroids in limited disease

• tetracycline + nicotinamide is effective for some cases

• immunosuppressantssuch as azathioprine, mycophenolate mofetil, cyclosporine

• For refractory cases:1Vlg, rituximab,dupilumab,or omalizumab

Pemphigus Vulgaris g

Clinical Features

• autoimmune blistering disease characterized by flaccid, non-pruritic intraepidermal bullae/vesicles

on an erythematous or normalskin base

• may present with erosions and secondary bacterial infection

• sites:mouth (90%),scalp,face, chest, axillae, groin, umbilicus

• Nikolsky’ssign:epidermal detachment with shearstress

• Asboe-Hansen sign: pressure applied to bulla causes it to extend laterally

Pathophysiology

• IgG against epidermal desmoglein-l and -3lead to loss of intercellular adhesion in the epidermis

Epidemiology

• 40-60 yr, M=F, higher prevalence in Jewish, Mediterranean, Asian populations

• paraneoplastic pemphigus may be associated with thymoma, myasthenia gravis,malignancy, and use

of D-penicillamine

Investigations

• immunofluorescence:shows intraepidermal IgG and G3 deposition

• circulating scrum anti-desmoglcin IgG antibodies

Prognosis

• lesions heal with hyperpigmentation but do not scar

• may be fatal unless treated with immunosuppressive agents

Pemphigus Vulgaris vs. Bullous

Pemphigoid

VUlgariS = Superficial,intraepidermal.

flaccid iesions

PemphigoiD - Deeper, tense lesions at

the dermal-epidermal junction

Pemphigus Foliaceus

An autoimmune intraepidermal blistering

disease that is more superficial than

pemphigus vulgaris due to antibodies

against desmoglein-1. a transmembrane

adhesion molecule. Appears as crusted

patches, erosions and/or flaccid bullae

that usually start on the trunk. Localized

disease can be managed with topical

steroids. Active widespread disease is

treated like pemphigus vulgaris

Management

• prednisone 1-2 mg/kg until no new blisters, then 1-1.5 mg/kg until clear, then taper ± steroid-sparing

agents (e.g.azathioprine, cyclophosphamide, cyclosporine, 1Vlg, mycophenolate mofetil, rituximab)

+

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D24 Dermatology Toronto Notes 2023

Dermatitis Herpetiformis

Clinical Features

• grouped papules/vesicles/urticarial wheals on an erythematous base, associated with intense pruritus,

burning,stinging, excoriations

• lesions grouped,bilaterally symmetrical

• common sites:extensorsurfaces of elbows/knees,sacrum,buttocks,scalp

Pathophysiology

• transglutaminase IgA deposits in the skin alone or in immune complexesleading to eosinophil and

neutrophil infiltration

• almost all carry human leukocyte antigen (HLA) DQ2 or DQ8,other haplotypes include B8, DR3, and

DQWZ

• 90% have gluten-sensitive enteropathy, 20% have intestinal symptoms of celiac disease

• 30% have thyroid disease;increased risk of intestinal lymphoma in untreated comorbid celiac disease;

Fe/folate deficiency'is common

Epidemiology

. 20-60 yr,M:F=2:l

Investigations

• biopsy

• immunofluorescence shows IgA depositsin perilesionalskin

Management

• dapsone (sulfapvridine if contraindicated or poorly tolerated)

• gluten-free diet for life:this can reduce risk of lymphoma

Porphyria Cutanea Tarda

Clinical Features

• skin fragility followed by formation of tense vesicles/bullae and erosions on photo-exposed skin

• gradual healing to scars,milia

• periorbital violaceous discolouration,diffuse hypermelanosis,facial hypertrichosis

• common sites:light-exposed areassubjected to trauma, dorsum of hands and feet, nose, and upper

trunk

Pathophysiology

• uroporphyrinogen decarboxylase deficiency leadsto excess heme precursors

• can be associated with hemochromatosis, alcohol abuse.DM,drugs(estrogen therapy, NSAIDs), HIV,

hepatitis C,increased iron indices

Epidemiology

• 30-40 yr,M>F

Investigations

• urine and HC15% shows orange-red fluorescence under Wood’

slamp (UV rays)

• 24 h urine has elevated uroporphyrins

• stool contains elevated coproporphyrins

• immunofluorescence shows IgE at dermal-epidermal junctions

Management

• discontinue aggravating substances (alcohol, estrogen therapy)

• phlebotomy to decrease body iron load

• low dose hydroxychloroquine

Drug Eruptions Diagnosis

G

of a Drug Reaction

Classification by Naranjo et al. has 4

criteria:

t Temporal relationship between drug

exposure and reaction

2.Recognized response tosuspected

Exanthematous

z :

- z L J

EXANTHEMATOUS DRUG REACTION 3.Improvement after drug withdrawal

4.Recurrence of reaction on rechallenge with the drug

Definite drug reaction requires all 4

criteria to be met

Probable drug reaction requires 41-3

to be met

Possible drug reaction requires only #1

Clinical Features

• morphology:erythematous macules and papules ± scale

• spread:symmetrical, trunk to extremities

• time course:7-14 d after drug initiation, fades 7-14 d after withdrawal

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D25 Dermatology Toronto Notes 2023

