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Primary Care > Skin Disorders > Flashcards

Skin Disorders Flashcards

1
Q

How many different skin phototypes are there and what is this classification called? (TN)

A
  • Fitzpatrick
    • Phototype I (lightest) to VI (darkest)
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2
Q

How should a skin lesions be described? (TN)

A
  • SCALDA
    • Size and surface area
    • Colour – hyperpigmented, hypopigmented, erythematous
    • Arrangement – solitary, linear, reticulated, grouped, herpetiform
    • Lesion morphology – macule, patch, papule, plaque, nodule, tumour, vesicle, bulla
    • Distribution – dermatomal, intertriginous, symmetrical/asymmetrical, follicular
    • Always check hair, nails, mucous membranes and intertriginous areas
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3
Q

What are 8 different morphologies of lesions and differentiate based on size. (TN)

A
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4
Q

Differentiate between a cyst and pustule and an erosion and ulcer. (TN)

A
  • Cyst: epithelial-lined collection containing semi-solid or fluid material
  • Pustule: elevated lesion containing purulent fluid (white, grey, yellow, green)
  • Erosion: disruption of the skin involving the epidermis alone; heals without scarring
  • Ulcer: disruption of the skin that extends into the dermis or deeper; heals with scarring
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5
Q

What are 7 secondary morphological lesions? (TN)

A
  • Crust: dried fluid (serum, blood, or purulent exudate) originating from a lesion (e.g. impetigo)
  • Scale: excess keratin (e.g. seborrheic dermatitis)
  • Lichenification: thickening of the skin and accentuation of normal skin markings (e.g. chronic atopic dermatitis)
  • Fissure: linear slit-like cleavage of the skin
  • Excoriation: a scratch mark
  • Xerosis: pathologic dryness of skin (xeroderma), conjunctiva (xerophthalmia), or mucous membranes
  • Atrophy: histological decrease in size and number of cells or tissues, resulting in thinning or depression of the skin
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6
Q

What is purpura and the three different types? (TN)

A
  • Purpura: extravasation of blood into dermis resulting in hemorrhagic lesions; non-blanchable, 3mm-1cm in size
    • Petechiae: small pinpoint purpura, <3mm in size
    • Ecchymoses: larger flat purpura, >1 cm in size, aka a “bruise”
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7
Q

What are 10 different patterns and distribution of skin lesions? (TN)

A
  • Acral: relating to the hands and feet (e.g. hand, foot and mouth disease)
  • Annular: ring-shaped
  • Follicular: involving hair follicles (e.g. folliculitis)
  • Guttate: lesions following a “drop-like” pattern (e.g. guttate psoriasis)
  • Morbilliform: a maculopapular rash resembling measles
  • Reticular: lesions following a net-like pattern (e.g. livedo reticularis)
  • Satellite: lesions scattered outside of primary lesions (e.g. candida diaper dermatitis)
  • Serpiginous: lesions following a snake-like pattern (e.g. cutaneous larva migrans)
  • Target/Targetoid: concentric ring lesions, like a dartboard (e.g. EM)
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8
Q

Provide possible diagnoses for each type of skin lesion: brown macule, discrete red papule, red scales, vesicle, bulla, pustule, oral ulcer and skin ulcer. (TN)

A
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9
Q

Eczema

What should be considered in the differential diagnosis for eczema?

A
  • Atopic dermatitis (Eczema)
  • Contact dermatitis
  • Seborrheic dermatitis
  • Impetigo
  • Psoriasis
  • Candidiasis
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10
Q

Eczema

What is the atopic triad? (DFCM)

A
  • Asthma
  • Allergic rhinitis
  • Atopic dermatitis
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11
Q

Eczema

How does atopic dermatitis look like on the skin? (DFCM)

A
  • Erythematous papules, patches and plaques with poorly defined borders
  • Dry skin and pruritus – leads to Itch Cycle – can lead to lichenification and inflammation
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12
Q

Eczema

What should be considered in patients with atopic dermatitis as a potential complication? (DFCM)

A
  • Secondary Impetigo
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13
Q

Eczema

Where do atopic dermatitis typically affect infants and children? (DFCM)

A
  • Infants: cheeks, scalp, extensor surfaces
    • Spares diaper area
  • Children: face, neck, flexural surfaces
    • Increased lichenification
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14
Q

Eczema

In patients with suspected atopic dermatitis that have crusted or vesicular lesions, what test could be performed? (DFCM)

A
  • Viral cultures to rule out HSV infection
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15
Q

Eczema

What are 4 important points to educate to patients and parents about the management of atopic dermatitis?

A
  • Emollients – Cetaphil or Vaseline
    • Ceramide containing – CeraVe or Restoraderm
    • Shower with warm (not hot) water, use emulsifier oil or Oatmeal in baths and use emollient after
  • Keep house cool and humidified
  • Clothing
    • 100% cotton
    • Mild detergents – i.e. Ivory Snow
    • Rinse laundry twice if possible
    • No fabric softener or bleach
  • Children
    • Don’t play in grass or leaves
    • Apply moisturizer to face before feeding
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16
Q

Eczema

What is first-line treatment for atopic dermatitis?

A
  • Topical steroids
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17
Q

Eczema

How should the dose of topical steroids for atopic dermatitis be determined?

A
  • Tailor potency to disease and degree of lichenification
    • BID to QID for low and mid potency
    • OD to BID for high and ultra high potency (max 2-4 weeks)
  • Mild potency: face, groin and any joints
    • Hydrocortisone (Hyderm or Emo-Cort) 1% or 2.5%
  • Moderate potency for <2 weeks is okay
    • Betamethasone valerate (Betaderm) 0.05% or 0.1%
  • High potency – consult with Derm
    • Betamethasone dipropionate (Diprosone) 0.05%
  • Ultra-high potency
    • Clobetasol propionate (Dermovate) 0.05%
  • Ointment > Cream > Lotion in terms of potency
    • Avoid ointment for open lesions and intertriginous folds
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18
Q

Eczema

What are 5 potential adverse effects of topical steroids for atopic dermatitis? (TN)

A
  • Atrophy
  • Striae
  • Telangectasia
  • Corticosteroid acne
  • Tachyphylaxis
  • ***No adrenal suppression or growth changes until regular use of high-potency steroids
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19
Q

Eczema

What is second-line therapy for atopic dermatitis?

A
  • Topical Calcineurin Inhibitors
    • Pimecrolimus 1% (Elidel)
    • Tacrolimus 0.03%, 0.1% (Protopic)
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20
Q

Eczema

How would topical calcineurin inhibitors be prescribed for atopic dermatitis?

A
  • Used for short-term (BID therapy) or long-term intermittent therapy (2x/week) for Mod-Severe
  • Pimecrolimus currently not approved for maintenance therapy
  • For use in patient >2 years of age
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21
Q

Eczema

What is the benefit of topical calcineurin inhibitors over topical steroids and what are the potential risks?

A
  • No skin atrophy – may be better for face, neck and skin folds
  • No tachyphylaxis
  • Black-box warning: ?link to lymphoma or immunosuppression
  • Side effects: transient skin irritation or burning, pruritus
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22
Q

Eczema

What can be used to treat atopic dermatitis refractory to topical treatments or with widespread disease?

A
  • Phototherapy
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23
Q

Eczema

What would be a Mild Approach and Moderate-Severe Approach long-term for atopic dermatitis?

A
  • Mild
    • Steroids are first-line for flares once daily
    • Return to emollient-only treatment after flares
  • Moderate-Severe
    • 2x/week steroids with emollient use for maintenance
      • Get control with higher potency, then taper strength
    • Or Calcineurin Inhibitors BID
    • Consider phototherapy
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24
Q

Seborrheic Dermatitis

What is seborrheic dermatitis called in infants? (TN)

A
  • Cradle Cap
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25
Q

Seborrheic Dermatitis

What is the uninflamed form of seborrheic dermatitis called? (TN)

A
  • Pityriasis capitis (Dandruff)
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26
Q

Seborrheic Dermatitis

How does seborrheic dermatitis typically appear? (TN)

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
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27
Q

Seborrheic Dermatitis

What is the suspected pathophysiology of seborrheic dermatitis? (TN)

A
  • Malassezia spp. (YEAST)
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28
Q

Seborrheic Dermatitis

What can be used to treat seborrheic dermatitis on the face? (TN)

A
  • Ketoconazole (Nizoral) cream daily or BID + mild steroid cream daily or BID
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29
Q

Seborrheic Dermatitis

What can be used to treat seborrheic dermatitis on the scalp? (TN)

A
  • Salicylic acid in olive oil or Derma-Smoothe FS lotion (peanut oil, mineal oil, fluocinolone acetonide 0.01%) to remove dense scales
  • 2% ketoconazole shampoo (Nizoral)
    • Shampoos used twice weekly for at least 1 month
  • Ciclopirox (Stieprox) shampoo
    • Shampoos used twice weekly for at least 1 month
  • Selenium sulfide (Selsun Blue) or Zinc pyrithione (Head and Shoulders) shampoo
    • Shampoos used twice weekly for at least 1 month
  • Steroid lotion (betamethasone valerate 0.1% lotion BID)
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30
Q

What are the two mechanisms of contact dermatitis? (TN)

A
  • Irritant
  • Allergic
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31
Q

What are the top ten allergens identified in contact dermatitis? (TN)

A
  • Nickel sulfate – jewelry, belt buckles
  • Neomycin sulfate – topical antibiotic in Polysporin
  • Balsam of Peru – fragrance material
  • Fragrance mix – fragrance components for allergen testing in cosmetics
  • Thimerosal – preservative used in vaccines, contact lens solution, cosmetics
  • Sodium gold – jewelry, dentistry, electronics
  • Formaldehyde – colourless gas
  • Quaternium-15 – component in shampoos, moisturizers, conditioners, soaps
  • Cobalt chloride – cosmetics, jewelry, buttons, tools
  • Bacitracin – topical antibiotic in Polysporin
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32
Q

How does irritant and allergic contact dermatitis present clinically?

