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LMCC > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is pruritus?

A

A sensation provoking a desire to scratch, with or without skin lesions

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2
Q

What are the categories of etiology for pruritus?

A
  • Dermatologic - generalized
  • Dermatologic - local
  • Systemic disease – usually generalized
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3
Q

What systemic diseases can cause pruritus?

A
  • Hepatic: obstructive biliary disease, cholestatic liver disease of pregnancy
  • Renal: chronic renal failure, uremia secondary to hemodialysis
  • Hematologic: Hodgkin’s lymphoma, multiple myeloma, leukemia, polycythemia vera, hemochromatosis, Fe deficiency anemia, cutaneous T-cell lymphoma
  • Neoplastic: lung, breast, gastric (internal solid tumours), non-Hodgkin’s lymphoma
  • Endocrine: carcinoid, DM, hypothyroid/thyrotoxicosis
  • Infectious: HIV, trichinosis, echinococcosis, hepatitis C
  • Psychiatric: depression, psychosis
  • Neurologic: post-herpetic neuralgia, multiple sclerosis
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4
Q

What local dermatologic diseases can cause pruritus?

A
  • Atopic and contact dermatitis, lichen planus, urticaria, insect bites, dermatitis herpetiformis
  • Infection: varicella, candidiasis
  • Lichen simplex chronicus
  • Prurigo nodularis
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5
Q

What generalized dermatologic diseases can cause pruritus?

A
  • Asteatotic dermatitis (“winter itch” due to dry skin)
  • Pruritus of senescent skin (may not have dry skin, any time of year)
  • Infestations: scabies, lice
  • Drug eruptions: ASA, antidepressants, opiates
  • psychogenic states
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6
Q

What should be asked on history for pruritus?

A
  • New cosmetics or creams - Allergic contact dermatitis, urticaria, photodermatitis
  • New medications, supplements, or illicit drugs - Urticaria, fixed drug eruptions
  • Recent travel - Pediculosis, scabies infestation, photodermatitis, urticaria
  • Hobby or occupational exposure to solvents, adhesives, cleaners - Irritant contact dermatitis, xerosis, atopic dermatitis, eczema
  • New animal exposures - Flea infestation, allergic contact dermatitis, urticaria
  • Sick contacts, especially those with febrile diseases and rashes - Rubeola, mumps, varicella, scarlet fever, cellulitis, fifth disease, folliculitis
  • Unexplained weight changes, menstrual irregularity, heat/cold intolerance - Thyroid disease with secondary urticaria or xerosis
  • Unexplained weight loss, night sweats, unexplained fevers, fatigue - Lymphoma with secondary generalized pruritus
  • Malaise, nausea, decreased urine output - Renal failure with generalized pruritus
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7
Q

What should be done on physical exam for pruritus?

A
  • An evaluation of the liver, spleen, and lymph nodes.
  • Organomegaly increases the likelihood of an underlying systemic disease, such as lymphoma.
  • The skin should also be examined. Finger webs, intertriginous regions, and the genitals should be evaluated for the presence of scabies or lice.
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8
Q

Investigations for pruritus?

A

CBC, TSH, fasting glucose, ALP, bili, Cr, BUN, LFT, stool culture

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9
Q

General management for pruritus?

A
  • Treat underlying cause
  • Cool water compresses to relieve pruritus
  • Bath oil and emollient ointment (especially if xerosis is present)
  • Topical corticosteroid and antipruritics (e.g. menthol, camphor, phenol, mirtazapine, capsaicin)
  • Systemic antihistamines: H1 blockers are most effective, most useful for urticaria
  • Phototherapy with UVB or PUVA
  • Doxepin, amitriptyline
  • Immunosuppressive agents if severe: steroids and steroid-sparing
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10
Q

How do you describe skin lesions?

A
  • Size
  • Colour
  • Arrangement
  • Lesion Morphology
  • Distribution
  • ALWAYS remember scalp, hair, nails, mucous membranes, feet
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11
Q

Type I acne

A

Type I: comedonal, sparse, no scarring

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12
Q

Type II acne

A

Type II: comedonal, papular, moderate ± little scarring

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13
Q

Type III acne

A

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

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14
Q

Type IV acne

A

Type IV: nodulocystic acne, risk of severe scarring

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15
Q

Pathophysiology of acne

A
  • Hyperkeratinization at the follicular ostia (opening) blocks the secretion of sebum leading to the formation of microcomedones
  • Androgens promote excess sebum production
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16
Q

Treatment of mild acne?

A
  • Topical OTC therapies: benzoyl peroxide, salicylic acid
  • Antimicrobials: clindamycin
  • Retinoids: Vitamin A acid
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17
Q

Treatment of moderate acne?

A
  • Tetracycline, minocycline

- Spironolactone

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18
Q

Treatment of severe acne?

A

Isotretinoin

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19
Q

What is rosacea

A

Chronic inflammation of skin and is especially associated with triggers that increase body temperature.

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20
Q

Triggers for rosacea

A
  • Hot weather, hot drinks, spicy food
  • Stress, alcohol, nicotine
  • Demodex mites
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21
Q

Clinical features of erythematotelangiectatic rosacea

A
  • Facial flushing

- Persistent erythema of the face (together with telangiectasias)

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22
Q

Clinical features of papulopustular rosacea

A
  • Papules, pustules, and erythema

- Comedones are not present in patients with rosacea.

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23
Q

Clinical features of phymatous rosacea

A
  • Skin and sebaceous glands thicken
  • Inflammatory, widespread nodules
  • Rhinophyma: enlarged, bulbous nose (almost exclusively in males)
  • Similar changes may occur on the chin, forehead, cheeks, and ears
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24
Q

Clinical features of ocular rosacea

A
  • Conjunctival hyperemia (most common)
  • Blepharitis (inflammation of the eyelid margin), stye (hordeolum externum), chalazion
  • Dry eyes and foreign-body sensation
  • Keratitis
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25
Q

Treatment of rosacea

A
  1. Avoid triggers
  2. Medical therapy
  3. Laser therapy: for erythema, telangiectasias, and phymatous rosacea
  4. Surgical therapy: for phymatous rosacea; includes electrocautery and dermabrasion
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26
Q

Clinical features of atopic dermatitis?

A
  • Subacute and chronic eczematous reaction associated with prolonged severe pruritus
  • Inflammation, lichenification, excoriations are secondary to relentless scratching
  • Atopic Palms: hyperlinearity of the palms
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27
Q

Pathophysiology of atopic dermatitis?

A

T-cell driven inflammatory process with epidermal barrier dysfunction

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28
Q

Epidemiology of atopic dermatitis?

A

Frequently affects infants/children/young adults; 10-20% children in developed countries under the age of 5 are affected - associated with PMHx/FHx of atopy (asthma, hay fever), anaphylaxis, eosinophilia

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29
Q

Distribution of atopic dermatitis?

A
  • Infants: head + flexure surfaces (elbows)
  • Children: neck + extensor surfaces (behind knees, in elbows)
  • Adults: neck + hands/feet (lichenification of skin in adults)
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30
Q

Non-pharmacology treatment of atopic dermatitis?

A
  • AVOID triggers: irritants, contact allergens, environmental, inappropriate bathing habits – long hot shower, sweating, microbes, stress
  • Moisturizers: apply liberally and reapply at least BID with goal of minimizing xerosis; include in treatment of mild-severe disease as 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&raquo_space;> immediately apply topical agents/moisturizers after this - use fragrance free hypoallergenic non-soap cleansers
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31
Q

Pharmacology treatment of atopic dermatitis?

A
  1. Topical Corticosteroids: effective in reducing acute/chronic sx as well as prevention of flares
  2. Topical Calcineurin Inhibitors (Tacrolimis, Pimecrolimus): use as steroid-sparing agents in the long-term
  3. Adjuncts: antihistamines + psychological interventions
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32
Q

Treatment of erythema, flushing, skin sensitivity, xerosis in rosacea

A

Topical brimonidine, Topical oxymetazoline

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33
Q

Treatment of mild papules and pustules in rosacea

A

Metronidazole (also for ocular rosacea), Azelaic acid, Ivermectin, Sodium sulfacetamide

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34
Q

Treatment of moderate to severe papules and pustules in rosacea

A

Tetracyclines: e.g., doxycycline (also for ocular rosacea), tetracycline, minocycline, Isotretinoin (first-line for phymatous rosacea)

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35
Q

Refractory treatment of atopic dermatitis?

A

Azathioprine + MTX + PO cyclosporine + PO steroids + phototherapy + potent topical steroids + psychotherapeutics

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36
Q

Two types of contact dermatitis?

A
  • Irritant Dermatitis

- Allergic Contact Dermatitis

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37
Q

Mechanism of reaction for irritant dermatitis?

A

Toxic injury to skin; non-immune mechanism

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38
Q

Clinical features of irritant dermatitis?

A
  • 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
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39
Q

Management of irritant dermatitis?

A
  • Avoidance of irritants
  • Wet compresses with Burrow’s solution
  • Barrier moisturizers
  • Topical/oral steroids
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40
Q

Mechanism of reaction for allergic contact dermatitis?

A

Cell-mediated delayed (Type IV) hypersensitivity reaction

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41
Q

Clinical features of allergic contact dermatitis?

