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Dermatology > Common skin lesions > Flashcards

Common skin lesions Flashcards

1
Q

Epidermal cyst presentation

A

Round, yellow/flesh-coloured, slow growing, mobile, firm, fluctuant, nodule or tumour

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2
Q

Epidermal cyst pathophysiology

A

Epithelial cells displaced into dermis, epidermal lining becomes filled with keratin and lipid-rich debris

May be post-traumatic, rarely syndromic

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3
Q

Epidermal cyst epidermiology

A

most common cutaneous cyst in youth - middle age

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4
Q

Epidermal cyst clinical course

A

central punctum may rupture (foul, cheesy odour, creamy colour) and produce inflammatory reaction Can increase in size and number over time)

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5
Q

Epidermal cyst management

A

no treatment elective excision

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6
Q

Pilar cyst (Trichillemmal) clinical presentation

A

Multiple, hard, variable sized nodules under the scalp, lacks central punctum

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7
Q

Pilar cyst (Trichillemmal) pathophysiology

A

Thick-walled cyst lined with stratified squamous epithelium and filled with dense keratin Idiopathic Posttraum

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8
Q

Pilar cyst (Trichillemmal) epidemiology

A

2nd most common cutaneous cyst F>M

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9
Q

Pilar cyst (Trichillemmal) clinical course

A

rupture causes pain and inflammation

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10
Q

Pilar cyst (Trichillemmal) management

A

no tx, elective excision

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11
Q

dermoid cyst clinical presentation

A

Firm nodule most commonly found at lateral third of eyebrow or midline under nose

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12
Q

dermoid cyst pathophys

A

Rare congenital hamartomas, which arise from inclusion of epidermis along embryonal cleft closure lines, creating a thick-walled cyst filled with dense keratin

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13
Q

dermoid cyst epi

A

rare

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14
Q

dermoid cyst clinical course

A

If nasal midline, risk of extension into CNS

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15
Q

dermoid cyst management

A

no tx, elective excision

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16
Q

ganglion cyst clinical presentation

A

Usually solitary, rubbery, translucent; a clear gelatinous viscous fluid may be extruded

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17
Q

ganglion cyst pathophys

A

Cystic lesion that originates from joint or tendon sheath, called a digital mucous cyst when found on fingertip

Associated with osteoarthritis

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18
Q

ganglion cyst epi

A

older age

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19
Q

ganglion cyst clinical course

A

stable

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20
Q

ganglion cyst management

A

no treatment
incision and experession of contents
elective excision

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21
Q

milium clinical presentation

A

1-2 mm superficial, white to yellow subepidermal papules occurring on eyelids, cheeks and forehead

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22
Q

milium pathophys

A

Small epidermoid cyst, primarily arsing from pluripotential cells in epidermal or adnexal epithelium Can be secondary to blistering, ulceration, trauma, topical corticosteroid atrophy, or cosmetic procedures

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23
Q

milium epi

A

any age

40-50$ of infants

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24
Q

milium clinical course

A

in newborns spontaneously resolves in first 4 weeks of life

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25
Q

milium tx

A

no tx

incision and expression of contents

electrodessication

topical retinoid therapy

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26
Q

Fitzpatrick scale

A

I - always burns, never tans
II - always burns, little tan
III - slight burn, slow tan
IV (pale brown) - slight burn, faster tan
V - (brown) - rarely burns, dark tan
VI (dark brown or black) - never burns, dark tan

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27
Q

Dermatofibroma clinical presentation

A

button-like, firm dermal papule or nodule, skin-coloured to red-brown

  • majority are asymptomatic but may be pruritic and/or tender
  • site: legs > arms > trunk
  • dimple sign (Fitzpatrick’s sign): lateral compression causes dimpling of the lesion
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28
Q

Dermatofibroma pathophy

A

benign tumour due to fibroblast proliferation in the dermis

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29
Q

Dermatofibroma etiology

A
  • unknown; may be associated with history of minor trauma (e.g. shaving or insect bites)
  • eruptive dermatofibroma can be associated with SLE
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30
Q

Dermatofibroma epi

A

adults F>M

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31
Q

Dermatofibroma ddx

A

• dermatofibrosarcoma protuberans

malignant melanoma

Kaposi’s sarcoma

blue nevus

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32
Q

Dermatofibroma investigations

A

biopsy if diagnosis uncertain

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33
Q

Dermatofibroma management

A

no tx required, excision if bothersome

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34
Q

skin tags clinical presentation

A
  • small (1-10 mm), soft, skin-coloured or darker pedunculated papule, often polypoid
  • sites: eyelids, neck, axillae, inframammary, and groin
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35
Q

skin tags pathophys

A

benign outgrowth of skin

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36
Q

skin tags epi

A

• middle-aged and elderly, F>M, obese, can increase in size and number during pregnancy

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37
Q

skin tags ddx

A

• pedunculated seborrheic keratosis

compound or dermal melanocytic nevus

neurofibroma

fibroepithelioma of Pinkus (rare variant of BCC)