A
  • Irritant (Right)
    • Usually the hands (palmar surface)
    • Burning and pruritus
    • Erythema, dry and fissured skin
    • Less distinct borders
  • Allergic (Left)
    • Exposed skin areas, often the hands (dorsal surface)
    • Pruritus is the dominant symptoms
    • Erythema, vesicles and bullae
    • Distinct angles, lines and borders
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33
Q

What is the evidence for steroid use for contact dermatitis?

A
  • Irritant – No evidence
  • Allergic – Good evidence
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34
Q

What should management be for contact dermatitis?

A
  • Irritant
    • Avoidance of irritants
    • Wet compresses with Burow’s solution
    • Trial cool compresses, calamine lotion and colloidal oatmeal baths
    • Topical/oral steroids
  • Allergic
    • Consider patch testing if persistent
    • Avoid allergen and its cross-reactants
    • Wet compresses soaked in Burow’s solution (drying agent)
    • Steroid cream (e.g. HC 1%, betamethasone valerate 0.05%, betamethasone valerate 0.1% cream; BID)
    • Systemic steroids prn (prednisone 1 mg/kg, taper over 2 week)
    • Antihistamines not effective, sedation probably helps the most
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35
Q

What is the prevalence of psoriasis in Canada? (DFCM)

A
  • 1.7%
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36
Q

At what ages does psoriasis incidence peak? (DFCM)

A
  • 20-30 and 50-60
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37
Q

What type of disease is psoriasis classified as? (PBSG)

A
  • Autoimmune with a genetic predisposition
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38
Q

How does psoriasis typically appear on the body? (DFCM)

A
  • Erythematous papules coalescing into plaques with silver-white scales, and well-defined borders
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39
Q

What areas of the body are classically affected by psoriasis? (DFCM)

A
  • Elbows
  • Knees
  • Sacral-gluteal region
  • Scalp
  • Lower back
  • Palms and Soles
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40
Q

What are 7 possible triggers of psoriasis? (DFCM/PBSG)

A
  • Physical trauma (e.g. vaccinations, tattoos, sunburn)
  • Stress
  • Infections (e.g. HIV)
  • Medications (e.g. systemic glucocorticoids, oral lithium, interferon, beta-blockers)
  • Alcohol
  • Cigarette smoking
  • Cold weather with low humidity
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41
Q

What is important to determine on clinical history in a patient presenting with psoriasis?

A
  • Family history (1/3 of patients)
  • No or mild pruritus, sometimes painful
  • Localization of lesions: scalp, elbows, knees, and lower back
  • Arthritis
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42
Q

What areas should be examined specifically in patients with psoriasis as they are often missed? (PBSG)

A
  • Scalp
  • Ears
  • Nails
  • Natal cleft
  • Genitalia
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43
Q

How does the majority of psoriasis appear? (PBSG)

A
  • 80-90% is Plaque Psoriasis
    • Sharply demarcate erythematous papules and plaques with a silver scale
    • Bathing can remove the scale
    • Often symmetrical
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44
Q

What is inverse psoriasis and what are 2 diagnoses to also consider in the differential? (PBSG)

A
  • Inverse psoriasis: plaque psoriasis with minimal scaling in the intertriginous areas (axillae, groin, natal cleft, under breasts)
  • Intertrigo: moist, erythematous lesions in intertriginous areas
  • Cutaneous T-cell lymphoma: erythematous patches/plaques in intertriginous areas, diagnosis confirmed with skin biopsy
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45
Q

What is guttate psoriasis, in what patients is it more common, what areas of the body does it affect, and what is a common precipitant? (PBSG)

A
  • Guttate Psoriasis: small papules of short duration (weeks to months)
    • Usually in those <30
    • Evidence on trunk, proximal limbs or face (does NOT affect palms/soles)
    • Commonly precipitated by URTI (streptococcal)
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46
Q

What are 2 diagnoses to also consider for guttate psoriasis? (PBSG)

A
  • Secondary syphilis
  • Pityriasis rosea: 1-2 weeks after vague viral episode, a single patch appears on trunk (Herald patch) and similar smaller lesions along skin cleavage lines (associated with human herpes virus type 6)
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47
Q

What are 2 signs on history associated with psoriasis? (DFCM)

A
  • Koebner phenomenon: new psoriatic lesions appearing at site of injury or trauma
  • Auspitz’s sign: bleeding after removal of psoriatic scales
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48
Q

What % of psoriasis patients have scalp involvement? (DFCM)

A
  • 86% - pruritus and scaling
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49
Q

What % of psoriasis patients have nail involvement and what are they? (DFCM)

A
  • 25% - pitting, leukonychia, red spots in lunula, nail plate crumbling, subungual hyperkeratosis, onycholysis, splinter hemorrhage, oil spot
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50
Q

What should be considered in the differential diagnosis for psoriasis?

A
  • Seborrheic dermatitis
  • Lichen simplex chronicus
  • Atopic dermatitis
  • Tinea corporis
  • Secondary Syphilis
  • Mycosis fungoides
    • Often are sharply demarcated and red, but limited scale and can itch
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51
Q

What potential comorbidities of psoriasis need to be investigated for?

A
  • Psoriatic arthritis
  • Depression
  • IBD (Crohn’s)
  • Lymphoma
  • Metabolic syndrome
  • CAD
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52
Q

What % of patients with psoriasis are affected by psoriatic arthritis? (DFCM)

A
  • 30%
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53
Q

How is psoriasis severity defined? (PBSG)

A
  • Extent of body surface area (BSA) involvement
    • Mild: <5%
    • Moderate: 5 to <10%
    • Severe: ≥10%
      • Involvement of hands, feet, facial or genital regions
  • Estimated using the palm (subject’s flat hand and thumb together, includes fingers) which ~1% of the total BSA
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54
Q

What topical treatment should all patients with psoriasis do?

A
  • Emollients (moisturizers) daily applied to entire body after shower/bath
    • Helps to minimize skin irritation and decrease likelihood of new lesions at the sites of minor trauma
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55
Q

What are 4 different types topical therapies for psoriasis?

A
  • Steroids
  • Vitamin D Analogues
  • Calcineurin Inhibitors
  • Retinoids
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56
Q

What are 6 different forms of vehicles for topical therapies for psoriasis? (PBSG)

A
  • Ointments
  • Creams
  • Solutions
  • Oils
  • Lotions
  • Foams
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57
Q

What is an advantage of using foam formulations as a topical therapy for psoriasis? (PBSG)

A
  • Quick drying
  • Ease of application
  • Lack of fragrance
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58
Q

How much topical agent is typical required to cover the whole body? In a patient with a 10% BSA involvement, how much would be required? (PBSG)

A
  • 30 g required to cover the whole body
  • 10% BSA = 3 g BID or 6 g daily
    • i.e. 60 g tube of ointment should last the patient 10 days
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59
Q

What are the different topical steroid doses that can be used for psoriasis?

A
  • Moderate: Betamethasone valerate (Betaderm): 0.05% or 0.1%
    • Only for the most mild cases or as foam for the scalp
    • Higher potency has longer disease free intervals
  • High: Betamethasone dipropionate (Diprosone): 0.05%
    • Comes in lotion for use on scalp
  • Ultra-High: Clobetasol propionate (Dermovate): 0.05%
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60
Q

For which areas of the body are low potency corticosteroids recommended to be used? (PBSG)

A
  • Thin-skinned areas: face, body folds, genitals
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61
Q

How frequently can topical steroids be applied per day for psoriasis? (PBSG)

A
  • Daily to TID (depending on type)
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62
Q

What are examples of mild, moderate and high potency topical steroids for scalp psoriasis? (PBSG)

A
  • Mild: Hydrocortisone 2.5% BID-TID
  • Moderate: Betamethasone valerate 0.1% lotion BID-TID
  • High: Betamethasone dipropionate 0.05% OD-BID
  • Ultra-High: Clobetasol propionate 0.05% shampoo OD, spray BID
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63
Q

What are known adverse effects associated with topical steroids? (PBSG)

A
  • Burning
  • Irritation
  • Pruritus
  • Dryness
  • Atrophy
  • Contact dermatitis
  • Rosacea
  • Striae
  • Purpura
  • HPA axis suppression
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64
Q

What topical treatment for psoriasis is considered “steroid sparing”? (DFCM)

A
  • Topical Vitamin D3 analogues
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65
Q

What other topical treatment can be used on its own or with steroids for psoriasis?