A
  • Type of reaction: Erythema with a papulovesicular eruption, swelling, pruritus
  • Distribution: Areas exposed to allergen
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42
Q

Treatment of allergic contact dermatitis?

A
  • 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
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43
Q

Clinical features of dyshidrotic dermatitis

A
  • “tapioca pudding” papulovesicular dermatitis of hands and feet that coalesce into plaques, followed by painful fissuring
  • Acute stage often very pruritic
  • Lesions heal with desquamation and may lead to chronic lichenification
  • Sites: palms and soles¬ ± dorsal surfaces of hands and feet
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44
Q

Pathophysiology of dyshidrotic dermatitis

A
  • unknown
  • NOT caused by hyperhidrosis (excessive sweating)
  • Emotional stress may precipitate flares
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45
Q

Management of dyshidrotic dermatitis

A
  • Topical: high potency corticosteroid with plastic cling wrap occlusion to increase penetration
  • Intralesional triamcinolone injection
  • Systemic
    o prednisone in severe cases
    o alitretinoin (Toctino) for all types of chronic hand dermatitis, including dyshidrotic dermatitis
    o antibiotics for secondary S. aureus infection
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46
Q

Clinical features of nummular dermatitis

A
  • Nummular (coin-shaped), pruritic, dry, scaly, erythematous plaques
  • Often associated with atopic and dyshidrotic dermatitis
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47
Q

Management of nummular dermatitis

A
  • Moisturization

- Mid to high potency corticosteroid ointment twice daily

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48
Q

Distribution of seborrheic dermatitis

A
  • 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
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49
Q

Clinical features of seborrheic dermatitis

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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50
Q

Pathophysiology of seborrheic dermatitis

A

Possible etiologic association with Malassezia spp. (yeast)

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51
Q

Management of seborrheic dermatitis

A
  • Face: ketoconazole cream daily or bid and/or mild steroid cream daily or bid
  • Scalp: salicylic acid in olive oil or Derma-Smoothe lotion to remove dense scales, 2% ketoconazole shampoo, ciclopirox, shampoo, selenium sulfide or zinc pyrithione (e.g. Head and Shoulders) shampoo, steroid lotion (e.g. betamethasone valerate 0.1% lotion bid)
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52
Q

Clinical features of stasis dermatitis

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
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53
Q

Pathophysiology of stasis dermatitis

A
  • Chronic venous insufficiency leads to venous stasis

- Surrounding soft tissue inflammation and fibrosis results

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54
Q

Investigations of stasis dermatitis

A
  • Doppler and colour-coded Duplex sonography if suspicious for DVT
  • Swab for bacterial culture if there is crusting
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55
Q

Management of stasis dermatitis

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
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56
Q

Clinical features of lichen simplex chronicus

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
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57
Q

Pathophysiology of lichen simplex chronicus

A
  • Skin hyperexcitable to itch, continued rubbing/scratching of skin results
  • Eventually lichenification occurs
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58
Q

Investigations of lichen simplex chronicus

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
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59
Q

Management of lichen simplex chronicus

A

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

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60
Q

Clinical features of lichen planus

A
  • Morphology: pruritic, well-demarcated, violaceous, polygonal, flat-topped papules
  • Characterized by the six P’s (pruritus, polygonal, planar, purple, papules, plaques)
  • Koebner phenomenon
  • Wickham’s striae: reticulate white-grey lines over mucosal surface; pathognomonic but may not be present
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61
Q

Pathophysiology of lichen planus

A
  • autoimmune, antigen unknown

- lymphocyte activation leads to keratinocyte apoptosis

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62
Q

Investigations of lichen planus

A
  • Clinical diagnosis but consider a punch biopsy

- Hepatitis C serology if patient has risk factors

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63
Q

Distribution of lichen planus

A
  • Common sites: wrists, ankles, mucous membranes in 60% (mouth, vulva, glans), nails, scalp
  • Distribution: symmetrical and bilateral
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64
Q

Management of lichen planus

A
  • Topical or intralesional corticosteroids
  • Short courses of oral prednisone (rarely)
  • Phototherapy or oral retinoids or systemic immunosuppressants (e.g. azathioprine, methotrexate, cyclosporine) for extensive or recalcitrant cases
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65
Q

Clinical features of initial eruption of pityriasis rosea?

A

Initial eruption: herald patch (mother patch)

  • Single ovoid macule or patch, 2-10 cm in diameter
  • Slightly raised, dark red border with a central salmon-colored clearing zone
  • Surrounded by a collarette: a collar of fine, white scales (like cigarette paper)
  • Typically on the back
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66
Q

Clinical features of secondary eruption of pityriasis rosea?

A
  • Bilateral diffuse, oval-shaped, salmon-colored papules and plaques (< 1.5 cm) with scaly collarette
  • Papules appear along Langer lines, which align on the back like the branches of a Christmas tree (Christmas tree appearance)
  • Typically seen on the trunk (thorax, back, abdomen), neck, and upper extremities
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67
Q

Etiology of pityriasis rosea?

A

Suspected HHV-7 or HHV-6 reactivation

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68
Q

Management of pityriasis rosea?

A
  • None required; clears spontaneously in 6-12wk

- Symptomatic: topical glucocorticoids if pruritic, cool compresses, emollients

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69
Q

Classification of psoriasis

A
  1. plaque psoriasis
  2. guttate psoriasis
  3. erythrodermic psoriasis
  4. pustular psoriasis
  5. inverse psoriasis
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70
Q

Clinical features of plaque psoriasis

A
  • Chronic and recurrent disease characterized by well-circumscribed erythematous papules/plaques with silvery-white scales
  • Often worse in winter (lack of sun)
  • Auspitz sign: bleeds from minute points when scale is removed
  • Common sites: scalp, extensor surfaces of elbows and knees, trunk (especially buttocks), nails, pressure areas
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71
Q

Management of mild (<3% BSA) plaque psoriasis

A
  • topical steroids, topical vitamin D3 analogues, or a combination of the two are first line
  • topical retinoid ± topical steroid combination, anthralin, and tar are also effective but tend to be less tolerated than first line therapies
  • emollients
  • phototherapy or systemic treatment may be necessary if the lesions are scattered or if it involves sites that are difficult to treat such as palms, soles, scalp, genitals
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72
Q

Management of moderate (3-10% BSA) to severe (>10% BSA) plaque psoriasis

A
  • goal of treatment is to attain symptom control that is adequate from patient’s perspective
  • phototherapy if accessible
  • systemic or biological therapy based on patient’s treatment history and comorbidities
  • topical steroid ± topical vitamin D3 analogue as adjunct therapy
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73
Q

Clinical features of guttate psoriasis

A
  • Discrete, scattered salmon-pink small scaling papules
  • Sites: diffuse, usually on trunk and legs, sparing palms and soles
  • Often antecedent streptococcal pharyngitis
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74
Q

Management of guttate psoriasis

A
  • UVB phototherapy, sunlight, lubricants, topical steroids

- Penicillin V or erythromycin if Group A β-hemolytic Streptococcus on throat culture

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75
Q

Clinical features of erythrodermic psoriasis

A
  • Generalized erythema (>90% of BSA) with fine desquamative scale on surface
  • Associated signs and symptoms: arthralgia, pruritus, dehydration, electrolyte imbalance
  • Triggered by having a Hx of psoriasis then start new drug/steroids/etc.
  • Aggravating factors: lithium, β-blockers, NSAIDs, antimalarials, phototoxic reaction, infection
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76
Q

Management of erythrodermic psoriasis

A
  • IV fluids, monitor fluids and electrolytes, may require hospitalization
  • Treat underlying aggravating condition, suna voidance
  • Cyclosporine, acitretin, methotrexate, UV, biologics
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77
Q

Clinical features of pustular psoriasis

A
  • Sudden onset of erythematous macules and papules which evolve rapidly into pustules, can be painful
  • May be generalized or localized
  • Patient usually has a history of psoriasis; may occur with sudden withdrawal from steroid therapy
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78
Q

Management of pustular psoriasis

A
  • methotrexate, cyclosporine, acitretin, UV, biologics
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79
Q

Clinical features of inverse psoriasis

A
  • Erythematous plaques on flexural surfaces such as axillae, inframammary folds, gluteal fold, inguinal folds
  • Lesions may be macerated
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80
Q

Management of inverse psoriasis

A
  • Low potency topical corticosteroids
  • Topical vitamin D derivatives (e.g. calcipotriene, calcitriol)
  • Topical calcineurin inhibitors (e.g. tacrolimus, pimecrolimus)
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81
Q

Clinical features of bullous pemphigoid

A
  • Chronic autoimmune bullous eruption characterized by pruritic, tense, subepidermal bullae on an erythematous or normal skin base. Affects skin, not mucous membranes. Tense bullae – may be serous or hemorrhagic. As the bullae age, they eventually become flaccid and rupture, leaving erosions and serous or hemorrhagic crusts. NEGATIVE NIKOLSKY’S SIGN.
  • Can present as urticarial plaques without bullae
  • Common sites: flexor aspect of forearms, axillae, medial thighs, groin, abdomen
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82
Q

Pathophysiology of bullous pemphigoid

A
  • IgG produced against dermal-epidermal basement membrane proteins (hemidesmosomes) leads to subepidermal bullae
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83
Q