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38
Q

skin tags management

A

excision

electrodessication

cryosurgery

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39
Q

skin tags are also known as

A

acrochordones

fibroepithelial polyps

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40
Q

seb keratosis clinical presentation

A

known as ‘wisdom spots,’ ‘age spots,’ or ‘barnacles of life’

  • well-demarcated waxy papule/plaque with classic “stuck on” appearance
  • rarely pruritic
  • over time lesions appear more warty, greasy and pigmented
  • sites: face, trunk, upper extremities (may occur at any site except palms or soles)
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41
Q

seb keratosis pathophys

A

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

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42
Q

seb keratosis epi

A
  • unusual <30 yr old
  • M>F
  • autosomal dominant inheritance
  • Leser-Trelat sudden appearance of SK that can be associated with malignancy, commonly gastric adenocarcinomas
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43
Q

seb keratosis ddx

A

• malignant melanoma (lentigo maligna, nodular melanoma)

melanocytic nevi

pigmented BCC

solar lentigo

spreading pigmented AK

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44
Q

seb keratosis investigations

A

biopsy if unsure

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45
Q

seb keratosis management

A

none req, cosmetic only

cryotherapy, electrodessication, excision

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46
Q

Corns (helomata) clinical presentation

A
  • 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
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47
Q

Corns (helomata) pathophys

A

• localized hyperkeratosis induced by pressure on hands and feet

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48
Q

Corns (helomata) epi

A

• F>M, can be caused by chronic microtrauma

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49
Q

Corns (helomata) ddx

A

callus

plantar wart

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50
Q

Corns (helomata) management

A
  • relieve pressure with padding or alternate footwear, orthotics
  • paring, topical salicylic acid
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51
Q

corns vs warts vs calluses

A
  • 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
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52
Q

keloids clinical presentation

A
  • firm, shiny, skin-coloured or red-bluish papules/nodules that most often arise from cutaneous injury (e.g. piercing, surgical scar, acne), but may appear spontaneously
  • extends beyond the margins of the original injury, and may continue to expand in size for years with claw-like extensions
  • can be pruritic and painful
  • sites: earlobes, shoulders, sternum, scapular area, angle of mandible
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53
Q

keloids pathophy

A

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

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54
Q

keloids epi

A
  • most common in black patients, followed by those of Asian descent (predilection for darker skin)
  • M=F, all age groups
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55
Q

keloids managemetn

A
  • intralesional corticosteroid injections

* silicone compression

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56
Q

keloids vs hypertrophic scars

A

keloids extend beyond margins of original injury with claw-like extensions

hypertrophic scars are confined to original margins of injury

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57
Q

congenital nevomelanocytic nevi (CNMN) clinical presentation

A

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

• classified by size: small (<1.5 cm),
medium M1: 1.5-10 cm, M2: >10-20 cm),
large (L1: >20-30 cm, L2 >30-40 cm),
giant (G1: >40-60 cm, G2: >60 cm)

• may be surrounded by smaller satellite nevi

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58
Q

congenital nevomelanocytic nevi (CNMN) pathophy

A

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

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59
Q

congenital nevomelanocytic nevi (CNMN) epi

A
  • present at birth or develops in early infancy to childhood
  • malignant transformation is rare (1-5%) and more correlated with size of the lesion
  • neurocutaneous melanosis can occur in giant CNMN (melanocytes in the central nervous system)
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60
Q

congenital nevomelanocytic nevi (CNMN) management

A
  • take a baseline photo and observe lesion for change in shape, colour, or size out of proportion of growth
  • surgical excision if suspicious, due to increased risk of melanoma
  • MRI if suspicious for neurological involvement
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61
Q

ddx of hyperpigmented macules

A
  • Purpura (e.g. solar, ASA, anti-coagulants, steroids, hemosiderin stain)
  • Post-inflammatory
  • Melasma
  • Melanoma
  • Fixed drug eruption
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62
Q

cafe-au-lait macule clinical presentation

A

Flat light brown lesions with smooth or jagged borders

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63
Q

cafe-au-lait macule patohophys

A

Areas of increased melanogenesis

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64
Q

cafe-au-lait macule epi

A

6 or more is suggestive of neurofibromatosis type I

Also associated with McCune Albright syndrome

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65
Q

cafe-au-lait macule ddx

A

Flat congenital melanocytic nevus, speckled lentiginous nevus

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66
Q

cafe-au-lait macule clinical course and management

A

enlarge in proportion to the child

No effective treatment

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67
Q

speckled lentiginous nevus (nevus spilus) clinical presentation

A

Brown pigmented macular background (caféau-lait macule-like) with dark macular or papular speckles

