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Dermatology > Vesiculobullous Diseases > Flashcards

Vesiculobullous Diseases Flashcards

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1
Q

Bullous pemphigoid clinical presentation

A
  • chronic autoimmune bullous eruption characterized by pruritic, tense, subepidermal bullae on an erythematous or normal skin base
  • can present as urticarial plaques without bullae
  • common sites: flexor aspect of forearms, axillae, medial thighs, groin, abdomen, mouth in 33%
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2
Q

Bullous pemphigoid pathophysiology

A

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

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3
Q

Bullous pemphigoid epi

A

• mean age of onset: 60-80 yr old, F=M

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4
Q

Bullous pemphigoid invesigations

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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5
Q

Bullous pemphigoid prognosis

A

heals without scarring, usually chronic

rarely fatal

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6
Q

Bullous pemphigoid management

A
  • prednisone 0.5-1 mg/kg/day until clear, then taper ± steroid-sparing agents (e.g. immunosuppressants such as 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
  • IVIg and plasmapheresis for refractory cases
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7
Q

Pemphigus vulgaris clinical presentation

A
  • autoimmune blistering disease characterized by flaccid non-pruritic intraepidermal bullae/vesicles on an erythematous or normal skin base
  • 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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8
Q

Pathophysiology pemphigus vulgaris

A

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

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9
Q

Pemphigus vulgaris epidemiology

A
  • 40-60 yr old, M=F, higher prevalence in Jewish, Mediterranean, Asian populations
  • paraneoplastic pemphigus may be associated with thymoma, myasthenia gravis, malignancy, and use of D-penicillamine
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10
Q

Pemphigus vulgaris investigations

A
  • immunofluorescence: shows IgG and C3 deposition intraepidermally
  • circulatng serum anti-desmoglein IgG antibodies
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11
Q

Pemphigus vulgaris prognosis

A
  • lesions heal with hyperpigmentation but do not scar

* may be fatal unless treated with immunosuppressive agents

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12
Q

Pemphigus vulgaris management

A

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

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13
Q

Pemphigus vulgaris vs Bullous pemphigoid

A

VulgariS = Superficial, intraepidermal, flaccid lesions

PemphigoiD = Deeper, tense lesions at the dermal-epidermal junction

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14
Q

Pemphigus Foliaceus description, pathophysiology and treatment

A

An autoimmune intraepidermal blistering disease that is more superficial than pemphigus vulgaris due to antibodies against desmoglein-1, a transmembrane adhesion molecule.

Appears as crusted patches, erosions and/or flaccid bullae that usually start on the trunk.

Localized disease can be managed with topical steroids. Active widespread disease is treated like pemphigus vulgaris

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15
Q

Dermatitis herpetiformis clinical presenntation

A
  • grouped papules/vesicles/urticarial wheals on an erythematous base, associated with intense pruritus, burning, stinging, excoriations
  • lesions grouped, bilaterally symmetrical
  • common sites: extensor surfaces of elbows/knees, sacrum buttocks, scalp
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16
Q

Dermatitis herpetiformis pathophysiology

A
  • transglutaminase IgA deposits in the skin alone or in immune complexes leading to eosinophil and neutrophil infiltration
  • 90% have HLA B8, DR3, DQWZ
  • 90-100% associated with an often subclinical gluten-sensitive enteropathy (i.e. celiac disease)
  • 30% have thyroid disease; increased risk of intestinal lymphoma in untreated comorbid celiac disease; iron/folate deficiency is common
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17
Q

Dermatitis herpetiformis epidemiology

A

20-60 year old

M:F = 2:1

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18
Q

Dermatitis herpetiformis investigations

A

biopsy

immunofluorescencce shows IgA depots in perilesional skin

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19
Q

Dermatitis herpetiformis management

A
  • dapsone (sulfapyridine if contraindicated or poorly tolerated)
  • gluten free diet for life – this can reduce risk of lymphoma
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20
Q

Porphyria Cutanea Tarda clinical presentation

A
  • skin fragility followed by formation of tense vesicles/bullae and erosions on photoexposed 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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21
Q

Porphyria Cutanea Tarda Pathophysiology

A
  • uroporphyrinogen decarboxylase deficiency leads to excess heme precursors
  • can be associated with hemochromatosis, alcohol abuse, DM, drugs (estrogen therapy, NSAIDs), HIV, hepatitis C, increased iron indices
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22
Q