Investigations of bullous pemphigoid

A
  • Immunofluorescence shows linear deposition of IgG and C3 along the basement membrane
  • Anti-basement membrane antibody (IgG) (pemphigoid antibody detectable in serum)
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84
Q

Management of bullous pemphigoid

A
  • Prednisone 0.5-1 mg/kg/d until clear, then taper ¬ ± steroid-sparing agents (e.g. azathioprine, cyclosporine, mycophenolate mofetil)
  • Topical potent steroids (clobetasol) may be as effective as systemic steroids in limited disease
  • Tetracycline ¬ ± nicotinamide is effective for some cases
  • Immunosuppressants such as azathioprine, mycophenolate mofetil, cyclosporine
  • IVIg and plasmapheresis for refractory cases
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85
Q

Clinical features of pemphigus vulgaris

A
  • Autoimmune blistering disease characterized by flaccid, non-pruritic intraepidermal bullae/vesicles on an erythematous or normal skin base. Affects skin and mucous membranes
  • May present with erosions and secondary bacterial infection
  • Sites: mouth (90%), scalp, face, chest, axillae, groin, umbilicus
  • Nikolsky’s sign: epidermal detachment with shear stress
  • Asboe-Hansen sign: pressure applied to bulla causes it to extend laterally
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86
Q

Pathophysiology of pemphigus vulgaris

A

IgG against epidermal desmoglein-1 and -3 lead to loss of intercellular adhesion in the epidermis

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87
Q

Epidemiology of pemphigus vulgaris

A

Paraneoplastic pemphigus may be associated with thymoma, myasthenia gravis, malignancy, and use of D-penicillamine

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88
Q

Investigations of pemphigus vulgaris

A
  • Immunofluorescence: shows IgG and C3 deposition intraepidermally
  • Circulating serum anti-desmoglein IgG antibodies
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89
Q

Management of pemphigus vulgaris

A

Prednisone 1-2mg/kg until no new blisters, then 1-1.5mg/kg until clear, then taper ¬ ± steroid-sparing agents (e.g. azathioprine, cyclophosphamide, cyclosporine, IVIg, mycophenolate mofetil, rituximab)

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90
Q

Clinical features of dermatitis herpetiformis

A
  • Grouped papules/vesicles/urticarial wheals on an erythematous base, associated with intense pruritus, burning, stinging, excoriations
  • Lesions grouped,bilaterallysymmetrical
  • Common sites: extensor surfaces of elbows/knees, sacrum, buttocks, scalp
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91
Q

Pathophysiology of dermatitis herpetiformis

A

Transglutaminase IgA deposits in the skin alone or in immune complexes leading to eosinophil and neutrophil infiltration

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92
Q

Investigations of dermatitis herpetiformis

A
  • Biopsy

- Immunofluorescence shows IgA deposits in perilesional skin

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93
Q

Management of dermatitis herpetiformis

A
  • Dapsone (sulfapyridine if contraindicated or poorly tolerated)
  • Gluten-free diet for life – this can reduce risk of lymphoma
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94
Q

Diagnosis of Drug Reaction

A

1-4 = DEFINITE, #1-3 = PROBABLE, #1 only = POSSIBLE

  1. Temporal relationship between drug exposure and reaction
  2. Recognized response to suspected drug
  3. Improvement after drug withdrawal
  4. Recurrence of reaction on re-challenge with the drug
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95
Q

Clinical features of porphyria cutaneous tarda

A
  • Skin fragility followed by formation often sevesicles/bullae and erosions on photo exposed skin gradual healing to scars, milia
  • Periorbital violaceous discolouration, diffuse hypermelanosis, facial hypertrichosis
  • Common sites: light-exposed areas subjected to trauma, dorsum of hands and feet, nose, and upper trunk
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96
Q

Pathophysiology of porphyria cutaneous tarda

A
  • Uroporphyrinogen decarboxylase deficiency leads to excess hemeprecursors
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97
Q

Investigations of porphyria cutaneous tarda

A
  • Urine and 5% HCl shows orange-red fluorescence under Wood’s lamp (UV rays)
  • 24h urine has elevated uroporphyrins
  • Stool contains elevated coproporphyrins
  • Immunofluorescence shows IgE at dermal-epidermal junctions
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98
Q

Management of porphyria cutaneous tarda

A
  • Discontinue aggravating substances (alcohol, estrogen therapy)
  • Phlebotomy to decrease body iron load
  • Low dose hydroxychloroquine
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99
Q

Presentation of exanthematous drug reaction

A

Erythematous macules/papules +/- scale, symmetrical, trunk to extremities

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100
Q

Typical course of exanthematous drug reaction

A

7-14d after drug initiation, fades 7-14d after drug d/c

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101
Q

Management of exanthematous drug reaction

A

d/c drug (weigh risks/benefits) + antihistamines + emollients + topical steroids

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102
Q

Clinical presentation of drug reaction with eosinophilia + systemic symptoms (DRESS)

A
  • morbilliform rash (face, trunk, arms) + can have facial edema
  • systemic Features: fever + malaise + arthralgia + cervical lymphadenopathy + internal organ involvement (hepatitis, nephritis, pneumonitis, hematologic abnormalities, thyroid dysfunction)
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103
Q

Typical spread of DRESS

A

Starts with face/periorbital + spread CAUDALLY + no mucosal involvement

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104
Q

Classic triad of DRESS

A

Fever + exanthematous eruption + internal organ involvement

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105
Q

Management of DRESS

A
  • Discontinue drug +/- prednisone (0.5mg/kg/d) + consider cyclosporine if severe
  • MAY progress to generalized exfoliative dermatitis/erythroderma if drug is NOT discontinued
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106
Q

Clinical presentation of drug induced urticarial angioedema

A
  • Intensely pruritic, well-circumscribed, erythematous, elevated wheals lasting >24hr (unlike non-drug induced urticarial). Individual lesions may coalesce and wax and wane over several hours + angioedema (face and mucous membranes)
  • Systemic Features: ~ associated with systemic anaphylaxis (bronchospasm, laryngeal edema, shock)
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107
Q

Management of drug induced urticarial angioedema

A

d/c drug + antihistamines + steroids + epinephrine if anaphylactic

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108
Q

Clinical features of serum sickness-like reaction

A
  • Morphology: symmetrical cutaneous eruption (usually urticarial)
  • Systemic features: malaise, low grade fever, arthralgia, lymph adenopathy
  • Time course: appears 1-3 wk after drug initiation, resolve 2-3 wk after withdrawal
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109
Q

Management of serum sickness-like reaction

A

Discontinue off ending drug ¬ ± topical/oral corticosteroids

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110
Q

What is stevens-johnson syndrome

A
  • Type IV Hypersensitivity Reaction
  • A consequence of rapid, synchronous cell death of deeper layer keratinocytes resulting in separation of the skin at the dermal– epidermal junction (therefore subepidermal cleavage)
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111
Q

Clinical features of stevens-johnson syndrome?

A
  • Morphology: prodromal rash (morbilliform/targetoid lesions ± purpura, or diffuse erythema), confluence of flaccid blisters, positive Nikolsky sign (epidermal detachment with shear stress), full thickness epidermal loss; dusky tender skin, bullae, desquamation/skin sloughing, atypical targets. PAINFUL macular exanthem. Most drug rashes are itchy, not painful
  • Systemic features: fever (higher in TEN), cytopenias, renal tubular necrosis/AKI, tracheal erosion, infection, contractures, corneal scarring, phimosis, vaginal synechiae
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112
Q

Classification of stevens-johnson syndrome

A

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

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113
Q

Spread of stevens-johnson syndrome

A

Face and extremities; may generalize; scalp, palms, soles relatively spared; erosion of mucous membranes (lips, oral mucosa, conjunctiva, GU mucosa)

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114
Q

Causes of stevens-johnson syndrome

A

Often associated with medications (e.g. antibiotics, analgesics, antihistamines, contrast agents)! The most well recognized is SJS/TEN in response to carbamazepine therapy in Han Chinese individuals carrying the HLA-B*1502 allele.

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115
Q

Management of stevens-johnson syndrome

A
  • Discontinue offending drug
  • Admit to intermediate/intensive care/burn unit
  • Supportive care: IV fluids, electrolyte replacement, nutritional support, pain control, wound care, sterile handling, monitor for and treat infection
  • IVIg or cyclosporine or etanercept
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116
Q

Clinical presentation of impetigo

A

Vesicles, bullae (large vesicles), and pustules which become covered by golden yellow crust (honey brown).

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117
Q

Etiology of impetigo

A
  • Group A beta-hemolytic streptococci, but also staph aureus.
  • Certain strains of Group A will cause post-streptococcal glomerulonephritis; uncommon, but can happen during nephritogenic strain epidemics. If suspect endemic like this, follow pt for glomerulonephritis and urinalysis 7 weeks following impetigo. Phage group II staphylococci can cause bullous impetigo.
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118
Q

Investigations of impetigo

A

Gram stain and culture of lesion fluid or biopsy

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119
Q

Treatment of impetigo

A
  • Remove crusts, use saline compresses, and topical antiseptic soaks bid
  • Topical antibacterials (e.g. 2% mupirocin or fusidic acid (Canada only) tid; continue for 7-10d after resolution)
  • Systemic antibiotics (e.g. cloxacillin or cephalexin for 7-10d)
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120
Q

Etiology of erysipelas

A

GAS

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121
Q

Clinical features of erysipelas?