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68
Q

speckled lentiginous nevus (nevus spilus) pathophys

A

Increased melanocyte concentration

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69
Q

speckled lentiginous nevus (nevus spilus) epi

A

Risk of melanoma similar to that of a CNMN of the same size

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70
Q

speckled lentiginous nevus (nevus spilus) ddx

A

Café-au-lait macule, agminated lentigines, Becker’s nevus

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71
Q

speckled lentiginous nevus (nevus spilus) clinical course and management

A

usually the light macular background is present at birth and speckles develop over time. Management is similar to that of CNMNs

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72
Q

Dermal melanocytosis (historically known as Mongolian Spot) clinical presentation

A

Congenital greyblue solitary or grouped macules commonly on lumbosacral area

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73
Q

Dermal melanocytosis (historically known as Mongolian Spot) pathophys

A

Ectopic melanocytes in dermis

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74
Q

Dermal melanocytosis (historically known as Mongolian Spot) epi

A

99% occurs in Asian and Indigenous infants

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75
Q

Dermal melanocytosis (historically known as Mongolian Spot) ddx

A

Ecchymosis

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76
Q

Dermal melanocytosis (historically known as Mongolian Spot) clinical course and management

A

usually fades, may persist

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77
Q

halo nevus

A

often a typical appearing nevus surrounded by a ring of depigmentation; not rare in children; uncommonly associated with vitiligo; no treatment required unless irregular colour or borders

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78
Q

blue nevus

A

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

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79
Q

acquired nevomelanocytic nevi clinical presentation

A
  • common mole: well circumscribed, round, uniformly pigmented macules/papules <1.5 cm
  • average number of moles per person: 18-40
  • 3 stages of evolution: junctional NMN, compound NMN, and dermal NMN
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80
Q

acquired nevomelanocytic nevi management

A
  • new or changing pigmented lesions should be evaluated for aypical features which could indicate a melanoma
  • excisiona biopsy should be considered if the lesion demonstrates asymmetry, varied colours, irregular borders, pruritus or persistent bleeding
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81
Q

junctional acquired nevomelanocytic nevi onset, clinical presentation and histology

A

childhoood, majority progress to compound

Flat, regularly bordered, uniformly tan-dark brown, sharply demarcated macul

Melanocytes at dermal-epidermal junction above basement membrane

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82
Q

compound acquired nevomelanocytic nevi onset, clinical presentation and histology

A

Any age

Domed, regularly bordered, smooth, round, tan-dark brown papule Face, trunk, extremities, scalp NOT found on palms or soles

Melanocytes at dermal-epidermal junction; migration into dermis

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83
Q

dermal acquired nevomelanocytic nevi onset, clinical presentation and histology

A

Adults

Soft, dome-shaped, skin-coloured to tan/brown papules or nodules Sites: face, neck

Melanocytes exclusively in dermis

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84
Q

Atypical nevus (dysplastic nevus) clinical presentation

A

Variegated macule/ papule with irregular distinct melanocytes in the basal layer Risk factors: family history

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85
Q

Atypical nevus (dysplastic nevus) pathophys

A

Hyperplasia and proliferation of melanocytes extending beyond dermal compartment of the nevus Often with region of adjacent nests

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86
Q

Atypical nevus (dysplastic nevus) epi

A

> 5 atypical nevi increases risk for melanoma Numerous dysplastic nevi may be part of familial atypical mole and melanoma syndrome

87
Q

Atypical nevus (dysplastic nevus) ddx

88
Q

Atypical nevus (dysplastic nevus) clinical course and management

A

Follow with baseline photographs for changes Excisional biopsy if lesion changing or highly atypica

89
Q

ephelides (freckles) presentation

A

Small (<5 mm) welldemarcated light brown macules Sites: sun-exposed skin

90
Q

ephelides (freckles) pathophys

A

Increased melanin within basal layer keratinocytes secondary to sun exposure

91
Q

ephelides (freckles) epi

A

Skin phototypes I-II most commonly

92
Q

ephelides (freckles) ddx

A

Junctional nevi

Juvenile lentigines

93
Q

ephelides (freckles) clinical course and management

A

Multiply and darken with sun exposure, fade in winter

No treatment required

Sunscreen and sun avoidance may prevent the appearance of new freckles

94
Q

Solar lentigo (liver spot) clinical presentation

A

Well-demarcated brown/black macules Sites: sun-exposed skin

95
Q

Solar lentigo (liver spot) pathophys

A

Benign melanocytic proliferation in dermal- epidermal junction due to chronic sun exposure

96
Q

Solar lentigo (liver spot) epid

A

Most common in Caucasians >40 yr Skin phototypes I-III most commonly

97
Q

Solar lentigo (liver spot) ddx

A

Lentigo maligna, seborrheic keratosis, pigmented actinic keratosis

98
Q

Solar lentigo (liver spot) clinical course and management

A

Laser therapy, shave excisions, cryotherapy

99
Q

Becker’s Nevus presentation

A

Hairy, light brown macule/patch with a papular verrucous surface Sites: trunk and shoulders onset in teen years