A
  • Vitamin D Analogues – better effect when combined with steroids
  • Dovonex (Calcipotriene) and Vectical (Calctriol)
    • Dovobet – Betamethasone dipropionate + Calcipotriol
      • Comes in ointment or lotion
      • Scalp gel can be applied once daily at bedtime, washout in morning
    • Slower onset of action, but longer disease-free intervals
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66
Q

What are known adverse effects associated with topical vitamin D analogues? (PBSG)

A
  • Burning
  • Pruritus
  • Edema
  • Peeling
  • Dryness
  • Erythema – mitigated with ongoing use
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67
Q

What is the maximum amount of topical Vitamin D analogues that should be used? (DFCM)

A
  • <40% BSAS or <100 g/week
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68
Q

In what patients should there be caution in the use of Vitamin D analogues for psoriasis?

A
  • Renal failure – can cause Hypercalcemia and PTH suppression
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69
Q

What are 2 examples of topical calcineurin inhibitors for psoriasis and their indications?

A
  • Pimecrolimus (Elidel) or Tacrolimus (Protopic)
    • For use in patients >2 years of age
    • Less effective for plaque psoriasis
    • First-line for facial or intertriginous psoriasis
    • Important as steroid sparing agents if need to use continual therapy
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70
Q

What is an example of a topical retinoid that can be used for psoriasis and its indications and side effects?

A
  • Tazarotene (Tazorac) – 0.05% or 0.1%
    • Side effects (often peri-lesion) – itch and burning
      • Use every-other-day or with steroid/moisturizer to decrease SE
    • As good as steroids, but longer disease free interval
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71
Q

Which topical therapy for psoriasis has the most ADEs? (DFCM)

A
  • Topical retinoids
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72
Q

What is a good topical therapy for scalp psoriasis? (DFCM)

A
  • Mid to high potency topical corticosteroids (e.g. Betamethasone dipropionate) and calcipotriol
  • Available shampoo formulations: clobetasol propionate solution or shampoo
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73
Q

Does scalp psoriasis cause hair loss?

A
  • No
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74
Q

What is a good topical therapy for psoriasis on the palms and soles?

A
  • Clobetasol with occlusive dressing
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75
Q

When should systemic treatment be considered for psoriasis?

A
  • >5% of body surface area (BSA) involved
  • Genitals, hands, feet or face involved
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76
Q

What are options for systemic treatment in psoriasis?

A
  • Phototherapy + Systemic (Methotrexate, Biologics)
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77
Q

What are 2 systemic immunosuppressives that can be used for psoriasis? (PBSG)

A
  • Methotrexate
  • Cyclosporine
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78
Q

What are 3 severe toxicities that are associated with methotrexate use? (PBSG)

A
  • Liver
  • Renal
  • Bone marrow
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79
Q

What is prescribed with methotrexate to protect against adverse reactions such as stomatitis? (PBSG)

A
  • Folic acid
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80
Q

What are 4 biologic agents that can be used for psoriasis? (PBSG)

A
  • Adalimumab (Humira)
  • Etanercept (Enbrel)
  • Infliximab (Remicade)
  • Ustekinumab (Stelara)
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81
Q

How often should phototherapy be used for psoriasis and what type of wavelength is required? (PBSG)

A
  • Phototherapy 1-4x per week
  • UVB – higher success rates and low risk of malignancy
    • UVA used in tanning beds – risk of skin cancer and carcinogenesis
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82
Q

What is the prevalence of acne among those aged 12 to 24 years? (CMAJ/PBSG)

A
  • 85%
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83
Q

What is the medical term for common acne? (CMAJ)

A
  • Acne vulgaris
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84
Q

Describe the pathobiology of acne.

A
  • Follicular hyperproliferation and abnormal desquamation – the normal dead cells are blocked from leaving the follicle by hyperkeratinization
  • Increased sebum production – an androgenic effect
  • Propionibacterium acnes proliferation
  • Inflammation
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85
Q

What are 4 diagnoses to consider in the differential diagnosis of acne. (DFCM/PBSG)

A
  • Rosacea – telangiectasia and no comedones
  • Perioral dermatitis – erythematous papules on chin and nasolabial folds, with a thin rim sparing around the vermilion border
    • May occur spontaneously or with topical steroid use
  • Pseudofolliculitis barbae – ingrown hairs in the beard area of individuals with curly hair who shave closely
  • Milaria – heat rash with nonfollicular papules, pustules and vesicles
  • Bacterial Folliculitis – variable distribution that spreads with shaving or scratching
  • Hidradenitis suppurativa – painful boils and sinus tracts
  • Sebaceous hyperplasia – no erythema
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86
Q

What should women with acne be asked about specifically? (DFCM)

A
  • Signs of hyperandrogenism (PCOS)
    • Hirsutism
    • Acanthosis nigricans
    • Menstrual irregularity
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87
Q

What complications of acne are more common in individuals with darker skin? (PBSG)

A
  • PIH
  • Keloid scarring
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88
Q

What is first line therapy for patients with acne in skin of colour to reduce PIH? (PBSG)

A
  • Topical retinoids
    • Azelaic acid (Finacea) – indicated for acne rosacea
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89
Q

What are the 3 categories of acne based on severity? (CMAJ)

A
  • Comedonal acne (NONinflammatory)
    • Small white papules (closed comedones) – white heads
    • Grey-white papules (open comedones) – black heads
  • Mild-to-moderate Papulopustular acne
    • Inflammatory lesions that are mostly superficial
  • Severe acne
    • Deep pustules and/or nodules, which may be painful, may extend over large areas and can lead to tissue destruction
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90
Q

What is a rare subtype of severe acne? (CMAJ)

A
  • Conglobate acne: extensive inflammatory papules, nodules and cysts
    • Can lead to disfiguring scars
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91
Q

What was considered superior efficacy in the CMAJ guidelines on acne? (CMAJ)

A
  • Statistical significant (p < 0.05)
  • Clinical relevance (minimum 10% difference in lesion counts)
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92
Q

What is first-line treatment for comedonal acne and mild papulopustular acne? (CMAJ)

A
  • Topical therapies
    • Retinoids OR
    • Benzoyl peroxide OR
    • Fixed-dose combinations of retinoids with benzoyl peroxide or Clindamycin
      • BPO/clinda
      • BPO/adapalene
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93
Q

What topical therapy can be tried if the initial first-line options fail for comedonal acne or mild papulopustular acne? (CMAJ)

A
  • Clindamycin/Tretinoin fixed-dose combination
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94
Q

What is a second-line option for comedonal acne or mild papulopustular acne if topical therapies fail? (CMAJ)

A
  • Combined oral contraceptives + Topical
  • Systemic antibiotics + Topical (only for Mild papulopustular)
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95
Q

What is the first-line option for moderate papulopustular acne? (CMAJ)

A
  • COC or Systemic antibiotics + Topical
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96
Q

What is the first-line treatment option for severe papulopustular/nodular acne? (CMAJ)

A
  • Oral isoretinoin
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97
Q

If a patient with severe acne is unwilling, unable or intolerant to oral isoretinoin, what treatment can then be tried? (CMAJ)

A
  • Systemic antibiotics with topical BPO +/- topical retinoid OR COC
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98
Q

Summarize the clinical treatment algorithm for acne. (CMAJ)

A
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99
Q

What type of topical formulation is better for dry or sensitive skin and what type for oily skin? (CMAJ)

A
  • Cream/Lotion for Dry/Sensitive
  • Gel for Oily
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100
Q

What are 4 points to educate patients about with acne?

A
  • Acne is NOT a hygiene problem
  • There is NO relationship to diet
  • Acne causes stress, NOT vice versa
  • Acne usually worsens the week before menses
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101
Q

What should patients be advised to do to help with acne that does not involve pharmacotherapies?

A
  • Limit face washing to 1-2x daily with mild soap (or soapless cleanser)
    • Neutrogena Oil Free Acne wash or Cetaphil or CeraVe
    • Dove bar soap or body wash
  • Consistency with washing/treatment is key
  • Gently wash face (men)
  • Use water-based or non-comedogenic makeup, sunscreen and lotions rather than oil-based
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102
Q

What are common adverse effects related to all topical acne therapies? (CMAJ)

A
  • Dryness
  • Redness
  • Burning
  • Irritation
  • Peeling
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103
Q

What doses can benzoyl peroxide be prescribed in? (CMAJ)

A
  • Benzoyl Peroxide 2.5%, 5% 10% gel, cream or lotion
    • 10% not for comedonal
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104
Q

What is the primary active ingredient in Proactiv? (PBSG)

A
  • BPO
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105
Q

What are 3 types of topical retinoids and which seems to be inferior? (CMAJ)

A
  • Tretinoin 0.025%, 0.04%, 0.05% gel or cream (Retin A, Stieva A)
    • Inferior
  • Adapalene 0.1% and 0.3% gel or cream (Differin)
  • Tazarotene 0.1% gel (Tazorac)
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106
Q

What is the fixed-dose combination of adapalene-BPO? (CMAJ)

A
  • Adapalene 0.1% and BPO 2.5% gel (TactuPump)
  • Adapalene 0.3% and BPO 2.5% gel (TactuPump Forte)
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107
Q

What is the fixed-dose combination of clindamycin-BPO? (CMAJ)

A
  • Clindamycin 1% and BPO 5% gel (BenzaClin, Clindoxyl)
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108
Q

What is the fixed-dose combination of clindamycin and tretinoin? (CMAJ)

A
  • Clindamycin 1.2% and tretinoin 0.025% (Biacna)
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109
Q

What topical acne treatment can be effective for hormone acne (premenstrual) that occurs near the jawline?