A
  • Superficial cellulitis involving the upper dermis and lymphatics
  • Confluent, erythematous, sharp raised edge, warm plaque, well demarcated
  • Very painful (“St. Anthony’s fire”)
  • Erysipelas is nonpurulent
  • Sites: face and legs
  • Systemic symptoms: fever, chills, headache, weakness (if present, sign of more serious infection)
  • Classic descriptions of erysipelas note “butterfly” involvement of the face
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122
Q

Clinical features of cellulitis?

A
  • Involves lower dermis/subcutaneous fat
  • Unilateral erythematous flat lesion, often with vesicles poorly demarcated, not uniformly raised
  • May present with or without purulence
  • Tender
  • Sites: commonly on legs
  • Systemic symptoms (uncommon): fever, leukocytosis, lymphadenopathy
123
Q

Etiology of cellulitis?

A

Staphylococci (penetrating trauma) and group A/B Streptococcus (hemolytic) (common in DM) or even haemophilus influenza (children)

124
Q

Investigations of cellulitis/erysipelas?

A
  • Laboratory testing is not required for patients with uncomplicated infection in the absence of comorbidities or complications.
  • Basic Labs: CBC + lytes + Urea/Cr + lactate (if suspicious of necrotizing fasciitis)
  • Basic Microbiology: swab the portal of entry or any open draining wound for gram stain + C&S + blood C&S (if systemic symptoms are present)
125
Q

Treatment of mild cellulitis?

A

Cephalexin 500mg PO QID or clindamycin 300mg PO QID x 5-14 days

126
Q

Treatment of mild erysipelas?

A

Penicillin 500mg PO QID or amoxicillin 500mg PO TID

127
Q

Treatment of systemic/severe cellulitis?

A

Cefazolin 1-2g IV q8h or ceftriaxone 1g IV q24h

128
Q

Treatment of systemic/severe erysipelas?

A

Ceftriaxone 1g IV q24h or cefazolin 1-2g IV q8h x 5-14 days

129
Q

What is staphylococcal scalded skin syndrome (SSSS)?

A

Desquamation of skin cells and breaking down of connections in superficial epidermis, scalded appearance (skin peels off in large sheets), diffuse erythema and exfoliation, often in pediatrics/neonates or immunosuppressed adults

130
Q

Pathophysiology of staphylococcal scalded skin syndrome (SSSS)?

A

Staph toxin exfoliatin binds to the epidermal granular zone

131
Q

Treatment of staphylococcal scalded skin syndrome (SSSS)?

A

Semisynthetic penicillin derivatives or cephalosporins >2 wks or erythromycin, prognosis great even without therapy

132
Q

Clinical features of necrotizing fasciitis?

A
  • Systemic symptoms: fever, chills, altered mental status
  • Cutaneous findings
    o Diffuse erythema (often manifests initially as suspected cellulitis that is not responding to initial antibiotic therapy)
    o Extreme tenderness and pain out of proportion to the area of erythema
    o Significant induration of the subcutaneous tissue
    o Crepitus: due to the production of methane and CO2 by bacteria
    o Purple skin discoloration (skin necrosis, ecchymosis)
    o Bullae
    o Loss of sensation in the affected area (paresthesias)
133
Q

Definition of necrotizing fasciitis?

A

Rare life threatening infection of superficial + deep fascia resulting in thrombosis of subcutaneous vessels + gangrene

134
Q

Predisposing conditions to necrotizing fasciitis?

A

Diabetes mellitus, peripheral vascular disease, intravenous drug use, obesity, malnutrition, cutaneous trauma

135
Q

Treatment of necrotizing fasciitis?

A

Surgical debridement and re-exploration 24 hr later, systemic Abx with culture

136
Q

Local signs and symptoms of gas gangrene?

A
  • Excruciating muscle pain
  • Massive edema with skin discoloration that progresses from bronze to red-purple to black and overlying bullae
  • Sweet and foul-smelling or nonodorous discharge produced by anaerobic metabolic products
  • Crepitus: Palpation reveals crackling of the skin due to gas production (skin emphysema)
  • Spreading infection
137
Q

Etiology of gas gangrene?

A
  • Clostridium perfringens (> 80% of cases): a gram-positive, obligate anaerobic, spore-forming bacterium
  • Less common: C. septicum , C. histolyticum
138
Q

Path of infection for gas gangrene?

A

Wounds with compromised blood supply create an optimal anaerobic environment for the proliferation of C. perfringens - necrosis that progresses within 24-36 hours

139
Q

Systemic toxicity signs of gas gangrene?

A
  • Early signs – Fever, Tachycardia, Altered mental status

- Late signs - Shock, Multi-organ failure, Hemolytic anemia, ARDS, Kidney and liver failure

140
Q

Treatment of gas gangrene?

A
  • Surgical exploration and debridement: If applicable, amputation of the affected extremity may be necessary.
  • Antibiotic therapy: penicillin plus clindamycin or tetracycline
141
Q

Clinical features of dermatophytoses?

A

Infection of skin, hair, and nails caused by dermatophytes (fungi that live within the epidermal keratin or hair follicle and do not penetrate into deeper structures)

142
Q

Investigations of dermatophytoses?

A

Skin scrapings, hair, and/or nail clippings analyzed with potassium hydroxide (KOH) prep to look for hyphae and mycelia

143
Q

What is tinea corporis?

A

Infection of the glabrous (smooth, without terminal hairs) skin with superficial dermatophytes – fungus.

144
Q

Treatment of tinea corporis?

A

Topical imidazole derivatives, topical polyenes (nyastatin), and topical allylamines (terbinafine). Resistant cases may require systemic oral griseofulfvin, terbinafine, ketoconazole.

145
Q

Clinical presentation of tinea capitis?

A
  • Round, several patches of alopecia, pruritic
  • Kerion (boggy, elevated, purulent inflamed nodule/ plaque) may form secondary to infection by bacteria and result in scarring
  • May have occipital lymphadenopathy
  • Affects children (mainly black), immunocompromised adults
146
Q

Investigations for tinea capitis?

A

Exam scalp under UVA/Wood’s light to see greenish yellow fluorescence. Some don’t fluoresce though, so doesn’t rule out. Hairs should be plucked from the area and sent for fungal culture – should see spores inside the hair shaft (endothrix infection) or coating the outside of the hair shaft (exothrix infection).

147
Q

Treatment of tinea capitis?

A

Oral terinbafine x4wk

148
Q

Predisposing factors of tinea pedis?

A

Predisposing factors: heat, humidity, occlusive footwear

149
Q

Clinical features of tinea pedis?

A
  • Pruritic scaling and/or maceration of the web spaces, and powdery scaling of soles
  • Acute infection: interdigital (especially 4th web space) red/white scales, vesicles, bullae, often with maceration
  • Secondary bacterial infection may occur
  • Chronic: non-pruritic, pink, scaling keratosis on soles, and sides of feet
  • May present as flare-up of chronic tinea pedis
150
Q

Clinical features of tinea cruris?

A
  • Scaly patch/plaque with a well-defined, curved border and central clearing
  • Pruritic, erythematous, dry/macerated
  • Sites: starts medial thigh, spreads centrifugally to perineum, gluteal cleft, buttocks
151
Q

Management of tinea cruris or tinea pedis?

A

Topicals as first line agents for tinea corporis/cruris and tinea pedis (interdigital type): clotrimazole, or terbinafine or ciclopirox olamine cream applied bid

152
Q

What is tinea versicolor?

A

Tinea versicolor (pityriasis versicolor) is a benign superficial skin infection that occurs most often in young adults during hot and humid weather and is most commonly caused by the fungi Malassezia globosa and Malassezia furfur.

153
Q

Clinical features of tinea versicolor?

A
  • Round, well-demarcated macules that reveal a fine, subtle scale with gentle scraping that can coalesce into patches (which may have irregular shapes)
  • Pityriasis versicolor alba: pale patches (hypopigmentation)
  • Pityriasis versicolor rubra: reddish-brown (hyperpigmentation)
  • Milder pruritus (compared to dermatophyte infections)
  • Patients often become aware of the disease after sun exposure because the lesions do not tan and become more visible against the recently tanned surrounding skin.
154
Q

Treatments of tinea versicolor?

A
  1. Topical antifungals (first-line therapy)
    - Selenium sulfide or zinc pyrithione in form of lotion or shampoo
    - Azoles (miconazole or ketoconazole) or allylamines (terbinafine) in form of creams
  2. Oral antifungals
    - Reserved for infections that are severe, widespread, or unresponsive to topical therapy to reduce the possible risks of systemic medication (not typically used in children)
    - Oral fluconazole or itraconazole are the preferred oral agents.
155
Q

Primary lesion of scabies?

A

Superficial linear burrows, inflammatory papules/nodules in the axilla/groin

156
Q

Secondary lesion of scabies?

A

Small urticarial crusted papules, eczematous plaques, excoriations

157
Q

Sites of scabies?

A

Axillae, groin, buttocks, hands/feet (esp. web spaces), sparing of head and neck (except in infants)

158
Q

Pathophysiology of scabies?

A

Scabies mites remains alive 2-3d on clothing/sheets, incubation 1mo > then pruritus begins, re-infection followed by hypersensitivity in 24hrs

159
Q

Risk factors of scabies?