Epidemiology

. most common cutaneous drug reaction; increased in presence of infections

• common causative agents: penicillin,sulfonamides, phenytoin

Management

• weigh risks and benefits of drug discontinuation

• antihistamines, emollients, topical steroids

w

Drug Hypersensitivity Syndrome Triad

Fever

Exanthematous eruption

Internal organ Involvement DRUG-INDUCED HYPERSENSITIVITY SYNDROME (DIHS)/DRUG REACTION WITH

EOSINOPHILIA AND SYSTEMIC SYMPTOMS (DRESS)

Clinical Features

• morphology: morbilliform rash involving face,trunk,arms;can have facial edema

• systemic features:fever, malaise, cervical lymphadenopathy, internal organ involvement (e.g.

hepatitis, arthralgia, nephritis,pneumonitis,lymphadenopathy, hematologic abnormalities, thyroid

abnormalities)

• spread:starts with face or periorbitally and spreads caudally; no mucosal involvement

• time course:onset 1-6 wk after first exposure to drug; persists wk after withdrawal of drug

Epidemiology

• rare:incidence varies considerably depending on drug

• common causative agents:anticonvulsants(e.g.phenytoin, phenobarbital, carbamazepine,

lamotrigine),sulfonamides, and allopurinol

• 10% mortality ifsevere, undiagnosed, and untreated

Management

• discontinue offending drug ± prednisone 0.5 mg/kg/d, consider cyclosporine in severe cases

• may progress to generalized exfoliative dermatitis/erythroderma if drug is not discontinued

Urticarial

DRUG-INDUCED URTICARIA AND ANGIOEDEMA

Clinical Features

• morphology: wheals lasting >24 h unlike non-drug induced urticaria, angioedema (face and mucous

membranes)

• systemic features: may be associated with systemic anaphylaxis (bronchospasm, laryngeal edema,

shock)

• time course: h-d after exposure depending on the mechanism

Epidemiology

• second most common cutaneous drug reaction

• common causative agents: penicillins,ACE1, analgesics/anti-inflammatories, radiographic contrast

media

Management

• discontinue offending drug,treatment with antihistamines,oral corticosteroids, epinephrine if

anaphylactic

SERUM SICKNESS-LIKE REACTION

Clinical Features

• morphology:symmetrical cutaneous eruption (usually urticarial)

• systemic features:malaise, low grade fever, arthralgia,lymphadenopathy

• time course:appears 1-3 wk after drug initiation,resolves 2-3 wk after withdrawal

Epidemiology

• more prevalent in children (0.02-0.2%)

• common causative agents: cefaclor in children; bupropion in adults

Management

• discontinue offending drug ± topical/oral corticosteroids L

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D26 Dermatology Toronto Notes 2023

Pustular

ACUTE GENERALIZED EXANTHEMATOUS PUSTULOSIS (AGEP)

Clinical Features

• morphology:extensive erythematous, edematous,and sterile pustules

• systemic features:high fever,leukocytosis with neutrophilia

• spread:startsin face and intertriginous areas,spreads to trunk and extremities

• time course: appears I wk after drug initiation, resolves 2 wk after withdrawal

Epidemiology

• rare: 1-5/million

• common causative agents:aminopenicillins, cephalosporins, clindamycin, calcium channel blockers

Management

• discontinue offending drug and systemic corticosteroids

Bullous K E

STEVENS-JOHNSON SYNDROME (SJS)/TOXIC EPIDERMAL NECROLYSIS (TEN)

Clinical Features

• morphology: prodromal rash (morbilliform/targetoid lesions ± purpura, or diffuse erythema),

confluence of flaccid blisters, positive Nikolsky sign (epidermal detachment with shear stress),full

thickness epidermal loss;dusky tenderskin, bullae,desquamation/skin sloughing, atypical targets

• classification:

BSA with epidermal detachment: <10% in SJS,10-30% in SJS/TEN overlap, and >30% in TEN

spread:face and extremities;may generalize;scalp, palms,soles relatively spared; erosion of mucous

membranes (lips,oral mucosa, conjunctiva, GU mucosa)

• systemic features:fever (higher in TEN), cytopenias, renal tubular necrosis/AKl, tracheal erosion,

infection, contractures, cornealscarring, phimosis, vaginal synechiae

• time course: appears 1-3wk after drug initiation; progression <4 d; epidermal regrowth in 3 wk

• can have constitutional symptoms: malaise, fever, hypotension, tachycardia

Epidemiology

• SJS: 1.2-6/million;TEN:0.4-1.2/million

• risk factors:SLE, HIV/A IDS, HLA-B1502 (reaction most prevalent in East Asians, associated with

carbamazepine), HLA-B5801 (reaction most prevalent in Asian and White populations, associated

with allopurinol)

• common causative agents:drugs (allopurinol, anti-epileptics,sulfonamides, NSAlDs,cephalosporins)

responsible in 50% of SJS and 80% of TEN; viral or mycoplasma infections

• prognosis:5% mortality in SJS,30% in TEN due to fluid loss and infection

Differential Diagnosis

• scarlet fever, phototoxic eruption, GVHD, SSSS, exfoliative dermatitis, AGEP, paraneoplastic

pemphigus

SCORTEN Score (or TEN Prognosis

One point for each o(

:age >40,