Porphyria cutanea tarda epidemiology

A

• 30-40 yr old, M>F

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23
Q

Porphyria Cutanea Tarda investigations

A
  • urine + 5% HCl shows orange-red fluorescence under Woods lamp (UV rays)
  • 24 h urine for uroporphyrins (elevated)
  • stool contains elevated coproporphyrins
  • immunofluorescence shows IgE at dermal-epidermal junctions
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24
Q

Porphyria Cutanea Tarda management

A

discontinue aggravating substances (alcohol, estrogen therapy)

  • phlebotomy to decrease body iron load
  • low dose hydroxychloroquine
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25
Q

Exanthematous drug reaction clinical presentation

A
  • morphology: erythematous macules and papules ± scale
  • spread: symmetrical, trunk to extremities
  • time course: 7-14 d after drug initiation, fades 7-14 d after withdrawal
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26
Q

Exanthematous drug reaction epidemiology

A

most common cutaneous drug reaction; increased in presence of infections

common causative agents: penicillin, sulfonamides, phenytoin

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27
Q

Exanthematous drug reaction management

A

weight risks and benefits of drug discontinuation

antihistamins, emollients, topical steroids

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28
Q

Drug induced hypersensitivity syndrome (DIHS)/Drug reaction with eosinophilia and systemic symptoms (DRESS) clinical presentation

A
  • morphology: morbilliform rash involving face, trunk arms; can have facial edema
  • systemic features: fever, malaise, cervical lymphadenopathy, internal organ involvement (e.g. hepatitis, arthralgia, nephritis, pneumonitis, lymphadenopathy, hematologic abnormalities, thyroid abnormalities)
  • spread: starts with face or periorbitally and spreads caudally; no mucosal involvement
  • time course: onset 1-6 weeks after first exposure to drug; persists weeks after withdrawal of drug
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29
Q

Drug induced hypersensitivity syndrome (DIHS)/Drug reaction with eosinophilia and systemic symptoms (DRESS) epidemiology

A
  • rare: incidence varies considerably depending on drug
  • common causative agents: aniconvulsants (e.g. phenytoin, phenobarbital, carbamazepine, lamotrigine), sulfonamides, and allopurinol
  • 10% mortality if severe, undiagnosed, and untreated
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30
Q

Drug induced hypersensitivity syndrome (DIHS)/Drug reaction with eosinophilia and systemic symptoms (DRESS) management

A
  • discontinue offending drug ± prednisone 0.5mg/kg per day, consider cyclosporine in severe cases
  • may progress to generalized exfoliative dermatitis/erythroderma if drug is not discontinued
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31
Q

Diagnosis of a drug reaction

A

Classification by Naranjo et. al has 4 criteria:

  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

Definite drug reaction requires all 4 criteria to be met

Probable drug reaction requires #1-3 to be met

Possible drug reaction requires only #1

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32
Q

Drug hypersensitivity syndrome triad

A

Fever

exanthematous eruption

internal organ involvement

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33
Q

Drug induced urticaria and angioedema clinical presentation

A

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

  • systemic features: may be associated with systemic anaphylaxis (bronchospasm, laryngeal edema, shock)
  • time course: hours to days after exposure depending on the mechanism
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34
Q

Drug induced urticaria and angioedema epidemiology

A
  • second most common cutaneous drug reaction

* common causative agents: penicillins, ACEI, analgesics/anti-inflammatories radiographic contrast media

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35
Q

Drug induced urticaria and angioedema management

A

• discontinue offending drug, treatment with antihistamines, steroids, epinephrine if anaphylactic

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36
Q

Serum sickness like reaction clinical presentation

A
  • morphology: symmetrical cutaneous eruption (usually urticarial)
  • systemic features: malaise, low grade fever, arthralgia, lymphadenopathy
  • time course: appears 1-3 wk after drug initiation, resolve 2-3 wk after withdrawal
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37
Q

Serum sickness like reaction epidemiology

A
  • more prevalent in kids 0.02-0.2%

* common causative agents: cefaclor in kids; bupropion in adults

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38
Q

Serum sickness like reaction management

A

• discontinue offending drug ± topical/oral corticosteroids

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39
Q

Acute generalized exanthematous pustulosis (AGEP) clinical presentation

A
  • morphology: erythematous edema and sterile pustules prominent in intertriginous areas
  • systemic features: high fever, leukocytosis with neutrophilia
  • spread: starts in face and intertriginous areas and spread to trunk and extremities
  • time course: appears 1 wk after drug initiation, resolve 2 wk after withdrawal
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40
Q