100
Q

Becker’s Nevus pathophys

A

Pigmented hamartoma with increased melanin in basal cells

101
Q

Becker’s Nevusepi

A

M>F Often becomes noticeable at puberty

102
Q

Becker’s Nevus ddx

A

Hairy congenital melanocytic nevus

103
Q

Becker’s Nevus clinical course and managemetn

A

hair growth follows onset of pigmentation

Cosmetic management (usually too large to remove

104
Q

melasma clinical presentation

A

Dark, usually symmetrical, skin discolouration on sunexposed areas of face (forehead, upper lip, cheeks, chin)

105
Q

melasma pathophys

A

Increase in number and activity of melanocytes Associated with estrogen and progesterone

106
Q

melasma epi

A

F>M Common in pregnancy and women taking OCP or HRT Risk factors: sun exposure, dark skin tone Can occur with mild endocrine disturbances, antiepileptic medications and other photosensitizing drug

107
Q

melasma ddx

A

Post-inflammatory hyperpigmentation

108
Q

melasma course and tx

A

often fades over several months after stopping hormone treatment or delivering baby

Treatment: hydroquinone, azelaic acid, retinoic acid, topical steroid, combination creams, destructive modalities (chemical peels, laser treatment), camouflage make-up, sunscreen, sun avoidance

109
Q

Hmangiomas of infancy clinical presentation

A

Hot, firm red to blue plaques or tumours

110
Q

Hmangiomas of infancy pathophys

A

benign vascular proliferation of endothelial lining

111
Q

Hmangiomas of infancy epi

A

Appears shortly after birth; rarely may be congenital

112
Q

Hmangiomas of infancy clinical course

A

Appears shortly after birth, increases in size over months, then regresses 50% of lesions resolve spontaneously by 5 yr

113
Q

Hmangiomas of infancy management

A

10% require treatment due to functional impairment (visual compromise, airway obstruction, high output cardiac failure) or cosmesis Consider treatment if not gone by school age; topical timolol, propranolol; systemic corticosteroids; laser treatment; surgery

114
Q

spider angioma (Campbell telengiectasia) clinical presentation

A

Central red arteriole with slender branches, blanchable

spider angioma will blanch when the tip of a paperclip is applied to the centre of the lesion

115
Q

spider angioma (Campbell telengiectasia) pathophys

A

Can be associated with hyperestrogenic state (e.g. in hepatocellular disease, pregnancy, OCP) but often is not

116
Q

spider angioma (Campbell telengiectasia) epi

117
Q

spider angioma (Campbell telengiectasia) clinical course

A

Increase in number over tim

118
Q

spider angioma (Campbell telengiectasia) management

A

reassurance

electrodessication or laser if patient wishes

119
Q

cherry angioma (Campbell De Morgan Spot) clinical presentation

A

Bright red to deep maroon, domeshaped vascular papules, 1-5 mm Site: trunk Less friable compared to pyogenic granulomas

120
Q

cherry angioma (Campbell De Morgan Spot) pathophys

A

Benign vascular neoplasm

121
Q

cherry angioma (Campbell De Morgan Spot) epi

A

> 30 years old

122
Q

cherry angioma (Campbell De Morgan Spot) clinical course

A

Lesions do not fade in time Lesions bleed infrequently

123
Q

cherry angioma (Campbell De Morgan Spot) management

A

usually no tx

Laser or elect ocautery for small lesions Excision of large lesions if necessary

124
Q

pyogenic granuloma clinical presentation

A

Bright red, dome-shaped sessile or pedunculated friable nodule Sites: fingers, lips, mouth, trunk, toes DDx: glomus tumour, nodular MM, SCC, nodular BCC

125
Q

pyogenic granuloma pathophys

A

Rapidly developing hemangioma Proliferation of capillaries with erosion of epidermis and neutrophilia

126
Q

pyogenic granuloma epi

127
Q

pyogenic granuloma clinical course

A

Lesion grows rapidly over weeks to months, then stabilizes Lesion may persist indefinitely if untreated

128
Q

pyogenic granuloma management

A

surgical excision with histologic examination Electrocautery; laser; cryotherapy

129
Q

what is a venous lake

A

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

130
Q

nevus flammeus (port-wine stain) clinical presentation

A

Red to blue macule present at birth that follows a dermatomal distribution, rarely crosses midline Most common site: nape of neck Never spontaneously regresses but grows in proportion to the child

131
Q

nevus flammeus (port-wine stain) pathophys

A

congenital vascular malformation of dermal capillaries; rarely associated with Sturge-Weber syndrome (V1, V2 distribution)

132
Q

nevus flammeus (port-wine stain) management

A

laser or make up

133
Q

nevus simplex (salmon patch) clinical presentation

A

Pink-red irregular patches Midline macule on glabella known as “Angel Kiss”; on nuchal region known as “Stork Bites Present in 1/3 of newborns Majority regress spontaneously