A

Sexual promiscuity + crowding + poverty + nosocomial + immunocompromised

160
Q

Investigations for scabies?

A

Microscopic exam of root and content of burro and mineral oil mount for mite/eggs/feces, skin bx may show scabies mite

161
Q

Management of scabies?

A
  • Bathe + apply permethrin 5% cream from neck down to soles of feet (must be left on for 8-14h and requires second treatment 7d after first treatment)
  • Change underwear and linens – wash 2x with detergent in HOT water > machine dry
  • Mid potency topic steroids and antihistamines for symptom management
  • Treat family + close contacts
162
Q

Clinical features of lice (pediculosis)?

A
  • Intensely pruritic, red excoriations, morbilliform rash, caused by louse (a parasite)
  • Scalp lice: nits (i.e.louse eggs) on hairs; red, excoriated skin with secondary bacterial infection, lymphadenopathy
  • Pubic lice: nits on hairs; excoriations
  • Body lice: nits and lice in seams of clothing; excoriations and secondary infection mainly on shoulders, belt-line, and buttocks
163
Q

Etiology of lice (pediculosis)?

A
  • Phthirus pubis (pubic), Pediculus humanus capitis (scalp), Pediculus humanus humanus (body): attaches to body hair and feeds on the nearby body site
164
Q

Management of lice (pediculosis)?

A
  • Permethrin 1% (Nix cream rinse) (ovicidal) or permethrin 1% (RC & Cor, Kwellada-P¬shampoo)
  • Comb hair with fine – toothed comb using dilute vinegar solution to remove nits
  • Repeat in 7d after first treatment
  • Shave hair if feasible, change clothing and linens; wash with detergent in hot water cycle then machine dry
165
Q

Clinical feature of herpes simplex?

A
  • Herpetiform (i.e. grouped) vesicles on an erythematous base on skin or mucous membranes
  • Transmitted via contact with erupted vesicles or via asymptomatic viral shedding
  • Ulcer crusts over in ~4 days, forms scab (falls off), complete healing in 8-9 days.
166
Q

Features of primary herpes simplex?

A
  • Children and young adults
  • usually asymptomatic; may have high fever, regional lymphadenopathy, malaise
  • followed by antibody formation and latency of virus in dorsal nerve root ganglion
167
Q

Features of secondary herpes simplex + triggers for recurrence?

A
  • recurrent form seen in adults; much more common than primary
  • Prodrome: tingling, pruritus, pain
  • Triggers for recurrence: fever, excess sun exposure, physical trauma, menstruation, emotional stress, URTI
168
Q

Complications of herpes simplex?

A

Dendritic corneal ulcer, EM, herpes simplex encephalitis (infants at risk), HSV infection on AD causing Kaposi’s varicelliform eruption (eczema herpeticum)

169
Q

Features of HSV-1 and where do they occur?

A
  • Typically “cold sores” (grouped vesicles at the mucocutaneous junction which quickly burst)
  • Recurrent on face, lips, and hard palate, but NOT on soft, non-keratinized mucous membranes (unlike aphthous ulcers)
170
Q

Features of HSV-2 and where do they occur?

A
  • usually sexually transmitted; incubation 2-20 d
  • gingivostomatitis: entire buccal mucosa involved with erythema and edema of gingiva
  • vulvovaginitis: edematous, erythematous, extremely tender, profuse vaginal discharge
  • urethritis: watery discharge in males
  • recurrent on vulva, vagina, penis for 5-7 d
171
Q

Investigations of herpes simplex

A
  • Tzanck smear with Giemsa stain shows multinucleated giant epithelial cells
  • Viral culture, electron microscopy, and direct fluorescence antibody test of specimen taken from the base of a relatively new lesion
  • Serologic testing for antibody for current or past infection if necessary
172
Q

Management of HSV-1?

A
  • treat during prodrome to prevent vesicle formation
  • topical antiviral (Zovirax/Xerese) cream, apply 5-6x/d x 4-7 d for facial/genital lesions
  • oral antivirals (e.g. acyclovir, famciclovir, valacyclovir) are far more effective and have an easier dosing schedule than topicals
173
Q

Management of HSV-2?

A
  • rupture vesicle with sterile needle if you wish to culture it
  • wet dressing with aluminum subacetate solution, Burow’s compression, or betadine solution
  • 1st episode: acyclovir 200 mg PO 5x/d x 10 d. Maintenance: acyclovir 400 mg PO bid
  • famciclovir and valacyclovir may be substituted and have better enteric absorption and less frequent dosing
  • in case of herpes genitalis, look for and treat any other STIs
174
Q

Clinical features of herpes zoster (shingles)

A
  • Unilateral dermatomal eruption occurring 3-5d after pain and paresthesia of that dermatome
  • Vesicles, bullae, and pustules on an erythematous, edematous base
  • Lesions may be come eroded/ulcerated and last days to weeks
  • Pain can be pre-herpetic, synchronous with rash, or post-herpetic
  • Severe post-herpetic neuralgia often occurs in elderly
  • Hutchinson’s sign: shingles on the tip of the nose signifies ocular involvement - Shingles in this area involves the nasociliary branch of the ophthalmic branch of the trigeminal nerve (V1)
  • Distribution: thoracic (50%), trigeminal (10-20%), cervical (10-20%); disseminated in HIV
175
Q

Etiology + RF of herpes zoster (shingles)

A
  • Caused by reactivation of VZV

- Risk factors: immunosuppression, old age, occasionally associated with hematologic malignancy

176
Q

Investigations of herpes zoster (shingles)

A

None required, but can do Tzanck test, direct fluorescence antibody test, or viral culture to rule out HSV

177
Q

Prevention of herpes zoster (shingles)

A

Routine vaccination in 50+ yr old with Shingrix® (recombinant zoster vaccine) preferred to in 60+ yr old with Zostavax® (live zoster vaccine)

178
Q

Management of herpes zoster (shingles)

A
  • Compress with normal saline, Burow’s or betadine solution
  • Oral antivirals: famciclovir, valacyclovir, or acyclovir for 7d; must initiate within 72h to be of benefit
  • Analgesia: NSAIDs, acetaminophen for mild-moderate pain; opioids if severe
  • Post-herpetic neuralgia: TCAs, anticonvulsants (gabapentin, pregabalin)
179
Q

Clinical features of molluscum contagiosum

A
  • Discrete dome-shaped and umbilicated pearly, white papules caused by DNA Poxvirus (Molluscum contagiosum virus)
  • Common sites: eyelids, beard (likely spread by shaving), neck, axillae, trunk, perineum, buttocks
180
Q

Etiology of molluscum contagiosum

A
  • Virus is spread via direct contact, auto-inoculation, sexual contact
  • Common in children and sexually active young adults (giant molluscum and severe cases can be seen in the setting of HIV)
  • Virus is self-limited and can take 1-2 yr to resolve
181
Q

Investigations of molluscum contagiosum

A

None required, however can biopsy to confirm diagnosis

182
Q

Management of molluscum contagiosum?

A
  • Topical cantharidin (avesicant)
  • cryotherapy
  • curettage
  • topical retinoids
  • Aldara® (imiquimod): immunemodulator that produces a cytokine inflammation
183
Q

Clinical presentation of chicken pox (varicella)

A
  • Incubation period 2 weeks, mild prodome of slight fever and malaise.
  • Presentation: small blisters on an erythematous base (“dew drop on a rose petal”) appear over several days, distributed mainly on the trunk or face. Distinctive feature is the simultaneous presence of lesions in different stages of evolution.
184
Q

Treatment of chicken pox (varicella)

A

May be severe in children on systemic corticosteroid therapy / leukemia. Usually treat Sx with topical calamine lotions, examine for 2o bacterial infection. Salicylates are contraindicated (Reye’s Syndrome).

185
Q

Pathogenesis of warts?

A

Benign neoplasms caused by infection of keratinizing cell epidermal cells with the human papilloma virus (HPV) = proliferation = thickening and keratotic surface.

186
Q

Clinical features of verruca vulgaris

A
  • Hyperkeratotic, elevated discrete epithelial growths with papillated surface caused by HPV
  • Paring of surface reveals punctate, red-brown specks (thrombosed capillaries)
187
Q

Distribution of verruca vulgaris

A

Located at trauma sites: fingers, hands, knees of children and teens

188
Q

Clinical features of verruca plantaris (Plantar Warts) and verruca palmaris (Palmar Warts)?

A

Hyperkeratotic, shiny, sharply marginated growths Paring of surface reveals red-brown specks (capillaries), interruption of epidermal ridges

189
Q

Distribution of verruca plantaris (Plantar Warts) and verruca palmaris (Palmar Warts)?