A
  • Dapsone (Aczone)
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110
Q

What is the use of systemic (oral) antibiotics for acne on their own not recommended? (CMAJ)

A
  • Selection of antibiotic resistant bacteria
  • Addition of BPO recommended to limit the emergence of antibiotic resistant bacteria
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111
Q

What are the preferred systemic (oral) antibiotics for acne and why? (CMAJ)

A
  • Tetracycline or Doxycycline
  • Minocycline associated with an increased risk of drug-induced lupus and hepatitis
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112
Q

Which COC combinations have been shown to be effective for the treatment of acne? (CMAJ)

A
  • Ethinyl estradiol 20 ug and levonorgestrel 100 ug (Alesse)
  • Ethinyl estradiol 20 ug and drospirenone 3 mg (Yasmin)
  • Ethinyl estradiol 35 ug and norgestimate 180, 215 or 250 ug (Tri-cyclin 21)
  • Ethinyl estradiol 35 ug and cyproterone acetate 2 mg (Diane-35)
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113
Q

What are potential adverse effects associated with topical retinoids for acne?

A
  • Erythema
  • Scaling
  • Dryness
  • Pruritus
  • Burning
  • Photosensitivity
  • Potential exacerbation of acne within the first few weeks
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114
Q

What is a contraindication to use of topical retinoids and what ages are they recommended in? (CMAJ)

A
  • Pregnancy
    • Tazarotene category X
    • Adapalene and Tretinoin category C
  • Adapalene and Tazarotene for patients ≥12 years of age
    • No age limitation for Tretinoin
115
Q

What should patients using topical retinoids be counselled about?

A
  • Avoid prolonged exposure to the sun and wear sunscreen
  • Avoid waxing or laser hair removal due to skin fragility
116
Q

What are potential adverse effects associated with topical BPO for acne?

A
  • Contact dermatitis (1-2%)
    • Can cause severe reaction
    • Health Canada recommends spot trial on 1 or 2 small affected areas for 3 days to ensure no hypersensitivity symptoms develop
  • Erythema
  • Peeling
  • Dryness
  • Can bleach clothing, bedding, and hair (use old sheets and wear old t-shirt in bed)
117
Q

What are potential adverse effects associated with topical dapsone for acne?

A
  • Dryness
  • Erythema
  • Sunburn
  • Contact dermatitis
  • Methemoglobinemia and hemolytic anemia
  • Contraindicated in pregnancy and breastfeeding
118
Q

How long should systemic antibiotics be prescribed for acne?

A
  • 3 months – then stop and maintain with topical treatment
119
Q

How is Accutane (Isotretinoin) prescribed for acne?

A
  • Initial 0.5 mg/kg divided BID for 1 month, then increase to 1 mg/kg
  • Total dose is 120-150 mg/kg (often takes 4-5 months)
120
Q

What do females need to do before starting Accutane (Isotretinoin)?

A
  • 2 contraceptive methods 1 month pre-treatment to 1 month post-treatment
121
Q

What are potential adverse effects associated with Accutane (Isotretinoin) for acne?

A
  • Cheilitis
  • Conjunctivitis
  • Dry mucous membranes of the nose and mouth
  • Xerosis
  • Photosensitivity
  • Less common:
    • Arthalgias
    • Myalgias
    • CNS – headache, nyctalopia (inability to see in dim light or at night), pseudotumor cerebri
122
Q

What do patients treated with Accutane (Isotretinoin) need to be monitored for?

A
  • Hypertriglyceridemia
  • Elevated total cholesterol
  • Reduced HDLs
  • LFT and Platelets
123
Q

What bloodwork should be performed in patients on Accutane (Isotretinoin)?

A
  • Initial and at 2 weeks
    • CBC, ESR, beta-HCG (2 tests before beginning), glucose, lipids, AST/ALT, INR, Bilirubin and Albumin
  • Monthly
    • Beta-HCG, Lipids, AST/ALT, INR, Bilirubin and Albumin
124
Q

How can rosacea be differentiated from acne? (TN)

A
  • Rosacea has NO comedones
  • Rosacea distributed more along central face and has symptoms of flushing
125
Q

How does rosacea typically appear? (TN)

A
  • Dome-shaped papules +/- pustules
  • Flushing, non-transient erythema and telangiectasia
  • Central face: forehead, nose, cheeks and chin
  • Remissions and exacerbations
126
Q

What is rosacea on the nose called? (TN)

A
  • Rhinophyma: distinct swelling caused by lymphedema and hypertrophy of subcutaneous tissue
127
Q

What can be exacerbating factors for rosacea? (TN)

A
  • Heat
  • Cold
  • Wind
  • Sun
  • Stress
  • Drinking hot liquids
  • Alcohol
  • Caffeine
  • Spices (triggers of vasodilation)
128
Q

How is rosacea diagnosed? (TN)

A
  • Presence of 1 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 (blepharoconjunctivitis, keratitis, iritis)
    • Peripheral location
129
Q

What are 3 general recommendations to manage rosacea? (TN)

A
  • Trigger avoidance
  • Avoid topical corticosteroids
  • Make-up to mask erythema
130
Q

What are specific 1st line rosacea treatment? (TN)

A
  • Oral tetracyclines (250-500 mg PO BID)
  • Topical metronidazole
  • Oral erythromycin (250-500 mg PO BID)
  • Topical azelaic acid
131
Q

What is being promoted a new topical option for rosacea? (CMA POEM / Cochrane)

A
  • Doxycycline and Tetracycline are effective
  • Doxycycline 40 mg dose may be as effective as 100 mg dose (less side effects)
  • Oral tetracycline similar to Topical Metronidazole in effectives for papulopustular rosacea
  • Topical Brimonidine 0.33% gel (alpha agonist) reduces redness for up to 12 hours after use
  • Topical Ivermectin effective, similar to topical metronidazole
  • Oral isotretinoin more effective than doxycycline 100 mg
132
Q

What are the 3 stages of hair growth? (TN)

A
  • Anagen = growth stage
  • Catagen = transitional stage
  • Telogen = resting stage
133
Q

When a patient presents with alopecia, what is important to determine initially and how can this be determined? (TN)

A
  • Scarring (Cicatricial) vs Non-Scarring (Non-Cicatricial) Alopecia
    • Non-scarring: intact hair follicles on exam
    • Scarring: absent hair follicles on exam
134
Q

What acronym can help remember the important causes of alopecia? (TN)

A
  • TOP HAT
    • Telogen effluvium, tinea capitis
    • Out of Fe, Zn
    • Physical: trichotillomania, “corn-row” braiding
    • Hormonal: hypothyroidism, androgenic
    • Autoimmune: SLE, alopecia areata
    • Toxins: heavy metals, anticoagulants, chemotherapy, vitamin A, SSRIs
135
Q

What are 5 types of non-scarring (non-cicatricial) alopecia? (TN)

A
  • Androgenetic alopecia
  • Physical
    • Trichotillomania
    • Traumatic: ‘corn-row’ braiding
  • Telogen effluvium
  • Anagen effluvium
  • Alopecia areata
136
Q

What is the differential for non-scarring alopecia? (TN)

A
  • Autoimmune
    • Alopecia areata
  • Endocrine
    • Hypothyroidism
    • Androgens
  • Micronutrient deficiencies
    • Iron
    • Zinc
  • Toxins
    • Heavy metals
    • Anticoagulants
    • Chemotherapy
    • Vitamin A
  • Trauma to the hair follicle
    • Trichotillomania – causes scarring on DermNet
    • ‘Corn-row’ braiding – causes scarring on DermNet
  • Other
    • Syphilis
    • Severe illness
    • Childbirth
137
Q

How does androgenetic alopecia appear for men and women? (TN)

A
  • Males: fronto-temporal areas progressing to vertex, entire scalp may be bald
  • Females: widening of central part, “Christmas tree” pattern
138
Q

What are 5 treatment options for androgenetic alopecia? (TN)

A
  • Minoxidil (Rogaine) solution or foam
  • Spironolactone in women
  • Cyproterone acetate (Diane-35) in women
  • Finasteride (Propecia) in men
  • Hair transplant
139
Q

What are potential precipitants of telogen effluvium? (TN)

A
  • SEND hair follicles out of anagen and into telogen
    • Stress and Scalp disease (seborrheic dermatitis, allergic contact dermatitis)
    • Endocrine (hypothyroidism, post-partum)
    • Nutritional (iron and protein deficiency)
    • Drugs (acitretin, heparin, lithium, interferon, beta-blockers, valproic acid, SSRIs)
140
Q

How long after exposure to the precipitant does hair loss occur with telogen effluvium and how long for it to regrow? (TN)