134
Q

nevus simplex (salmon patch) pathophys

A

Congenital dilation of dermal capillaries

135
Q

nevus simplex (salmon patch) management

136
Q

lipoma clinical presentation

A
  • 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
137
Q

lipoma pathophys

A

• adipocytes enclosed in a fibrous capsule

138
Q

lipoma epi

A

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

139
Q

lipoma ddx

A

angiolipoma, liposarcoma

140
Q

lipoma investigations

A

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

141
Q

lipoma management

A

reassurance

excision or liposuction only if desired for cosmetic purposes

142
Q

Acne vulgaris/common acne clinical presentation

A

a common inflammatory pilosebaceous disease categorized with respect to severity
■ Type I: comedonal, sparse, no scarring
■ Type II: comedonal, papular, moderate ± little scarring
■ Type III: comedonal, papular, and pustular, with scarring
■ Type IV: nodulocystic acne, risk of severe scarring

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

143
Q

Acne vulgaris/common acne pathophysiology

A
  • hyperkeratinization at the follicular ostia (opening) blocks the secretion of sebum leading to the formation of microcomedones
  • androgens promote excess sebum production
  • Propionibacterium acnes metabolize sebum to free fatty acids and produces pro-inflammatory mediators
144
Q

Acne vulgaris/common acne epi

A
  • age of onset in puberty (10-17 yr in females, 14 19 yr in males)
  • in prepubertal children consider underlying hormonal abnormality (e.g. late onset congenital adrenal hyperplasia)
  • incidence decreases in adulthood
  • genetic predisposition: majority of individuals with cystic acne have parent(s) with history of severe acne
145
Q

Acne vulgaris/common acne ddx

A

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

146
Q

Treatment of acne scars

A
  • Tretinoin creams
  • Glycolic acid
  • Chemical peels for superficial scars
  • Injectable fillers (collagen, hyaluronic acid) for pitted scars
  • Fraxel laser
  • CO2 laser resurfacing
147
Q

Does eating greasy food and chocolate cause or worsen acne?

148
Q

Why are blackheads black?

A

Blackheads (comedones) are black because of oxidized fatty acids, not dirt

149
Q

Is acne caused by poor hygiene?

A

Acne is not caused by poor hygiene; on the contrary, excessive washing of face can be an aggravator

150
Q

Role of antibiotics in acne

A

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)

151
Q

Acne exacerbating factors

A
  • Systemic medications: lithium, phenytoin, steroids, halogens, androgens, iodides, bromides, danazol
  • Topical agents: steroids, tars, ointments, oily cosmetics
  • Mechanical pressure or occlusion, such as leaning face on hands
  • Emotional stress
152
Q

Management of mild acne

A

Mild acne - topical therapies OTC
Benzoyl peroxide (BPO) - solugel, benzac, desquam, fostex
Salicylic acid - Akurza Cream, dermalzone

  • prescription topical therapies
    Antimicrobials - Clindamycin (Dalacin T), Erythromycin
    Retinoids - Vit A Acid (tretinoin, Stieva-A, Retin A) Adapalene (Differin)
    Combination products - Clindoxyl (Clindamycin and BPO), Benzaclin (Clindamycin and BPO), Tactuo (Adapalene and bpo), biacna (clindamycin and tretinoin), benzamycine (bpo and erythromycin)

A combination of topical retinoids and topical erythromycin or clindamycin is more effective than either agent used alone

153
Q

Indication for intralesional corticosteroid injections for acne

A

Intralesional corticosteroid injections are effective in the treatment of individual acne nodules

154
Q

Salicylic acid indication in acne therapy

A

Used when patients cannot tolerate a topical retinoid due to skin irritation

155
Q

why not use antimicrobials as monotherapy for acne

A

high rate of resistance when used as monotherapy

156
Q

retinoids indication in acne therapy

A

Backbone of topical acne therapy

All regimens should include a retinoid unless patient cannot tolerate

157
Q

Benefit of combination acne products

A

greater adherence and efficacy by combining different MOAs to increase efficacy and maximize tolerability

158
Q

Benefit of combination acne products

A

greater adherence and efficacy by combining different MOAs to increase efficacy and maximize tolerability

159
Q

moderate acne therapy

A

tetracycline/minocycline/doxycycline (sumycin/minocin/vibramycin)

Cyproterone acetate-ethinyl estradiol (Diane 35)

Spironolactone (Aldactone)

160
Q

caution and duration before assessing efficacy for tetracycline/minocycline/doxycycline (sumycin/minocin/vibramycin)

A

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

Sun sensitivity

Antibiotics require 3 mo of use before assessing efficacy

161
Q

age limit for cyproterone acetate ethinyl estradiol

A

After 35 yr of age, estrogen/progesterone should only be considered in exceptional circumstances arefully weighing the risk/benefit ratio with physician guidance