A

Located at pressure sites: metatarsal heads, heels, toes

190
Q

Clinical features of verruca planae (Flat Warts)

A
  • Multiple discrete, skin coloured, flat topped papules grouped or in linear configuration
  • Common in children
191
Q

Clinical features of condyloma acuminata (Genital Warts)

A
  • Skin-coloured pinhead papules to soft cauliflower like masses in clusters
  • Can be asymptomatic, lasting months to years
  • Highly contagious, transmitted sexually and non-sexually (e.g. Koebner phenomenon via scratching, shaving), and can spread without clinically apparent lesions
192
Q

Treatment for warts

A
  • First line therapies: salicylic acid preparations (patches, solutions, creams, ointments), cryotherapy, topical cantharidin (Cantharone®)
  • Second line therapies: topical imiquimod, topical 5-fluorouracil, topical tretinoin, podophyllotoxin
  • Third line therapies: curettage, cautery, surgery for non plantar warts, CO2 laser, oral cimetidine (particularly children), intralesional bleomycin (plantar warts), trichloroacetic acid, diphencyprone
193
Q

Investigations of condyloma acuminata (Genital Warts)

A

Acetowhitening (subclinical lesions seen with 5% acetic acid x 5 min and hand lens)

194
Q

Etiology of candidiasis?

A

Candida (70-80% of infections are from Candida albicans)

195
Q

Clinical features of candidal paronychia

A

Painful red swelling of periungual skin

196
Q

Management of candidal paronychia

A

Topical agents not as effective; oral antifungals recommended

197
Q

Clinical features of candidal intertrigo

A
  • macerated/eroded erythematous patches that may be covered with papules and pustules, located in intertriginous areas often under breast, groin, or interdigitally
  • peripheral “satellite” pustules
  • starts as non-infectious maceration from heat, moisture, and friction
198
Q

Predisposing factors of candidiasis?

A

Obesity, DM, systemic antibiotics, immunosuppression, malignancy

199
Q

Management of candidiasis?

A

Keep area dry, terbinafine, ciclopirox olamine, ketoconazole/clotrimazole cream bid until rash clears

200
Q

Clinical features of vitiligo?

A

● Irregular, well-demarcated, depigmented (white) macules or patches , surrounded by normal skin

  • Unilateral or bilateral distribution, with stable or slowly progressive lesions [4]
  • Commonly on the face (e.g., perioral and periocular regions), neck, scalp, acral surfaces (e.g., hands), extensor surfaces, or genitalia
201
Q

Clinical features of vitiligo?

A
  • Irregular, well-demarcated, depigmented (white) macules or patches , surrounded by normal skin
  • Unilateral or bilateral distribution, with stable or slowly progressive lesions
  • Commonly on the face (e.g., perioral and periocular regions), neck, scalp, acral surfaces (e.g., hands), extensor surfaces, or genitalia
202
Q

Treatment of vitiligo?

A
  1. General measures
    - Sunscreen (to prevent burns)
    - Concealing makeup for cosmetic reasons
  2. Limited disease
    - Topical steroids (betamethasone, mometasone, etc.)
    - Alternative : topical calcineurin inhibitors (tacrolimus, pimecrolimus)
  3. Progressive or refractory disease
    - Oral steroids
    - Narrowband ultraviolet B phototherapy
    - PUVA phototherapy
203
Q

Clinical features of ichthyosis vulgaris?

A

o Generalized fine, white scaling
o Dry and coarse skin (xerosis): more common on extensor surfaces (skin folds are usually not affected)
o Hyperlinearity of palms and soles (accentuated skin lines)
o Symptoms generally worsen in winter and improve in summer

204
Q

Clinical features of ichthyosis vulgaris?

A
  • Generalized fine, white scaling
  • Dry and coarse skin (xerosis): more common on extensor surfaces (skin folds are usually not affected)
  • Hyperlinearity of palms and soles (accentuated skin lines)
  • Symptoms generally worsen in winter and improve in summer
205
Q

Management of ichthyosis vulgaris?

A

Immersion in bath and oils followed by an emollient cream, humectant cream, or creams/oil containing urea or alpha or beta-hydroxy acids

206
Q

Management of ichthyosis vulgaris?

A

Immersion in bath and oils followed by an emollient cream, humectant cream, or creams/oil containing urea or alpha or beta-hydroxy acids

207
Q

Diagnostic criteria for neurocutaneous syndromes?

A

Diagnostic criteria includes 2 or more of the following:

  1. more than 5 café-au-lait patches >1.5 cm in an adult or more than 5 café-au-lait macules >0.5 cm in a child <5yr
  2. axillary or inguinal freckling
  3. iris hamartomas (Lisch nodules)
  4. optic gliomas
  5. neurofibromas
  6. distinctive bony lesion (sphenoid wing dysplasia or thinning of long bone cortex)
  7. first degree relative with neurofibromatosis Type 1
208
Q

Pathophysiology of neurocutaneous syndromes?

A

Autosomal dominant disorder with excessive and abnormal proliferation of neural crest elements (Schwann cells, melanocytes), high incidence of spontaneous mutation

209
Q

Investigations for neurocutaneous syndromes?

A

Wood’s lamp to detect cafe-au-lait macules in patients with pale skin

210
Q

Management of neurocutaneous syndromes

A
  • Refer to orthopedics, ophthalmology, plastics, and psychology
  • Follow up annually for brain tumours (e.g. astrocytoma)
  • Excise suspicious or painful lesions
211
Q

Definition of lentigo maligna

A

Precancerous lesion with intraepithelial proliferation of dysplastic melanocytes

212
Q

Etiology of lentigo maligna

A

Exposure to UV light

213
Q

Lesion features of lentigo maligna

A
  • Mostly found in areas exposed to sun (e.g., face, neck)
  • Darkly pigmented macule
  • Irregular borders and varying size
  • Gradual growth, color irregularities, surrounding “island-like” speckling
214
Q

Treatment of lentigo maligna

A

Surgical excision with a safety margin

215
Q

Definition of actinic keratosis

A

UV-induced precancerous skin lesion that may progress to skin cancer.

216
Q

Etiology of actinic keratosis

A

Sun exposure (e.g., from working outdoors)

217
Q

Lesion features of actinic keratosis

A
  • Sites: areas of sun exposure (face, ears, scalp if bald, neck, sun-exposed limbs)
  • Initially: small lesion (papule or plaque) with rough surface (sandpaper-like texture)
  • Later: Lesions grow and become brown or erythematous and scaly.
218
Q

Pathophysiology and RF of actinic keratosis

A
  • UV radiation damage to keratinocytes from repeated sun exposure (especially UVB)
  • Risk of transformation of AK to SCC (~1/1000), but higher likelihood if AK is persistent UV-induced p53 gene mutation
  • Risk factors: increased age, light skin/eyes/hair, immunosuppression, syndromes such as albinism or xeroderma pigmenotsum
  • Risk factors for malignancy: immunosuppression, history of skin cancer, persistence of the AK
219
Q

What is actinic cheilitis

A

Actinic keratosis on the lower lip

220
Q

What is a cutaneous horn

A
  • Benign growth composed of keratin that resembles a horn
  • May develop from preexisting actinic and seborrheic keratoses or warts
  • Can progress to squamous cell carcinoma (SCC)
  • Treatment of choice is surgical excision with a margin.
221
Q

Management of actinic keratosis

A
  1. Destructive: cryotherapy, electrodessication, and curettage
  2. Topical pharmacotherapy (mechanism: destruction of rapidly growing cells or immune system modulation)
    - topical 5-fluorouracil cream (for 2-4 wk), imiquimod 5% (2x/wk for 16 wk), imiquimod 3.75% (daily for 2 wk then none for 2 wk then daily for 2 wk), ingenol Mmbutate gel 0.015% (daily for 3 d on the head and neck), ingenol mebutate 0.05% gel (daily for 2 d on the body)
  3. Photodynamic therapy
  4. Excision
222
Q

Clinical features of leukoplakia

A

● A morphologic term describing homogeneous or speckled white plaques with sharply demarcated borders
● Sites: oropharynx, most often floor of the mouth, soft palate, and ventral/lateral surfaces of the tongue

223
Q

Clinical features of leukoplakia

A
  • A morphologic term describing homogeneous or speckled white plaques with sharply demarcated borders
  • Sites: oropharynx, most often floor of the mouth, soft palate, and ventral/lateral surfaces of the tongue
224
Q

Pathophysiology of leukoplakia

A
  • Precancerous or premalignant condition

- Oral form is strongly associated with tobacco use and alcohol consumption

225
Q

Investigations for leukoplakia

A

Biopsy is mandatory due to risk of malignancy

226
Q

Management of leukoplakia

A
  • Low risk sites on buccal/labial mucosal or hard palate: eliminate carcinogenic habits, smoking cessation, follow-up
  • Moderate/dysplastic lesions: excision, cryotherapy
227
Q

Clinical features of noduloulcerative (typical) BCC?

A

Skin-coloured papule/nodule with rolled, translucent (“pearly”) telangiectatic border, and depressed/eroded/ulcerated centre

228
Q

Clinical features of pigmented variant BCC?

A
  • Flecks of pigment in translucent lesion with surface telangiectasia
  • May mimic malignant melanoma
229
Q

Clinical features of superficial variant BCC?

A
  • Flat, tan to red-brown plaque, often with scaly, pearly border, and fine telangiectasia at margin
  • Least aggressive subtype
230
Q

Clinical features of sclerosing (morpheaform) variant BCC?

A
  • Flesh/yellowish-coloured, shiny papule/plaque with indistinct borders, indurated
231
Q

Pathophysiology of basal cell carcinoma?

A

● Malignant proliferation of basal keratinocytes of the epidermis - low grade cutaneous malignancy, locally aggressive (primarily tangential growth), rarely metastatic

232
Q

Pathophysiology of basal cell carcinoma?