Acute generalized exanthematous pustulosis (AGEP) epidemiology

A
  • rare: 1-5/million

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

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41
Q

Acute generalized exanthematous pustulosis (AGEP) management

A

Discontinue offending drug and systemic corticosteroids

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42
Q

Steven Johnson Syndrome (SJS)/Toxic epidermal necrolysis (TEN) clinical presentation

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

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

  • spread: face and extremities; may generalize; scalp, palms, soles relatively spared; erosion of mucous membranes (lips, oral mucosa, conjunctiva, GU mucosa)
  • systemic features: fever (higher in TEN), cytopenias, renal tubular necrosis/AKI, tracheal erosion, infection, contractures, corneal scarring, phimosis, vaginal synechiae
  • time course: appears 1-3 wk after drug initiation; progression <4 d; epidermal regrowth in 3 wk
  • can have constitutional symptoms: malaise, fever, hypotension, tachycardia
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43
Q

Steven Johnson Syndrome (SJS)/Toxic epidermal necrolysis (TEN) epidemiology

A
  • SJS: 1.2-6/million; TEN: 0.4-1.2/million
  • risk factors SLE, HIV/AIDS, HLA-B1502 (associated with carbamazepine), HLA-B5801 (associated with allopurinol)
  • common causative agents: drugs (allopurinol, anti-epileptics, sulfonamides, NSAIDs, cephalosporins) responsible in 50% of SJS and 80% of TEN; viral or mycoplasma infections
  • prognosis: 5% mortality in SJS, 30% in TEN due to fluid loss and infection
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44
Q

Steven Johnson Syndrome (SJS)/Toxic epidermal necrolysis (TEN) differential diagnosis

A

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

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45
Q

Steven Johnson Syndrome (SJS)/Toxic epidermal necrolysis (TEN) management

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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46
Q

SCORTEN Score for TEN PROGNOSIS

A 
One point for each of: 
age ≥40
malignanc
body surface area detached ≥10%
tachycardia ≥120 bpm
serum urea >10 mmol/L
serum glucose >14 mmol/L
serum bicarbonate <20 mmol/L

Used to determine appropriate clinical setting:

score 0-1 can be treated in non-specialized wards

score ≥2 should be transferred to intensive care or burn unit

Score at admission is predictive of survival:
94% for 0-1, 
87% for 2, 
53% for 3, 
25% for 4, and 
17% for ≥5
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47
Q

Effect of IVIG IV at dosages over 2+ g/kg for SJS or TEN

A

Significantly decreased mortality in patients with SJS or TEN

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48
Q

Fixed drug eruption clinical presentation

A
  • morphology: sharply demarcated erythematous oval patches on the skin or mucous membranes
  • spread: commonly face, mucosa, genitalia, acral; recurs in same location upon subsequent exposure to the drug (fixed location)
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49
Q

Fixed drug eruption epidemiology

A

• common causative agents: antimicrobials (tetracycline, sulfonamides), anti-inflammatories, psychoactive agents (barbiturates), phenolphthalein

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50
Q

Fixed drug eruption management

A

• discontinue offending drug ± prednisone 1mg/kg/d x 2 wk for generalized lesions ± potent topical corticosteroids for non-eroded lesions or antimicrobial ointment for eroded lesions

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51
Q

Photosensitivity reaction clinical presentation

A
  • phototoxic reaction: “exaggerated sunburn” (erythema, edema, vesicles, bullae) confined to sun-exposed areas
  • photoallergic reaction: pruritic eczematous eruption with papules, vesicles, scaling, and crusting that may spread to areas not exposed to light
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52
Q

Photosensitivity reaction pathophysiology

A
  • phototoxic reaction: direct tissue injury

* photoallergic reaction: type IV delayed hypersensitiviy

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53
Q

Photosensitivity reaction epidemiology

A

common causative agents: chlorpromazine, doxycycline, thiazide diuretics, procainamide

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54
Q

Photosensitivity reaction management

A

sun protection +/- topical/oral corticosteroids

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55
Q

Ichthyosis vulgaris clinical presentation

A
  • xerosis with fine scaling as well as large adherent scales (“fish-scales”)
  • affects arms, legs, palms, soles, back, forehead, and cheeks; spares flexural creases
  • improves in summer, with humidity, and as the child grows into adulthood
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56
Q