162
Q

spironolactone adverse effects/black box warning

A

May cause hyperkalemia at higher doses

Black box warning for breast cancer

163
Q

Isotretinoin and pregnancy

A
  • Use of Isotretinoin during pregnancy is associated with spontaneous abortion and major birth defects such as facial dysmorphism and cognitive impairment
  • Pregnancy should be ruled out before starting isotretinoin
  • Patients should use 2 forms of contraception while on isotretinoin
164
Q

Severe acne treatment

A

isotretinoin (accutane, clarus, epuris)

165
Q

isotretinion adverse effects

A

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

Baseline lipid profile (risk of hypertriglyceridemia), LFTs and β-hCG before treatment

May transiently exacerbate acne before patient sees improvement

Refractory cases may require multiple courses of isotretinoin

166
Q

Clinical presentation perioral dermatitis

A

discrete erythematous micropapules that often become confluent, forming inflammatory plaques on perioral, perinasal, and periorbital skin commonly symmetrical, rim of sparing around vermillion border of lips

167
Q

perioral dermatitis epi

A
  • 15-40 yr old, occasionally in younger children

* predominantly females

168
Q

perioral dermatitis ddx

A

• contact dermatitis, rosacea, acne vulgaris

169
Q

perioral dermatitis mx

A
  • avoid all topical steroids
  • topical: metronidazole 0.75% gel or 0.75-1% cream to affected area bid
  • systemic: tetracycline family antibiotic (utilized for its anti-inflammatory properties)
  • occasional use of a non-steroidal anti-inflammatory cream (i.e. tacrolimus or pimecrolimus)
170
Q

Important controversies associate with isotretinoin therapy for acne

A
  1. The evidence on whether isotretinoin causes depression and suicide is inconsistent; however, numerous controlled studies have shown an improvement in anxiety and depression scores in those taking isotretinoin.
  2. There is no association between IBD and isotretinoin use. Only one study showed a significantly increased risk of UC. When considering using isotretinoin in a patient with IBD or with a strong family history, consider involving a gastroenterologist.
171
Q

Rosacea clinical presentation

A
  • dome-shaped inflammatory papules ± pustules
  • flushing, non-transient erythema, and telangiectasia
  • distribution: typically on central face including forehead, nose, cheeks, and chin; rarely on scalp, neck, and upper body
  • characterized by remissions and exacerbations
  • exacerbating factors: heat, cold, wind, sun, stress, drinking hot liquids, alcohol, caffeine, spices
  • all forms of rosacea can progress from mild to moderate to severe
  • rarely in longstanding rosacea, signs of thickening, induration and lymphedema in the skin can develop
  • phyma: a distinct swelling caused by lymphedema and hypertrophy of subcutaneous tissue, particularly affecting the nose (rhinophyma)
  • ocular manifestations: blepharoconjunctivitis, keratitis, iritis
172
Q

Rosacea pathophysiology

173
Q

Rosacea epi

A

all skin types, highest prevalence in fair-skinned people

30-50 year old; F>M

174
Q

Rosacea ddx

A

acne vulgaris, seborrheic dermatitis, perioral dermatitis, contact dermatitis

175
Q

Rosacea mx

A
  • trigger avoidance and daily sunscreen use for long-term management
  • avoid topical corticosteroids
  • telangiectasia: treated by physical ablation; electrical hyfrecators, vascular lasers, and intense pulsed light therapies
  • phymas: treated by physical ablation or removal; paring, electrosurgery, cryotherapy, laser therapy (CO2, argon, Nd:YAG)
1st line 
- Oral tetracyclines 
Topical metronidazole 
Oral erythromycin (250-500 mg PO bid) 
Topical azelaic acid 
Topical Ivermectin
2nd line 
Topical clindamycin 
Topical erythromycin 2% solution 
Topical benzoyl peroxide 
Oral metronidazole

3rd line
oral retinoids

176
Q

How can rosacea be differentiated from acne

A

Rosacea can be differentiated from acne by the absence of comedones,

a predilection for the central face

and symptoms of flushing

177
Q

Guidelines for the diagnosis of rosacea

A 
Presence of one or more of the following primary features: 
• Flushing (tansient erythema) 
• Nontransient erythema 
• Papules and pustules 
• Telangiectasia 
May include one or more of the following secondary features: 
• Burning or stinging 
• Dry appearance 
• Edema 
• Phymatous changes 
• Ocular manifestations 
• Peripheral location
178
Q

Dermatitis (eczema) definition

A

inflammation of the skin

179
Q

Dermatitis (eczema) clinical presentation

A
  • poorly demarcated erythematous patches or plaques
  • symptoms include pruritus and pain
  • acute dermatitis: papules, vesicles
  • subacute dermatitis: scaling, crusting, excoriations
  • chronic dermatitis: lichenification, xerosis, fissuring
180
Q