A

Malignant proliferation of basal keratinocytes of the epidermis - low grade cutaneous malignancy, locally aggressive (primarily tangential growth), rarely metastatic

233
Q

Etiology of basal cell carcinoma?

A
  1. Sun exposure
  2. Genetic predisposition
    - Skin types I and II (people with light complexions, red hair, and who sunburn easily)
    - Albinism
    - Xeroderma pigmentosum
  3. Nevoid basal-cell carcinoma syndrome (Gorlin syndrome)
  4. Chemicals: arsenic, polycyclic aromatic hydrocarbons (e.g., tars)
234
Q

Diagnosis of basal cell carcinoma?

A

full-thickness biopsy done at the edge of the lesion

235
Q

Diagnosis of basal cell carcinoma?

A

Full-thickness biopsy done at the edge of the lesion

236
Q

Management of basal cell carcinoma?

A
  • Imiquimod 5% cream (Aldara) or cryotherapy is indicated for superficial BCCs on the trunk
  • 5-fluorouracil and photodynamic therapy can also be used for superficial BCCs
  • Shave excision and electrodessication and curettage for most types of BCCs, not including morpheaform
  • Mohs surgery
  • Radiotherapy used in advanced cases of BCC
237
Q

Define squamous cell carcinoma (SCC)

A

Malignant transformation of keratinocytes in the stratum spinosum (prickle cell layer) of the epidermis

238
Q

Clinical features of squamous cell carcinoma (SCC)

A
  • Hyperkeratotic indurated, pink/red/skin-coloured papule/plaque/nodule with surface scale/crust ¬ ± ulceration
  • More rapid enlargement than BCC + BCC does not metastazie to LN
  • Location: face, ears, scalp, forearms, dorsum of hands
239
Q

Risk factors for squamous cell carcinoma (SCC)

A
  • UV exposure (especially among light-skinned individuals): most significant risk factor
  • Exposure to ionizing radiation
  • Exposure to chemical carcinogens (e.g., coal tars through smoking, arsenic)
  • Areas of chronically damaged skin, nonhealing wounds (Marjolin ulcer)
  • Chronic immunosuppression (e.g., HIV, transplant patients who receive immunosuppressive therapy)
  • Precancerous skin lesions (especially actinic keratosis and Bowen disease)
240
Q

Management for squamous cell carcinoma (SCC)

A
  • Surgical excision with primary closure, skin flaps or grafting
  • Mohs surgery
  • Lifelong follow-up (more aggressive treatment than BCC)
  • Radiation therapy
241
Q

Classic presentation of squamous cell carcinoma (SCC)

A

The classic clinical presentation of cSCC is a painless, nonhealing, bleeding ulcer.

242
Q

Clinical features of keratoacanthoma

A
  • Rapidly growing, firm, dome-shaped, erythematous or skin-coloured nodule with central keratin-filled crater, resembling an erupting volcano
  • May spontaneously regress within a year, leaving a scar
  • Sites: sun-exposed skin
243
Q

Pathophysiology of keratoacanthoma

A
  • Epithelial neoplasm with atypical keratinocytes in epidermis
  • Low grade variant of SCC
244
Q

Etiology of keratoacanthoma

A

HPV, UV radiation, chemical carcinogens (tar, mineral oil)

245
Q

Management of keratoacanthoma

A
  • Surgical excision or saucerization (shave biopsy) followed by electrodesiccation of the base, treated similarly to SCC
  • Intralesional methotrexate injection
246
Q

What is malignant melanoma?

A

Cancer arising from melanocytes, usually skin. It can arise from a pre-existing nevus, or idiopathic.

247
Q

Risk factors for malignant melanoma

A
  • UV radiation exposure
  • Light skin
  • Dysplastic nevi , giant congenital nevi, or inherited skin conditions (e.g., dysplastic nevus syndrome, familial atypical mole, melanoma syndrome, xeroderma pigmentosa)
  • Immunosuppression
  • Genetics
    o BRAF gene mutations; V600E is the most common mutation
    o CDKN2A gene mutations
248
Q

Clinical features for malignant melanoma

A
  • Pruritic, persistently bleeding skin lesion

- ABCDE3 signs: (=ABCDE-cubed!)

249
Q

What are the ABCDE3 signs for malignancy?

A
  • Asymmetry: one half of the lesion does not resemble the other half.
  • Border: border is not regular. It may be scalloped in outline.
  • Color: color of the lesion is not uniform. There may be light brown, dark brown, black colors in same lesion.
  • Diameter: longest axis of the lesion is greater than 5 mm.
  • Evolving: lesion has been changing in shaped, color, etc.
  • Elevated: lesion is raised and feels ‘thicker’.
  • Eroded: surface of the lesion is eroded or ulcerated—it may bleed at times.
250
Q

Diagnosis for malignant melanoma

A

A full-thickness excisional biopsy (best diagnostic test) with 1–3 mm margins is indicated in all suspicious lesions?

251
Q

Treatment for malignant melanoma

A
  • Surgical excision: full-thickness excision with appropriate safety margins
  • 0.5-1 cm safety margin: melanoma in situ
  • Other margins according to Breslow depth: thickness from the granular layer to the lowest detectable tumor cell.
  • If > 1mm on microscopic, and ^risk for mets, sentinel LN biopsy can be used for regional LN met detection.
252
Q

DDx for hair loss

A

TOPHAT

  • 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, SSRls
253
Q

Define non-scarring alopecia?

A

Hair follicle is not permanently damaged, and therefore spontaneous or treatment-induced regrowth is possible

254
Q

Clinical features of androgenetic alopecia

A

o Male- or female-pattern alopecia
o Males: fronto-temporal areas progressing to vertex, entire scalp may be bald
o Females: widening of central part, “Christmas tree” pattern

255
Q

Clinical features of androgenetic alopecia

A
  • Male- or female-pattern alopecia
  • Males: fronto-temporal areas progressing to vertex, entire scalp may be bald
  • Females: widening of central part, “Christmas tree” pattern
256
Q

Pathophysiology of androgenetic alopecia

A
  • Action of dihydrotestosterone (DHT) on hair follicles

- Common genetically determined form of progressive

257
Q

Management of androgenetic alopecia

A
  • Minoxidil (Rogaine) solution or foam to reduce rate of loss/partial restoration
  • Females: spironolactone (anti-androgenic effects), cyproterone acetate (Diane-35®)
  • Males: finasteride (Propecia®) (5-α-reductase inhibitor) 1mg/d
  • Hair transplant
258
Q

When does telogen effluvium occur?

A

Occurs 3-5 mos after pathologic or normal physiologic change in health status;

259
Q

Clinical features of telogen effluvium

A

Uniform decrease in hair density secondary to hairs leaving the growth (anagen) stage and entering the resting (telogen) stage of the cycle

260
Q

Pathophysiology of telogen effluvium

A
  • Variety of precipitating factors (i.e. post-partum, psychological stress, major illness)
  • Hair loss typically occurs 2-4 mo after exposure to precipitant
  • Regrowth occurs within a few months but may not be complete
261
Q

Clinical features of anagen effluvium?

A

Hair loss due to insult of hair follicle impairing its mitotic activity (growth stage)

262
Q

Pathophysiology of anagen effluvium?

A
  • Precipitated by chemotherapeutic agents (most common), other meds (bismuth, levodopa, colchicine, cyclosporine), exposure to chemicals (thallium, boron, arsenic)
  • Dose-dependent effect
  • Hair loss 7-14d after single pulse of chemotherapy; most clinically apparent after 1-2mo
  • Reversible effect; follicles resume normal mitotic activity few weeks after agent stopped
263
Q

Clinical features of alopecia areata?

A
  • May be associated with dystrophic nail changes – fine stippling, pitting
  • “exclamation mark” pattern (hairs fractured and have tapered shafts, i.e. looks like “!”)
  • May be associated with pernicious anemia, vitiligo, thyroid disease, Addison’s disease
  • Spontaneous regrowth may occur within months of first attack
  • Frequent recurrence often precipitated by emotional distress
264
Q

What is alopecia areata

A

Autoimmune disorder characterized by patches of complete hair loss often localized to scalp, but can affect eyebrows, beard, eyelashes, etc.