Ichthyosis vulgaris pathophysiology

A
  • genetic deficiency in filaggrin protein leads to abnormal retention of keratinocytes (hyperkeratosis)
  • scaling without inflammation
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57
Q

Ichthyosis vulgaris epidemiology

A
  • 1:300 incidence
  • autosomal dominant inheritance
  • associated with AD and keratosis pilaris
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58
Q

Ichthyosis vulgaris investigations

A

electron microscopy keratohyalin granules

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59
Q

Ichthyosis vulgaris management

A
  • immersion in bath and oils followed by an emollient cream, humectant cream, or creams/oil containing urea or α or β-hydroxy acids
  • intermittent systemic retinoids for severe cases
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60
Q

Neurofibromatosis (Type I; von Recklinghausen’s Disease) clinical presentation

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 <5 yr
  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
  • associated with pheochromocytoma, astrocytoma, bilateral acoustic neuromas, bone cysts, scoliosis, precocious puberty, developmental delay, and renal artery stenosis
  • skin lesions less prominent in neurofibromatosis Type II
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61
Q

Neurofibromatosis (Type I; von Recklinghausen’s Disease) pathophysiology

A
  • autosomal dominant disorder with excessive and abnormal proliferation of neural crest elements (Schwann cells, melanocytes), high incidence of spontaneous mutation
  • linked to absence of neurofibromin (a tumour suppressor gene)
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62
Q

Neurofibromatosis (Type I; von Recklinghausen’s Disease) epidemiology

A

incidence 1: 3000

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63
Q

Neurofibromatosis (Type I; von Recklinghausen’s Disease) investigations

A

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

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64
Q

Neurofibromatosis (Type I; von Recklinghausen’s Disease) management

A
  • refer to orthopedics, ophthalmology, plastics, and psychology for relevant management
  • follow-up annually for brain tumours such as astrocytoma
  • excise suspicious or painful lesions
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65
Q

Vitiligo clinical presentation

A
  • primary pigmentary disorder characterized by depigmentation
  • acquired destruction of melanocytes characterized by sharply marginated white patches
  • associated with streaks of depigmented hair, chorioretinitis
  • sites: extensor surfaces and periorificial areas (mouth, eyes, anus, genitalia)
  • Koebner phenomenon, may be precipitated by trauma
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66
Q

Vitiligo pathophysiology

A

acquired autoimmune destruction of melanocytes

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67
Q

Vitiligo epidemiology

A
  • 1% incidence, polygenic

* 30% with positive family history

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68
Q

Vitiligo investigations

A
  • rule out associated autoimmune diseases: thyroid disease, pernicious anemia, Addison’s disease, Type I DM
  • Wood’s lamp to detect lesions: illuminates UV light onto skin to detect amelanosis (porcelain white discolouration)
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69
Q

Vitiligo management

A
  • sun avoidance and protection
  • topical calcineurin inhibitor (e.g. tacrolimus, pimecrolimus) or topical corticosteroids
  • PUVA or Narrow band UVB
  • make-up
  • “bleaching” normal pigmented areas (i.e. monobenzyl ether of hydroquinone 20%) if widespread loss of pigmentation
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70
Q

Level of skin that impetigo affects

A

Stratum corneum of the epidermis

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71
Q

Level of skin that erysipelas effects

A

Upper dermis and lymphatics only

Rarely involves the lower dermis

Subepidermal edema underlying an uninvolved epidermis

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72
Q

Level of skin that cellulitis effects

A

lower dermis and subcutaneous fat

primarily not raised and demarcation less distinct than erisypelas

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73
Q

Level of skin that necrotizing fasciitis effects

A

subcutaneous fat, fascial planes and deep muscle

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74
Q

Dermatological group A strep infections

A

Impetigo - just below stratum corneum

Erysipelas - epidermis and upper dermis only

cellulitis - primarily lower dermis and subcutis (primarily not raised, and demarcation less distinct than erysipelas)

Nec fasciitis - deep fascia and mucle

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75
Q

Impetigo clinical presentation

A
  • acute purulent infection which appears vesicular; progresses to golden yellow “honey-crusted” lesions surrounded by erythema
  • can present with bullae
  • common sites: face, arms, legs, and buttocks
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76
Q

Impetigo etiology

A

GAS, S. aureus or both

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77
Q

Impetigo epidemiology

A

Preschool and young adults living in crowded conditions, poor hygiene, neglected minor trauma