Asteatotic dermatitis clinical presentation

A
  • 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”
181
Q

Asteatotic dermatitis management

A

• skin rehydration with moisturizing routine ± corticosteroid creams

182
Q

Atopic dermatitis clinical presentation

A
  • subacute and chronic eczematous reaction associated with prolonged severe pruritus
  • distribution depends on age
  • inflammation, lichenification excoriations are secondary to relentless scratchng
  • atopic palms: hyperlinearity of the palms (associated with ichthyosis vulgaris)
  • associated with: keratosis pilaris (hyperkeratosis of hair follicles, “chicken skin”), xerosis, occupational hand dryness
183
Q

Atopic dermatitis epi

A
  • frequently affects infants, children, and young adults
  • 10-20% of children in developed countries under the age of 5 are affected
  • associated with personal or family history of atopy (asthma, hay fever), anaphylaxis, eosinophilia
  • polygenic inheritance: one parent >60% chance for child; two parents >80% chance for child
  • long-term condition with 1/3 of patients continuing to show signs of AD into adulthood
184
Q

Atopic dermatitis pathophysiolgoy

A

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

185
Q

Atopic dermatitis investigations

A
  • clinical diagnosis

* consider: skin biopsy, patch testing if allergic contact dermatitis is suspected

186
Q

Atopic dermatitis mx

A
  • goal: reduce signs and symptoms, prevent or reduce recurrences/flares
  • better outcome (e.g. less flare-ups, modified course of disease) if diagnosis made early

Initial assessment ->
patient education, daily emollient use ->
acute control of flare (topical corticosteroids or topical calcineurin inhibitor) ->
maintenance therapy if disease is persistent and/or frequent recurrences (topical corticosteroid or calcineurin inhibitor at earliest sign of flare, long-term maintenance use of calcineurin inhibitors) ->
Severe refractory disease
- azathioprine
- methotrexate
- oral cyclosporin
- oral steroids, potent topical steroids
- phototherapy
- psychotherapeutics

Adjunctive therapy 
• avoid triggers of AD 
- treat bacterial superinfections (topical or oral abx) 
- antihistamines 
- psychological interventions

• non-pharmacologic therapy
■ moisturizers
◆ apply liberally and reapply at least twice a day with goal of minimizing xerosis
◆ include in treatment of mild to severe disease as well as in maintenance therapy
■ bathing practices
◆ bathe in plain warm water for a short period of time once daily followed by lightly but not completely drying the skin with a towel; immediately apply topical agents or moisturizers after this
◆ use fragrance-free hypoallergenic non-soap cleansers

• pharmacologic therapy
■ topical corticosteroids
◆ effective in reducing acute and chronic symptoms as well as prevention of flares
◆ choice of steroid potency depends on age, body site, short vs. long-term use
◆ apply 1 adult fingertip unit (0.5 g) to an area the size of 2 adult palms bid for acute flares
◆ local side effects: skin atrophy, purpura, telangiectasia, striae, hypertrichosis, and acneiform eruption are all very rarely seen
■ topical calcineurin inhibitors
◆ tacrolimus 0.03%, 0.1% (Protopic®) and pimecrolimus 1% (Elidel®)
◆ use as steroid-sparing agents in the long-term
◆ advantages over long-term corticosteroid use: sustained effect in controlling pruritus; no skin atrophy; safe for the face and neck
◆ apply 2x/d for acute flares, and 2-3x/wk to recurrent sites to prevent relapses
◆ local side effects: stinging, burning, allergic contact dermatitis
◆ U.S. black box warning of malignancy risk: rare cases of skin cancer and lymphoma reported; no causal relationship established

187
Q

Atopic dermatitis complications

A

• infections
■ treatment of infections
◆ topical mupirocin or fusidic acid (Canada only, not available in US)
◆ oral antibiotics (e.g. cloxacillin, cephalexin) for widespread S. aureus infections

188
Q

Triggers for atopic dermatitis

A
  • 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
189
Q

Atopic dermatitis distribution in infants <6 months

A

Scalp

Extensor elbow

190
Q

Atopic dermatitis distribution in children >18 months

A

Neck

Flexor elbow

Flexor knee

191
Q

Atopic dermatitis distribution in adults

A

Scalp, neck

Hands, feet

192
Q

Contact dermatitis clinical presentation

A

cutaneous inflammation caused by an external agent(s)

193
Q

irritant contact dermatitis

mechanism of reaction

type of reaction

frequency

distribution

examples

management

A

mechanism of reaction - Toxic injury to skin; non-immune mechanism

type of reaction - Erythema, dryness, fine scale, burning
Acute: quick reaction, sharp margins (e.g. from acid/alkali exposure)
Cumulative insult: slow to appear, poorly defined margins (e.g. from soap), more common

frequency - Majority; will occur in anyone given sufficient concentration of irritants

distribution - hands most common site

examples - soaps, oils, detergents, weak alkali, organic solvents, alcohol

management - avoidance of irritants, wet compresses with Burrow’s solution, barrier moisturizers, topical/oral steroids