265
Q

What is alopecia totalis

A

Complete loss of hair on scalp

266
Q

What is alopecia universalis

A

Complete loss of scalp hair, eyelashes, eyebrows, and body hair

267
Q

Management of alopecia areata

A
  • Topical corticosteroids and intralesional triamcinolone acetonide (corticosteroids) can be used for isolated patches
  • Systemic immunosuppressants for refractory or extensive disease
  • Immunomodulatory (diphencyprone, anthralin)
268
Q

Clinical features of scarring alopecia

A

Irreversible loss of hair follicles with fibrosis

269
Q

Etiology of scarring alopecia

A

● Physical: radiation, burns
● Infections: fungal, bacterial, TB, leprosy, viral (HSV)
● Primary inflammatory - subdivided into lymphocytic, neutrophilic, and mixed
● Morphea: “coup de sabre” with involvement of centre of scalp

270
Q

Etiology of scarring alopecia

A
  • Physical: radiation, burns
  • Infections: fungal, bacterial, TB, leprosy, viral (HSV)
  • Primary inflammatory - subdivided into lymphocytic, neutrophilic, and mixed
  • Morphea: “coup de sabre” with involvement of centre of scalp
271
Q

Causes of lymphocytic scarring alopecia

A
  • Lichen planus (lichen planopilaris) - white scale around hair follicles, up to 50% have lichen planus at other body sites
  • DLE (note that SLE can cause an alopecia unrelated to DLE lesions which are non-scarring)
  • Central centrifugal cicatricial alopecia (CCCA): seen in up to 40% of black women, starting at central scalp; one of most commonly diagnosed scarring alopecias, may be associated with hair care practices in this population
272
Q

Causes of neutrophilic scarring alopecia

A
  • Folliculitis decalvans – discharge of pus and blood, tufting of hair follicles
  • Dissecting cellulitis of the scalp – follicular papules, pustutles, nodules, and abscesses develop on the scalp
273
Q

Causes of mixed scarring alopecia

A
  • Acne keloidalis nuchae – Dome-shaped papules, pustules, and plaques on the occipital scalp
274
Q

Management of scarring alopecia

A
  • Infections: treat underlying infection

- Inflammatory: topical/intralesional steroids, anti-inflammatory antibiotics, antimalarials

275
Q

Etiology for clubbing

A

Cyanotic heart disease, bacterial endocarditis, pulmonary disorders, GI disorders

276
Q

Define nail clubbing

A

Proximal nail plate has greater than 180° angle to nail fold, watch-glass nails, bulbous digits

277
Q

Define koilonychia

A

Spoon shaped nails

278
Q

Etiology of koilonychia

A

Fe deficiency, malnutrition, DM

279
Q

What is erythema nodosum

A

o Erythema nodosum (EN) is an inflammation of subcutaneous fat caused by a delayed hypersensitivity reaction.

280
Q

What is erythema nodosum

A

Erythema nodosum (EN) is an inflammation of subcutaneous fat caused by a delayed hypersensitivity reaction.

281
Q

Etiology of erythema nodosum

A
  • Idiopathic (most common)
  • Infection (e.g. streptococcal pharyngitis, histoplasmosis, coccidioidomycosis, TB, leprosy)
  • Autoimmune diseases (e.g. sarcoidosis, Crohn disease, ulcerative colitis, Behcet syndrome)
  • Drugs (oral contraceptives, sulfonamides, iodide)
  • Pregnancy
  • Malignancy
282
Q

Clinical features of erythema nodosum

A
  • Nonspecific symptoms: fever, arthralgia , malaise, hilar lymphadenopathy
  • Painful, subcutaneous nodules on both pretibial (anterior leg) surfaces (less common on other areas of skin)
    ● Firm, erythematous (1st week)
    ● Fluctuant (without suppuration) and bluish (2nd week)
    ● Progressively fades (i.e., yellow or brown hue)
283
Q

Treatment of erythema nodosum

A
  • Symptomatic treatment - Bed rest, Leg elevation, Heat or cool compresses, NSAIDS (e.g., ibuprofen), Potassium iodide
  • Treat underlying disease
284
Q

Etiology of erythema multiforme

A
  • Infections (most common): herpes simplex virus (HSV), Mycoplasma pneumoniae, and fungal infections
  • Drugs: e.g., barbiturates, phenytoin, NSAIDs, beta-lactam antibiotics (e.g., penicillins), and sulfonamides
  • Immunizations (rare): e.g., after diphtheria, tetanus, influenza, hepatitis B vaccination
285
Q

Rash characteristics of erythema multiforme

A
  • Acute onset, with progression from erythematous macules to papules and vesicles to target lesions
  • Target lesions
    o Characteristic of EM, appear a few days after the onset of rash, may be absent in some patients
    o Target lesions have 3 zones: an inner dark red/brown zone, surrounded by a pale zone, and an outer erythematous ring
    o Epithelial necrosis is present in the inner zone
  • May be asymptomatic or cause pruritus and painful burning
  • Nikolsky sign is negative
286
Q

Distribution of erythema multiforme

A
  • Symmetrical distribution
  • Affects backs of hands and feet first - spreads proximally and can affect the entire body, including palms and soles
  • Mucous membrane involvement
287
Q

Treatment of erythema multiforme

A
  • In most cases of EM, no treatment is necessary because the condition is self-limiting.
  • General: stop the offending drug or treat the underlying infection
  • Mild cases: symptomatic treatment
  • Analgesics, NSAIDs
  • Antihistamines (for pruritus)
  • Topical steroids and saline (gargling) solutions
  • Topical lubricants (for eye involvement)
288
Q

Clinical presentation of venous insufficiency ulcers?

A

Most common in women, obesity and old age. See stasis dermatitis, then after minor trauma to the skin, located in the medial malleolus, and less often the lateral malleolus. Can become large if untreated

289
Q

Treatment of venous insufficiency ulcers?

A

Stasis can be treated with topical CS, leg elevation, and compression stockings to decrease edema. Before compression stockings, must do U/S to measure ABI; compares arterial systemic pressure of the brachial and ankle arteries. If ankle arterial supply is abnormal then no compression stockings.

290
Q

Clinical presentation of arterial insufficiency ulcers?

A

Ischemia may include hair loss on the feet, and pulses diminished or absent. Cold feet/toe skin.

291
Q

Clinical presentation of neuropathic leg ulcers?

A

Neuropathic sx like numbness, pain, decreased sensation of leg and feet. Decreased sensation = pt not aware of trauma to feet, which may have preced ulcers – occur on soles, toes, and heels.

292
Q

Two types of angioedema?

A

o Histamine-mediated angioedema
▪ Clinical features: immediate onset, laryngeal edema, bronchospasm, urticaria, hypotension
▪ Causes:
● IgE-mediated: Food allergens, Drugs (e.g., NSAIDs and antibiotics), Stinging insects, Latex
● Direct mast cell activation (Non-IgE mediated):
o Drugs (NSAIDs, Opiates, Radiocontrast agents)
o Physical: Exercise, Temperature
▪ Vibration
▪ UV radiation
o Bradykinin-mediated angioedema
▪ Clinical features: GI symptoms, laryngeal edema, extremity or truncal edema, NOT ASSOCIATED with urticaria
▪ Hereditary angioedema
● Onset in childhood <20; 80% have positive family history
● Triggers: Estrogen fluctuation, Infection, Mental, Physical
▪ Acquired angioedema
● Acquired C1 inhibitor deficiency
● ACEi induced

293
Q

Two types of angioedema?

A
  • Histamine-mediated angioedema

- Bradykinin-mediated angioedema

294
Q

Causes of histamine-mediated angioedema

A
  1. IgE-mediated: Food allergens, Drugs (e.g., NSAIDs and antibiotics), Stinging insects, Latex
  2. Direct mast cell activation (Non-IgE mediated):
    - Drugs (NSAIDs, Opiates, Radiocontrast agents)
    - Physical: Exercise, Temperature
  3. Vibration
  4. UV radiation
295
Q

Clinical features of bradykinin-mediated angioedema

A

GI symptoms, laryngeal edema, extremity or truncal edema, NOT ASSOCIATED with urticaria

296
Q

Treatment of angioedema?

A

▪ IM epinephrine - oor response consider bradykinin-mediated angioedema
▪ Histamine-mediated angioedema: IV antihistamines, IV glucocorticoids
▪ Bradykinin-mediated: Purified C1-INH concentrate (protein replacement)

297
Q

Treatment of angioedema?

A
  • IM epinephrine - oor response consider bradykinin-mediated angioedema
  • Histamine-mediated angioedema: IV antihistamines, IV glucocorticoids
  • Bradykinin-mediated: Purified C1-INH concentrate (protein replacement)
298
Q

When would the onset be for hereditary angioedema

A

Onset in childhood <20; 80% have positive family history

299
Q

Triggers for hereditary angioedema

A

Triggers: Estrogen fluctuation, Infection, Mental, Physical

300
Q

Causes of acquired angioedema

A
  • Acquired C1 inhibitor deficiency

- ACEi induced

301
Q

Clinical features of urticaria (Hives)?

A
  • Transient, red, pruritic well-demarcated wheals

- Each individual lesion lasts less than 24h

302
Q

Ddx of urticaria (Hives)?

A

DAM HIVES

  • Drugs and foods
  • Allergic
  • Malignancy
  • Hereditary
  • Infection
  • Vasculitis
  • Emotions
  • Stings
303
Q

Types of of urticaria (Hives)?

A
  1. Acute urticaria:
    - Attacks last <6 wk
    - No immediate investigations needed; consider referral for allergy testing
  2. Chronic urticaria:
    - Attacks last > 6wks
    - Further investigations required: CBC and differential, urinalysis, ESR, TSH, LFTs to help identify underlying cause
  3. Urticarial Vasculitis
    - Individual lesions last >24 h, often painful, less likely pruritic, heals with bruise type lesions
    - Requires biopsy
304
Q

Types of of urticaria (Hives)?

A
  1. Acute urticaria:
    - Attacks last <6 wk
    - No immediate investigations needed; consider referral for allergy testing
  2. Chronic urticaria:
    - Attacks last > 6wks
    - Further investigations required: CBC and differential, urinalysis, ESR, TSH, LFTs to help identify underlying cause
  3. Urticarial Vasculitis
    - Individual lesions last >24 h, often painful, less likely pruritic, heals with bruise type lesions
    - Requires biopsy

LMCC (23 decks)

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