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78
Q

Impetigo differential diagnosis

A

infected eczema

HSV

VZV

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79
Q

Impetigo investigations

A

Gram stain and culture of lesion fluid or biopsy

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80
Q

Impetigo management

A

remove crusts, use saline compresses and topical antiseptic soaks bid

topical antibacterials such as 2% mupirocin or fusidic acid (Canada only) tid; continue for 7-10 days after resolution

systemic antibiotics such as cloxacillin or cephalexin for 7-10 days

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81
Q

Erysipelas clinical presentation

A

Involves upper dermis

Confluent, erythematous, sharp raised edge, warm plaque, well demarcated

Very painful (“St. Anthony’s fire”)

Sites: face and legs

Systemic symptoms: fever, chills, headache, weakness (if present, sign of more serious infection)

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82
Q

Erysipelas etiology

A

GAS

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83
Q

Erysipelas complications

A

Scarlet fever, streptococcal gangrene, fat necrosis, coagulopathy

Spreads via lymphatics

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84
Q

Erysipelas differential diagnosis

A

DVT (less red, less hot, smoother),

superficial phlebitis,

contact dermatitis,

photosensitivity reaction,

stasis dermatitis,

panniculitis,

vasculitis

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85
Q

Erysipelas investigations

A

Clinical diagnosis: rarely do skin/blood culture

If suspect necrotizing fasciitis: do immediate biopsy and frozen section, histopathology

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86
Q

Erysipelas management

A

1st line: penicillin, cloxacillin or cefazolin

2nd line: clindamycin or cephalexin

If allergic to penicillin, use erythromycin

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87
Q

Cellulitis clinical presentation

A

Involves lower dermis/subcutaneous fat

Unilateral erythematous flat lesion, often with vesicles poorly demarcated, not uniformly raised

Tender

Sites: commonly on legs

Systemic symptoms (uncommon): fever, leukocytosis, lymphadenopathy

88
Q

Cellulitis etiology

A

GAS

S. aureus (large sized wounds)

H. influenzae (periorbital)

Pasteurella multocida (dog/ cat bite)

89
Q

Cellulitis complications

A

Uncommon

90
Q

Cellulitis ddx

A

Same as erysipelas

91
Q

Cellulitis investigations

A

Same as erysipelas

92
Q

Cellulitis management

A

1st line: cloxacillin or cefazolin/cephalexin

2nd line: erythromycin or clindamycin Children: cefuroxime

If DM (foot infections): TMP/SMX and metronidazole

93
Q

Common hair follicle infections

A

Superficial folliculitis

Furuncles (Boils)

Carbuncles

94
Q

Superficial folliculitis clinical presentation

A

Superficial infection of the hair follicle (versus pseudofolliculitis: inflammation of follicle due to friction, irritation, or occlusion)

Acute lesion consists of a dome-shaped pustule at the mouth of hair follicle

Pustule ruptures to form a small crust

Sites: primarily scalp, shoulders, anterior chest, upper back, other hair-bearing areas

95
Q

Superficial folliculitis etiology

A

Normal non-pathogenic bacteria (Staphylococcus – most common; Pseudomonas – hot tub)

Pityrosporum

96
Q

Superficial folliculitis management

A

Antiseptic (Hibiclens)

Topical antibacterial (fusidic acid, mupirocin, erythromycin or clindamycin)

Oral cloxacillin for 7-10 d

97
Q

Furuncles (boils) clinical presentation

A

Red, hot, tender, inflammatory nodules with central yellowish point, which forms over summit and ruptures

Involves subcutaneous tissue that arises from a hair follicle

Sites: hair-bearing skin (thigh, neck, face, axillae, perineum buttocks)

98
Q

Furuncles (boils) etiology

A

S. aureus

99
Q

Furuncles (boils) management

A

Incise and drain large furuncles to relive pressure and pain

If afebrile: hot wet packs, topical antibiotic

If febrile/cellulitis: culture blood and aspirate pustules (Gram stain and C&S)

Cloxacillin for 1-2 wk (especially for lesions near external auditory canal/ nose, with surrounding cellulitis, and not responsive to topical therapy)

100
Q

Carbuncles clinical presentation

A

Deep-seated abscess formed by multiple coalescing furuncles

Usually in areas of thicker skin

Occasionally ulcerates

Lesions drain through multiple openings to the surface

Systemic symptoms may be associated

101
Q

Carbuncles etiology

A

S. aureus

102
Q

Carbuncles management

A

Same as for furuncles

103
Q

Dermatophytoses clinical presentation

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)