A
  • 2-4 months after exposure
  • Regrowth within a few months
141
Q

What are potential precipitants of anogen effluvium? (TN)

A
  • Chemotherapeutic agents, other medications (e.g. Levodopa, Colchicine, Cyclosporine), exposure to chemicals (thallium, arsenic)
142
Q

How long after exposure to the precipitant does hair loss occur with anogen effluvium and how long for it to regrow? (TN)

A
  • Hair loss 7-14 days after single pulse of chemotherapy
    • Most clinically apparent after 1-2 months
  • Reversible, follicles resume normal growth few weeks after agent stopped
143
Q

What is the pathophysiology of alopecia areata? (TN)

A
  • Autoimmune
144
Q

What are 2 subtypes of alopecia areata? (TN)

A
  • Alopecia totalis: loss of all scalp hair and eyebrows
  • Alopecia universalis: loss of all body hair
145
Q

What sign can be found on clinical exam in alopecia areata? (TN)

A
  • “Exclamation Mark” pattern: hairs fractured and have tapered shafts)
146
Q

What are 4 diseases that can be associated with alopecia areata? (TN)

A
  • Pernicious anemia
  • Vitiligo
  • Thyroid disease
  • Addison’s disease
147
Q

What are management options for alopecia areata? (TN)

A
  • Intralesional triamcinolone (corticosteroids)
  • UV or PUVA therapy
148
Q

In a patient with suspected scarring (Cicatricial) alopecia, what should be done? (TN)

A
  • Biopsy
149
Q

What are 2 types of lesions seen in pityriasis rosea? (TN)

A
  • “Herald patch” – precedes other lesions by 1-2 weeks
  • “Christmas Tree” pattern – lesions follow skin tension lines (Langer’s Lines) parallel to ribs on back
150
Q

How do lesions in pityriasis rosea appear? (TN)

A
  • Red, oval plaques/patches with central scale that does NOT extend to edge of lesion (collaret)
    • Some plaques may be annular (ring-shaped)
  • Sites: trunk, proximal aspects of arms and legs
  • Varied degree of pruritus
151
Q

What is believed to be the cause of pityriasis rosea? (TN)

A
  • HHV6/7
  • May follow a few days after a URTI
152
Q

What treatment options are available for pityriasis rosea? (TN)

A
  • None required as will clear spontaneously in 6-12 weeks
  • Topical corticosteroids when PIH is a concern or if uncomfortable
  • Oral erythromycin for 2 weeks
    • May clear up faster
  • Oral acyclovir for 7 days
    • May clear up faster
153
Q

What are the 3 most common genera of dermatophytes infecting humans? (DFCM)

A
  • Trichophyton
  • Microsporum
  • Epidermophyton
154
Q

How can the diagnosis of a fungal (dermatophyte) skin infection be confirmed? (DFCM)

A
  • Potassium bromide (KOH) microscopy of a skin scraping
    • Shows hyphae or Mycelia or with Fungal Culture
155
Q

What tool can be useful for the diagnosis of a fungal skin infection? (DFCM)

A
  • Wood’s lamp (UV-A light) – Tinea Versicolor
156
Q

What is in the differential diagnosis for a fungal skin infection? (DFCM)

A
  • Eczema
  • Contact dermatitis
  • Acne
  • Folliculitis
  • Psoriasis
  • Lichen planus
  • Trauma/irritation
157
Q

What are 8 types of fungal skin infections? (DFCM)

A
  • Tinea Capitis
  • Tinea Corporis (Ringworm)
  • Tinea Barbae
    • Tinea Faciei – non-bearded areas
  • Tinea Cruris (Jock Itch)
  • Tinea Pedis (Athlete’s Foot)
    • Tinea Mannum - hands
  • Tinea Unguum (Onychomycosis)
  • Tinea Versicolor (Pityriasis Versicolor)
  • Candida intertrigo
158
Q

How does Tinea Capitis appear, where is it located and what can it be associated with? (DFCM)

A
  • Scaling, itching and erythema of the scalp, eyelashes and eyebrows
  • Can also present as patchy alopecia, black-dot alopecia, occipital adenopathy, or a kerion (sterile inflammatory scalp mass)
  • More common in children, mainly black
  • Very contagious, may be transmitted from barber, hats, theatre seats, pets
159
Q

How does Tinea Corporis appear and where is it located? (DFCM)

A
  • Annular lesions, with scaly, well demarcated border and central clearing
  • Trunk, limbs, face
  • May be hyperpigmented in darker-skinned persons
160
Q

How does Tinea Barbae appear, where is it located and whom it is more common in? (DFCM)

A
  • Inflamed pustules, erythema and scaling on neck and beard area
  • More common in farm workers
161
Q

How does Tinea Cruris appear and where is it located? (DFCM)

A
  • Sharply demarcated areas of redness, scaling and pruritus on the medial thigh
  • Central clearing
  • Pruritic, erythematous, dry/macerated
  • No satellite lesions
162
Q

How does Tinea Pedis appear, where is it located and what is a potential complication? (DFCM)

A
  • Interdigital scaling, erythema, itching and sometimes blisters seen on the foot
  • Can also present as scaly, erythematous and hyperkeratotic lesions on the sole and sides of foot (refererd to as Moccasin Ringworm)
  • Strep cellulitis is a potential complication
163
Q

How does Tinea Unguum (Onychomycosis) appear, where is it located and what can it be associated with? (DFCM)

A
  • Thickened, raised, discolored, and cracked nails
  • More common in elderly, diabetic, and immunocompromised patients
  • Can be seen on the hand or foot
164
Q

What are the best predictors of onychomycosis on clinical exam? (CMA Infopoem)

A
  • Plantar desquamation
  • Interdigital tinea pedis
  • Previous diagnosis of fungal disease in the feet and subungual hyperkeratosis
165
Q

What are 2 topical option for the treatment of onychomycosis and their effectiveness? (TN/UTD)

A
  • Jublia (Efinaconazole) 10% solution
    • Applied directly to the nails once daily for 48 weeks
      • 1 drop per nail (2 drops for great toenail)
    • 4 weeks after 48-week treatment, complete cure achieved by 15-18% vs 3-6%
  • Penlac (Ciclopirox) 8% nail lacquer
    • Applied directly to the nails once daily for 48 weeks
    • After 48-week treatment, complete cured achieved by 7% vs 0.4%
166
Q

What is the recommended length of treatment for tinea unguum (onychomycosis)? (TN/UTD)

A
  • Terbinafine (Lamisil) 6 weeks for fingernail or 12 weeks for toenails
    • 76% cure rate after 3-4 months (UTD)
167
Q

What would a green discolouration of the nails suggest and what would be the treatment?

A
  • Pseudomonas nail infection
  • Vinegar soaks x15 min TID for 1 month
168
Q

How does Tinea Versicolor appear and where is it located? (DFCM)

A
  • Hypo or hyperpigmented circular macules on the trunk and extremities
169
Q

How does Candida intertrigo appear and where is it located? (DFCM)

A
  • Erythematous, macerated and pruritic plaques with peripheral scaling and satellite lesions
  • Typically occurs in moist area of friction such as groin, buttock, axillae and skin folds
170
Q

How should topical antifungals be applied and how long should their treatment be continued for? (DFCM)

A
  • Applied to the affected and surrounding area (1-2 inches beyond rash)
  • Treatment continued for 1 week after the symptoms are gone
171
Q

In which fungal skin infections is systemic antifungal therapy recommended? (DFCM)

A
  • Tinea capitis
  • Tinea barbae
  • Onychomycosis
  • Patients that have failed topical therapy
172
Q

What are 3 classes of topical antifungal agents and examples of each and their indications? (DFCM)

A
  • Azoles – clotrimazole (Canesten), ketoconazole (Nizoral)
    • Dermatophytes, tinea versicolor, candida
  • Allylamine – terbinafine (Lamisil)
    • Dermatophytes and tinea versicolor
  • Polyene – Nystatin
    • Candida
173
Q

What is the toxicity concern associated with terbinafine? (TN)

A
  • Liver toxicity
  • CYP 2D6 inhibitor
174
Q

What is the recommended management for Tinea Capitis? (TN)

A
  • Terbinafine (Lamisil) x 4 weeks
    • Oral agents required to penetrate the hair root where dermatophyte resides
  • Adjunctive antifungal shampoos or lotions for patient and HOUSEHOLD CONTACTS
    • Selenium sulfide shampoo 2.5% 3x per week
175
Q

What is the recommended management options for Tinea Corporis, Tinea Cruris, Tinea Pedis and Tinea Manuum? (TN)

A
  • Topical:
    • 1% clotrimazole
    • 2% ketoconazole
    • 2% miconazole
    • 1% Terbinafine (Lamisil)
    • Lotriderm (Clotrimazole & Betamethasone) BID for up to 2 weeks
  • Oral:
    • Terbinafine
    • Itraconazole
    • Fluconazole
    • Ketoconazole (if extensive)
176
Q

What are 5 types of bacterial skin infections? (DFCM)