194
Q

allergic contact dermatitis

mechanism of reaction

type of reaction

frequency

distribution

examples

management

A

mechanism of reaction - cell mediated delayed (Type IV) hypersensitivity reaction

type of reaction - erythema with a papulovesicular eruption, swelling, pruritus

frequency - Minority; patient acquires susceptibility to allergen that persists indefinitely

distribution - areas exposed

examples - many are same as irritants

management - Patch testing to determine specific allergen
Avoid allergen and its cross-reactants
Wet compresses soaked in Burrow’s solution (drying agent)
Topical Steroids BID prn Systemic steroids prn if extensive

195
Q

Dyshidrotic dermatitis clinical presentation

A
  • “tapioca pudding” papulovesicular dermatitis of hands and feet that coalesce into plaques, followed by panful fissuring
  • acute stage often very pruritic
  • secondary infections common
  • lesions heal with desquamation and may lead to chronic lichenification
  • sites: palms and soles ± dorsal surfaces of hands and feet
196
Q

Dyshidrotic dermatitis pathophysiology

A
  • NOT caused by hyperhidrosis (excessive sweating)

* emotional stress may precipitate flares

197
Q

Dyshidrotic dermatitis management

A
  • topical: high potency corticosteroid with plastic cling wrap occlusion to increase penetration
  • intralesional triamcnolone injection

• systemic
■ prednisone in severe cases
■ antibiotics for secondary S. aureus infection

198
Q

Nummular dermatitis clinical presentation

A
  • nummular (coin-shaped), pruritic, dry, scaly, erythematous plaques
  • often associated with atopic and dyshidrotic dermatitis
  • secondary infection common
199
Q

Nummular dermatitis pathophysiology

A

• 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

200
Q

Nummular dermatitis management

A
  • moisturization

* mid to high potency corticosteroid ointment bid

201
Q

Seborrheic dermatitis clinical presentation

A
  • greasy, erythematous, yellow, scaling, minimally elevated papules and plaques in areas rich in sebaceous glands, can look moist and superficially eroded in flexural regions
  • infants: “cradle cap”
  • children: may be generalized with flexural and scalp involvement • adults: diffuse involvement of scalp margin with yellow to white flakes, pruritus and underlying erythema
  • sites: scalp, eyebrows, eyelashes, beard, glabella, post-auricular, over sternum, trunk, body folds, genitalia
202
Q

Seborrheic dermatitis pathophysiology

A

possible etiologic association with Malassezia spp. (yeast)

203
Q

Seborrheic dermatitis epi

A
  • common in infants and adolescents
  • increased incidence and severity in immunocompromised patients
  • in adults, can cause dandruff (pityriasis sicca)
204
Q

Seborrheic dermatitis management

A
  • face: ketoconazole (Nizoral®) cream daily or bid + mild steroid cream daily or bid
  • scalp: salicylic acid in olive oil or Derma-Smoothe FS® lotion (peanut oil, mineral oil, fluocinolone acetonide 0.01%) to remove dense scales, 2% ketoconazole shampoo (Nizoral®), ciclopirox (Stieprox®) shampoo, selenium sulfide (e.g Selsun®) or zinc pyrithione (e.g. Head and Shoulders®) shampoo, steroid lotion (e.g. betamethasone valerate 0.1% lotion bid)
205
Q

Stasis dermatitis clinical presentation

A
  • erythematous, scaly, pruritic plaques in lower legs, particularly the medial ankle
  • brown hemosiderin deposition, woody fibrosis, atrophy blanche, and lipodermatosclerosis in late stages usually bilateral, accompanied by swelling, oozing, crusting, may have accompanying varicosities
206
Q

Stasis dermatitis pathophysiology

A
  • chronic venous insufficiency leads to venous stasis

* surrounding soft tissue inflammation and fibrosis results

207
Q

Stasis dermatitis investigations

A
  • Doppler and colour-coded Duplex sonography if suspicious for DVT
  • swab for bacterial culture if there is crusting
208
Q

Stasis dermatitis management

A
  • compression stockings
  • rest and elevate legs (above the level of the heart)
  • moisturizer to treat xerosis
  • mid-high potency topical corticosteroids to control inflammation
209
Q

Stasis dermatitis complications

A

• ulceration (common at medial malleolus)

secondary bacterial infections

210
Q

Lichen simplex chronicus clinical presentation

A
  • well-defined plaque(s) of lichenified skin with increased skin markings ± excoriations
  • common sites: neck, scalp, lower extremities, urogenital area
  • often seen in patients with atopy
211
Q

Lichen simplex chronicus pathophys

A
  • skin hyperexcitable to itch, continued rubbing/scratching of skin results
  • eventually lichenification occurs
212
Q

Lichen simplex chronicus investigations

A
  • if patient has generalized pruritus, rule out systemic cause: CBC with differential count, transaminases, bilirubin, renal and thyroid function tests, TSH, glucose, SPEP
  • CXR if lymphoma suspected
213
Q

Lichen simplex chronicus mx

A

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

Dermatology (11 decks)

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