A
  • Erysipelas – bacterial infection of the superficial dermis and superficial lymphatics
  • Cellulitis – bacterial infection of the deeper dermis and subcutaneous fat
  • Folliculitis – bacterial infection of the hair follicles with purulence in the epidermis
  • Furuncle (Boil) – bacterial infection of a hair follicle with purulence extending beyond the dermis into the subcutaneous tissue
  • Impetigo – contagious bacterial infection of the superficial skin commonly seen in the pediatric population
177
Q

How can erysipelas and cellulitis be differentiated on exam? (DFCM)

A
  • Erysipelas – RAISED lesions with WELL DEMARCATED borders, exhibit intense erythema, warmth and edema
    • ACUTE onset of symptoms
    • RAPID PROGRESSION to systemic symptoms of fever/chills
  • Cellulitis – NOT RAISED, SOMEWHAT demarcated, exhibit erythema, warmth and edema
    • SLOW onset of symptoms
    • May develop purulence or an underlying abscess requiring incision and drainage
178
Q

What are the 3 types of impetigo? (DFCM)

A
  • Non-bullous – mix of vesicles and pustules, form thick, characteristically GOLDEN-crusted exudates
  • Bullous – vesicles form yellow-brown bullae that can burst to form a BROWN crust
  • Ecythma – ulcerative lesions extend through the epidermis deep into the dermis, “PUNCHED-OUT” appearance
179
Q

Where is impetigo commonly seen? (DFCM)

A
  • Children aged 2-5
  • Common on face and extremities
180
Q

What would be the treatment for early folliculitis, mild folliculitis or mild impetigo, and moderate/severe folliculitis or impetigo? (DFCM)

A
  • Early Folliculitis = hot compresses and anti-septic cleansers daily
  • Mild = mupirocin 2% or fusidic 2% cream applied topical TID
  • Moderate/Severe = Keflex or Cloxacillin or Clindamycin or Erythromycin (all PO)
181
Q

What are 3 types of oral antibiotics that can treat community acquired (CA)-MRSA? (DFCM)

A
  • TMP/SMX PO
  • Doxycycline
  • Clindamycin
182
Q

What are 2 types of IV antibiotics that can treat CA-MRSA? (DFCM)

A
  • Vancomycin IV
  • Linezolid PO/IV
183
Q

What are 3 types of parasitic skin infections? (TN)

A
  • Scabies
  • Lice (Pediculosis)
  • Bed bugs (Hemiptera)
184
Q

What is scabies characterized by? (TN)

A
  • Skin infection due to Sarcoptes scabiei (MITE)
  • Superficial burrows
  • Intense pruritus (especially nocturnal)
  • Secondary infection
185
Q

How does the primary scabies lesion appear? (TN)

A
  • Superficial linear burrows
  • Inflammatory papules and nodules in the axilla and groin
186
Q

Where does scabies typically affect? (TN)

A
  • Axillae
  • Groin
  • Buttocks
  • Hands/Feet (especially WEB SPACES)
  • Sparing of head and neck (except in infants)
187
Q

How long do scabies mite remain alive on clothing/sheet? (TN)

A
  • 2-3 days
188
Q

How long is the incubation period for scabies? (TN)

A
  • 1 month then pruritus begins
189
Q

How should scabies be managed? (TN)

A
  • Bathe, then apply permethrin 5% cream (i.e. Nix) from neck down to soles of feet (must be left on for 8-14 hours) and requires 2nd treatment 7 days after first
  • Change underwear and linens – wash with detergent in hot water cycle then machine dry
  • Treat family and close contacts
  • Mild potency topical steroids and antihistamines for symptoms management
190
Q

How does lice typically present? (TN)

A
  • Intensely pruritic red excoriations, morbilliform rash, caused by louse (a parasite)
191
Q

What are the 3 locations that lice can present? (TN)

A
  • Scalp lice: nits (i.e. louse eggs) on hairs
    • Red excoriated skin
  • Pubic lice: nits on hairs
    • Excoriations
  • Body lice: nits and lice in seams of clothing
    • Excoriations (mainly shoulders, belt-line, buttocks)
192
Q

How should lice be managed? (TN)

A
  • Permethrin 1% (Nix cream rinse) (Ovicidal) or Permethrin 1% shampoo
  • Comb hair with fine-toothed comb using dilute vinegar solution to remove nits
  • Repeat in 7 days after first treatment
  • Shave hair if feasible
  • Change clothing and linens
  • Wash clothes and linens used 2 days prior with detergent in hot water cycle then machine dry
  • Put un-washable items in a sealed bag for 2 weeks
193
Q

What is an expensive option to treat head lice? (CMA Infopoem / NEJM)

A
  • Topical Ivermectin 0.5% ($260 per 4 oz bottle)
  • Applied once to scalp
194
Q

What treatment has been shown to be better than Permethrin for the treatment of lice? (TFP)

A
  • Dimeticone (NYDA) (silicone based product that suffocates lice and is applied to dry hair, left 8 hours, then repeated after 1 week)
  • 4% or 9.2% concentrations
  • NNT = 3-4 compared to permethrin for lice
195
Q

What causes bed bugs? (TN)

A
  • Cimex lectularius – small insect that feeds mainly at night
    • During day bedbugs hide in crevices in walls and furniture
196
Q

How does bed bugs typically present? (TN)

A
  • Burning wheals, turning to firm papules, often in groups of three – “breakfast, lunch and dinner” in areas with easy access (face, neck, arms, legs, hands)
197
Q

How should bed bugs be managed? (TN)

A
  • Professional fumigation of home
  • Topical steroids and oral H1-antagonists for symptomatic relief
  • Definitive treatment is removal of clutter in home and application of insecticides to walls and furniture
198
Q

What are most lower-limb ulcers? (PBSG)

A
  • Venous stasis ulcers
199
Q

Differentiate between venous stasis ulcers and arterial ulcers. (PBSG)

A
  • Venous Stasis Ulcers: caused by skin injury in patients with impaired venous circulation
  • Arterial Ulcers: caused by lack of blood flow distal to an area of vessel occlusion
200
Q

What is the definition of a pressure ulcer (decubitus ulcer)? (PBSG)

A
  • Localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction
201
Q

What are 5 risk factors for venous stasis ulcers? (PBSG)

A
  • Pregnancy, obesity, immobility, prolonged standing/sitting, leg trauma
  • Venous impairment (post-phlebitic syndrome, DVT, varicose veins, previous vein surgery, valve incompetence in perforator veins)
  • History of venous insufficiency ulcers
  • CHF
  • Nephrotic syndrome
202
Q

What are 4 risk factors for pressure ulcers? (PBSG)

A
  • Pressure on skin greater than arteriolar pressure (leads to hypoxia and compressive forces)
  • Friction, pressure and shearing forces from sitting or lying or from transfer/rolling methods
  • Moisture (sweat, feces, urine)
  • Immobility, Incontinence, Dietary Inadequacy
203
Q

How do venous stasis, arterial and pressure ulcers appear clinically? (PBSG)

A

Type of Ulcer

Clinical Clues

Venous stasis

  • May be large, relatively superficial and with RED/YELLOW base
  • Signs of venous pressure – EDEMA
  • “Champagne glass” ankle may be present
  • Often significant drainage
  • Peripheral pulses palpable

Arterial

  • Commonly distal with well-defined borders, a “PUNCHED-OUT” appearance
  • Often over the MEDIAL-MALLEOLAR region
  • DRIER and DEEPER than venous ulcers, with minimal granulation tissue
  • Typically covered with pale pink, yellow or black eschar
  • Often PAINFUL

Pressure

  • Located over areas of pressure (e.g. HEELS, TROCHANTERS, SACRUM)
  • Initially NON-BLANCHABLE erythema, increasing to open areas
204
Q

What should be assessed in all patients presenting with lower-extremity ulcers? (PBSG)

A
  • Clinical assessment
  • Palpable pedal pulses
  • Capillary refill
  • ABPI (Ankle Brachial Pressure Index)
205
Q

How are pressure ulcers staged? (PBSG)

A
  • NPUAP staging
    • Stage 1 – intact skin, non-blanchable redness, localized (usually over bony prominence)
    • Stage 2 – partial-thickness loss of dermis, shallow and open
    • Stage 3 – full-thickness tissue loss, subcutaneous fat may be visible (no tendons, muscles or bones), may be undermined or tunnelled
    • Stage 4 – full-thickness tissue loss, bone exposed, tendon or muscle visible or palpable, slough or eschar may be present
    • Unstageable – full-thickness tissue loss, base of ulcer bed covered by slough or eschar
206
Q

What are signs of a spreading wound infection? (PBSG)

A
  • Wound breakdown
  • Spreading erythema
  • Induration
  • Discolouration
  • Warmth
  • Crepitus
  • Lymphangitis
  • Pain
  • Malaise
207
Q

What are 3 indications to swab a wound for cultures? (PBSG)

A
  • Signs of spreading or systemic infection
  • Lack of response to appropriate antibiotic treatment
  • Protocol requirements for antibiotic-resistant organisms
208
Q

How should a wound be swabbed? (PBSG)

A
  • Clean the ulcer with warm tap water or saline first
  • Remove unhealthy tissue
  • Place the swab onto “clean” viable tissue, rotate and press firmly to obtain fluid from beneath the surface of the wound
209
Q

What are 4 practices to prevent pressure ulcers? (PBSG)

A
  • Education patients and caregivers about ischemic pain as a response to pressure
  • Move or reposition the patient to take pressure off
  • Maintain skin integrity through regular cleansing, moistening and inspection
  • Ensure adequate nutrition, ideally including a daily protein intake of 1.2-1.5 k/kg body weight
210
Q

What is recommended for all patients at risk of pressure ulcers? (PBSG)

A
  • High density foam mattress/seating
  • Sheepskin may be used over top of regular mattresses where high density foam mattresses are unavailable
211
Q

What is recommended for prevention of venous leg ulcers in patients with venous hypertension, leg edema or postphlebitic syndrome? (PBSG)

A
  • Continuous and indefinite awake-time use of compression stockings
212
Q

What are 4 principles of managing wound infections? (PBSG)

A
  • Appropriate dressing and dressing changes
  • Wound drainage and cleansing
  • Debridement as necessary
  • Antimicrobial therapy
213
Q

How much should a wound improve to indicate appropriate wound healing? (PBSG)

A
  • 30% reduction in wound measurement (length x width x depth) at 3-4 weeks
    • Most pressure ulcers show signs of healing within 2 weeks
214
Q

What are factors that can impair wound healing? (PBSG)

A
  • Nutritional status
  • Ischemia
  • Hepatic/Renal/Cardiac disease
  • Medications
    • Systemic steroids
    • NSAIDs (topical Voltaren)
    • Anti-neoplastics
  • Age
  • Smoking
  • Psychosocial status
215
Q

What should be considered when ulcers do not heal despite standard care? (PBSG)

A
  • Biopsy – to rule out malignancy
216
Q

What are 6 ways to treat venous leg ulcers? (PBSG)

A
  • Elevate legs
  • Calf pump exercises
  • Regular or range-of-motion exercise
  • Weight management
  • Skin care
  • Compression therapy
217
Q

What is required prior to initiating compression therapy in patients with venous leg ulcers? (PBSG)

A
  • ABPI
218
Q

At what ABPI can compression therapy be used and how much? (PBSG)

A
  • ABPI ≥0.8 mmHg
  • 40 mmHg compression stockings
219
Q

What is the benefit of keeping wounds moist? (PBSG)

A
  • Level 1 evidence
    • Decrease healing time
    • Less pain
    • Less risk of infection
    • Require fewer dressing changes
    • Cost-effective
220
Q

What is the benefit of debriding necrotic tissue in a skin ulcer? (PBSG)

A
  • Inhibit bacterial growth
  • Promote wound healing
221
Q

What are 5 ways to debride a wound or skin ulcer? (PBSG)

A
  • Sharp (scalpel or scissors)
  • Mechanical – superficial loose or necrotic exudate
  • Enzymatic
  • Autolytic (hydrocolloid or hydrogel dressings)
  • Biosurgery or Maggot Larvae
222
Q

What characteristics are associated with dermatofibromas? (TN)

A
  • Button-like, firm dermal papule or nodule, skin-coloured to red-brown colouring
  • Majority asymptomatic but may be PRURITIC and/or TENDER
  • Legs > Arms > Trunk
  • Dimple Sign: lateral compression causes dimpling of the lesion
223
Q

What should be done to treat bothersome dermatofibromas? (TN)

A
  • Excision
  • Cryosurgery
224
Q

Differentiate between corns vs warts vs calluses. (TN)

A
  • Corns: whitish yellow central translucent keratinous core
  • Warts: bleed with pairing, black speckled central appearance due to thrombosed capillaries
  • Calluses: layers of yellowish keratin revealed with paring
225
Q

Where are corns commonly found? (TN)

A
  • Dorsolateral 5th toe and dorsal aspects of other toes
226
Q

How can corns be treated? (TN)

A
  • Relieve pressure with padding or alternate footwear, orthotics
  • Paring, curettage
227
Q

Differentiate between keloids and hypertrophic scars. (TN)

A
  • Keloids – extended BEYOND margins of original injury with claw-like extensions
  • Hypertrophic scar – confined to original margins of injury
228
Q

What are risk factors for melanoma? (DFCM)

A
  • Intermittent intense sun exposure (like BCC, unlike SCC)
  • Immunosuppressive therapy
  • Family history of MM
  • Family history of pancreatic cancer
  • High number of common nevi
  • 1 or more atypical/dysplastic nevi
    • Should screen more often if have dysplastic nevi
    • Prophylactic excision is not recommended as most melanoma develop de novo, but having dysplastic nevi increases that risk
  • Light skin phenotype (Fitzpatrick 1/2)
229
Q

What are the screening recommendations for melanoma? (DFCM)

A
  • General Population – routine TBSE and counseling on SSE NOT recommended
    • No risk factors
  • High risk (5-10x) – screen by PCP annually for skin cancer, counsel about SSE (self-skin exam) and SCP (skin cancer prevention) by PCP
    • 2 or more of the following:
      • 1st degree relative with MM
      • 1 or more atypical nevi
      • Many (50-100) nevi
      • Naturally red or blonde hair
      • Tendency to freckle
      • Skin that burns easily and tans poorly or not at all
      • Outdoor occupation
      • Childhood in lower altitudes
      • Tanning bed use in teens and 20s
      • Radiation therapy as adult
  • Very high risk (>10x) – TBSE by dermatologist or trained PCP on yearly basis, counsel about SSE and SCP
    • Immunosuppressive therapy
    • Personal history of skin cancer
    • 2+ 1st degree relatives with MM
    • >100 nevi total or 5+ atypical nevi
    • >250 PUVA treatments for psoriasis
    • Radiation therapy for cancer as a child
230
Q

What is in the differential diagnosis for melanoma?

A
  • Dysplastic nevus
  • Traumatized nevus
  • Pigmented basal cell
  • Dermatofibroma
  • Seborrheic keratosis
231
Q

What are 4 types of NMSC? (DFCM)

A
  • BCC
  • SCC
  • Bowen disease (SCC in situ)
  • AK (solar keratosis, senile keratosis)
232
Q

What is the most common human cancer? (DFCM)

A
  • BCC
233
Q

Where are BCC commonly found? (DFCM)

A
  • Nose
234
Q

Which of BCC or SCC poses a greater metastasis risk? (DFCM)

A
  • SCC
235
Q

What is the risk of cancer associated with AKs? (DFCM)

A
  • Develop into SCC (1/1000)
236
Q

What are biopsy options for NMSC (except AKs)? (DFCM)

A
  • Shave biopsy
  • Punch biopsy
  • Deep shave (SCC and Bowen’s)
237
Q

What are options for field therapy in patients with a history of Bowen’s disease or AKs? (DFCM)

A
  • 5-FU (2-3 weeks)
  • 5% Imiquimod (8-10 weeks)
  • 3% Diclofenac gel (AKs)
238
Q

What should be asked on history for suspicious skin lesions?

A
  • A – Asymmetry
  • B – Borders irregular
  • C – Colour changing or multiple
  • D – Diameter >6 mm
  • E – Evolving
  • ABCDE Rule
    • 97% sensitivity if use on criteria, but only 43% specificity
    • Can consider biopsy if 1 criteria present
    • Consider referral if evolving +1 other criteria
239
Q

What are the 4 types of melanoma? (DFCM)

A
  • Superficial spreading
  • Nodular
  • Invasive lentigo maligna melanoma
  • Acral lentiginous melanoma
240
Q

How do most melanomas present?

A
  • Superficial spreading (70% of all melanomas)
    • Asymmetry and color variegation are characteristic
    • Majority arise de novo, only ¼ from dysplastic nevi
  • Nodular also possible
    • Discrete nodular, usually with dark pigmentation (although may be amelanotic as well)
241
Q

What are two specific types of melanoma that can appear on specific locations of the body?

A
  • Lentigo Maligna
  • Acral Lentiginous
242
Q

How does lentigo maligna appear typically?

A
  • Usually arises in areas of sun-damaged skin, particularly on the head and neck
  • Freckle-like, tan-brown macule and gradually enlarges and develops darker or lighter asymmetric foci and raised areas, which signify dermal invasion
243
Q

How does acral lentiginous appear typically?

A
  • Shows the asymmetry and color variegation of typical melanomas
  • They are distinguished clinically by their locations on the palms, soles or nails
244
Q

How should all suspicious skin lesions be investigated?

A
  • Biopsy all suspicious lesions
    • Excisional biopsy with 2mm of regular skin surrounding is best
    • Can do punch biopsy if lesion is large
  • Any concerning brown lesion should be biopsied – Don’t Watch and Wait
245
Q

How should melanomas be excised/treated? (DFCM)

A
  • Leave it to plastics
  • In situ melanomas can have margins of 0.5-1 cm
  • <1mm thick can have 1cm margins
  • >1mm thick can have 2cm margins
246
Q

What is pemphigus vulgaris?

A
  • Autoimmune blistering disease of the skin and mucous membranes
247
Q

What is in the differential diagnosis for pemphigus vulgaris?

A
  • Mouth ulcers
    • HSV
    • Aphthous ulcers
    • Erythema multiforme
  • Wide-spread erosions
    • Bullous pemphigoid
    • Bullous drug eruptions
    • Pyoderma gangrenosum
    • Impetigo
248
Q

How does pemphigus vulgaris appear?

A
  • Flaccid, non-pruritic, painful epidermal bullae/erosions
  • Typically begin in oropharynx, then spread to skin
  • Nikolsky’s Sign – pressure around a lesion leads to an erosion
249
Q

What is pemphigus vulgaris associated with?

A
  • Thymoma
  • Myasthenia gravis
  • Malignancy
250
Q

What is the treatment for pemphigus vulgaris?

A
  • High dose steroid – prednisone 1mg/kg
    • May require long-term or other immunomodulator
  • Refer immediately
251
Q

What is bullous pemphigoid?

A
  • Autoimmune bullous eruption
252
Q

How does bullous pemphigoid typically appear?

A
  • Pruritic, tense, subepidermal bullae on an erythematous or normal base
  • Prodromal urticarial for weeks to months that evolve into bullae
  • Locations – lower legs, medial thighs, groins, flexor forearm, axillae
253
Q

What is the treatment for bullous pemphigoid?

A
  • High dose steroid – prednisone 1mg/kg
    • May require long-term or other immunomodulator
  • Refer immediately
254
Q

How does cutaneous T-cell lymphoma appear?

A
  • Progressive patches/plaques with telangiectasia
  • May wax and wane
  • May be pruritic
  • May have scale
255
Q

How is cutaneous T-cell lymphoma diagnosed?

A
  • May need repeated skin biopsy
  • Keep a high degree of suspicion when presumed Psoriasis or Dermatitis does NOT respond to appropriate treatment
256
Q

What is the treatment for cutaneous T-cell lymphoma?

A
  • Topical alkylating agents for localized disease
  • Chemotherapy for extensive disease
257
Q

How does Stevens-Johnson syndrome present?

A
  • Prodrome of flu-like symptoms for 1-3 days
  • Vesicles and bullae develop over a few days
258
Q

What are potential triggers of SJS?

A
  • Medications – 50-80%
    • Allopurinol, Antibiotics, Antipsychotics, Antiepileptics, NSAIDs
    • Septra has a 20x risk compared to any other drug
  • Infections – 15%
259
Q

How should patients with burns be managed?

A
  • Fluid resuscitation
  • Tetanus prophylaxis
  • Early intubation if suspect inhalation injury
    • Closed space, unconscious, noxious chemical
  • Escharotomy – in circumferential full thickness burns
260
Q

How should fluid be replaced in burn patients?

A
  • Parkland Formula = 4cc/kg/%TBSA with RL in first 24h
    • ½ in first 8 hours, ½ in remaining 16h
    • 0 hour = time of burn (therefore if present 3h after burn, give ½ in 5h)
    • Add normal fluid maintenance to this formula
  • Urine output 50cc/hr (Adult) or 1cc/kg/hr (Children)
261
Q

What are specific things to look for with chemical and electrical burns?

A
  • Chemical – high volume irrigation before other treatment
  • Electrical – look for entrance and exit
262
Q

When can a patient presenting with a burn be discharged?

A
  • Asymptomatic
  • No significant cutaneous injury
  • No urine heme
  • Normal ECG
  • Observed 4-8h
263
Q

When should a patient presenting with a burn be admitted?

A
  • Partial thickness 15-20% (>10% if <5y or >60y)
  • Full thickness 2-5%
  • Smoke inhalation, high voltage electrical, circumferential
264
Q

What can be prescribed for patients topically for burns?

A
  • Flamazine 1% (Silver Sulfadiazine)
    • Apply to a thickness of 1/16 inch once or twice daily
    • Contraindicated in newborns, pregnancy, and lactation
  • Chlorhexidine
  • Bismuth-impregnated petroleum based gauze (e.g. Xeroform)
265
Q

What can be given to patients for post-burn pruritus?

A
  • H1 and H2 antihistamines (diphenhydramine, cetirizine, cimetidine)
  • Aloe vera, Vaseline based products, cocoa butter
266
Q

What is Wegener’s Granulomatosis?

A
  • Systemic vasculitis of small blood vessels
267
Q

What diagnostic triad is used to diagnose Wegener’s?

A
  • Necrotizing granulomatous vasculitis of respiratory tract
  • Glomerulonephritis
  • C-ANCA positive
268
Q

How does Wegener’s present clinically?

A
  • Chronic rhinosinusitis, nasal ulcerations, bloody discharge
  • Cough, SOB, hemoptysis, chest pain, CXR nodules
  • Renal failure
  • Skin lesions – irregular ulcers and erythematous plaques/papules and subcutaneous nodules
269
Q

What is the treatment for Wegener’s?

A
  • Steroids and Cyclophosphamide
  • Dialysis if needed
270
Q

What is systemic lupus erythematosus (SLE)?

A
  • Chronic inflammatory multi-system disease of unknown etiology
271
Q

What patients are at increased risk of SLE?

A
  • 10% have family history
  • F:M = 10:1, with onset during reproductive years (13-40)
  • More common in blacks and Asians
  • Can be secondary to drugs
272
Q

What is the criteria to diagnose SLE?

A
  • 4 or more of 11 must be present serially or simultaneously
    • “4, 7, 11 rule” à 4 out of 11 criteria (4 lab, 7 clinical)
  • 4 RASHES
    • 4 rashes: Malar rash, Discoid rash, Oral Ulcers, Photosensitivity
    • Renal – proteinuria (>0.5 g/day or >3+ dip) or Cellular Casts (RBC, Hb, granular, tubular, mixed)
    • Arthritis - ≥2 joints, symmetric, large or small, non-erosive
    • Serositis – Pleuritis, Pericarditis
    • Hematologic – Hemolytic anemia, Leukopenia, Lymphopenia, Thrombocytopenia
    • Excitation – seizures or psychosis
    • Serology
      • ANA (98% SN, not SP)
      • Anti-dsDNA and Anti-Sm (not SN, but >95% SP), anti-phospholipids or false positive VDRL
  • SOAP BRAIN MD
    • Serositis
    • Oral ulcers
    • ANA
    • Photosensitivity
    • Blood
    • Renal
    • Arthritis
    • Immune
    • Neurology
    • Malar rash
    • Discoid rash
273
Q

What investigations should be performed in patients suspected of having SLE?

A
  • CBC, GBCL, ESR, CRP
  • ANA (sensitive), anti-dsDNA (specific), C3, C4
    • ANA should be ordered when a patient has 2 organ systems of potential SLE origin that are otherwise unexplained
    • ENA panel ordered when ANA positive
    • Anti-dsDNA increases and Complement decreases with increasing disease severity
  • Urinalysis, ACR
  • Consider arthrocentesis for Cells, Culture and Crystals
274
Q

What are treatment options for the different complications of SLE?

A
  • Rituximab to treat underlying SLE pathology
  • Cutaneous lupus – sunscreen and hydroxychloroquine
  • Arthritis – NSAIDs, hydroxychloroquine, steroids, methotrexate
  • Nephritis and Neuritis – steroids, cyclophosphamide
  • Serositis – NSAIDs, steroids
  • Thrombocytopenia – steroids, IVID, splenectomy
  • Avoid exogenous estrogen – no OCP or HRT
275
Q

What are potential causes of drug induced lupus?

A
  • Anticonvulsants (phenytoin)
  • Antihypertensives (hydralazine)
  • Antiarrhythmics (procainamide)
  • Isoniazid (INH)
  • OCP can exacerbate
276
Q

How does drug-induced lupus differ from SLE?

A
  • Relative to SLE has:
    • Abrupt onset
    • Middle aged presentation
    • No gender preference
    • No racial discrimination
    • Less cutaneous, renal, neurologic and hematologic involvement
    • Similar joint, hepatic and constitutional symptoms
277
Q

What laboratory findings are expected in patients with drug-induced lupus?

A
  • Anti-histone positive
  • Anti-Smith/dsDNA negative
  • Complement normal
278
Q

What is the treatment for drug-induced lupus?

A
  • Discontinue offending agent
279
Q

What are two well-known types of drug reactions?

A
  • Erythema multiform
  • Serum sickness
280
Q

What is the etiology of erythema multiform?

A
  • Infection: HSV, Mycoplasma
  • Drugs: Sulfa, Penicillin, NSAIDs, anticonvulsants, allopurinol
281
Q

How does erythema multiform typically appear?

A
  • Classic “Bull’s Eye” pattern +/- bullae or erosions
  • Bilateral and Symmetric – usually asymptomatic rash
  • Can have mucosal involvement
  • Fever, Malaise, Weakness
282
Q

What is the treatment for Erythema multiform?

A
  • Stop Drug
  • Topical steroids, oral antihistamines
  • Acyclovir if HSV
283
Q

How does serum sickness present?

A
  • Symmetric drug eruptions with fever, arthralgia, LAD and rash
  • 5-10 days after the drug
284
Q

How should serum sickness be managed?

A
  • Symptomatic treatment with NSAIDs, Antihistamines
  • Oral steroids for more severe reactions
    • Temp >38.5
    • Extensive arthritis
    • Extensive rash

Primary Care (12 decks)

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