104
Q

Dermatophytoses pathophysiology

A

• digestion of keratin by dermatophytes results in scaly skin, broken hairs, crumbling nails/onycholysis

105
Q

Dermatophytoses etiology

A

Trichophyton, Microsporum, Epidermophyton species (Pityrosporum is a superficial yeast and not a dermatophyte)

106
Q

Dermatophytoses investigations

A

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

107
Q

Dermatophytoses management

A
  • topicals as first line agents for tinea corporis/cruris and tinea pedis (interdigital type): clotrimazole, or terbinafine or ciclopirox olamine cream applied bid
  • oral therapy is indicated for onychomycosis or tinea capitis: terbinafine (Lamisil® – liver toxicity, CYP2D6 inhibitor) or itraconazole (Sporanox® – CYP3A4 inhibitor, liver toxicity)
108
Q

Tinea capitis clinical presentation

A

Round, scaly patches of alopecia, possibly with broken off hairs; pruritic

Sites: scalp, eyelashes, and eyebrows; involvng hair shafts and follicles

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

Very contagious and may be transmitted from barber, hats, theatre seats, pets

109
Q

Tinea capitis ddx

A

Aloecia areata

psoriasis

seborrheic dermatitis

trichotillomania

110
Q

Tinea capitis investigations

A

Wood’s light examination of hair: green fluorescence only for Microsporum infection

Culture of scales/hair shaft

Microscopic examination of KOH preparation of scales or hair shaft

111
Q

Tinea capitis management

A

Terbinafine (Lamisil) x 4 weeks

NB: oral agents are required to penetrate the hair root where dermatophyte resides

Adjunctive antifungal shampoos or lotions may be helpful, and may prevent spread (e.g. selenium sulfide, ketoconozole, ciclopirox)

112
Q

Tinea corporis (ringworm) clinical presentation

A

Pruritic, scaly, round/oval plaque with active erythematous margin, and central clearing

Site: trunk, limbs, face

113
Q

Tinea corporis (ringworm) ddx

A

Granuloma annulare, pityriasis rosea, psoriasis, seborrheic dermatitis

114
Q

Tinea corporis (ringworm) investigations

A

Microscopic examinations of KOH prep of scales shows hyphae

Culture of scales

115
Q

Tinea corporis (ringworm) management

A

Topicals: 1% clotrimaole, 2% ketoconazole 2% miconazole, terbinafine or ciclopirox olamine cream bid for 2-4 wk

Oral terbinafine, or itraconazole, or fluconazole, or ketoconazole if extensive

116
Q

Tinea Cruris (“jock itch”) clinical presentation

A

Scaly patch/plaque with a well-defined, curved border and central clearing

Pruritic, erythematous, dry/macerated

Site: medial thigh

117
Q

Tinea Cruris (“jock itch”) ddx

A

Candidiasis (involvement of scrotum and satellite lesions), contact dermatitis, erythrasma

118
Q

Tinea Cruris (“jock itch”) investigations

A

Same as for tinea corporis

119
Q

Tinea Cruris (“jock itch”) management

A

Same as for tinea corporis

120
Q

Tinea pedis (athlete’s foot) clinical presentation

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

Predisposing factors: heat, humidity, occlusive footwear

121
Q

Tinea pedis (athlete’s foot) ddx

A

AD, contact dermatitis, dyshidrotic dermatitis, erythrasma, intertrigo, inverse psoriasis

122
Q

Tinea pedis (athlete’s foot) investigations

A

same as for tinea corporis

123
Q

Tinea pedis (athlete’s foot) management

A

same as for tinea corporis

124
Q

Tinea manuum clinical presentation

A

Primary fungal infection of the hand is rare; usually associated with tinea pedis

Acute: blisters at edge of red areas on hands

Chronic: single dry scaly patch

125
Q

Tinea manuum ddx

A

AD, contact dermatitis, granuloma annulare, psoriasis

126
Q

Tinea manuum investigations

A

same as for tinea corporis

127
Q

Tinea manuum management

A

same as for tinea corporis

128
Q

Tinea unguium (onychomycosis) clinical presentation

A

Crumbling, distally dystrophic nails; yellowish, opaque with subungual hyperkeratotic debris

Toenail infections usually precede fingernail infections

T. rubrum (90% of all toenail infections)

129
Q

Tinea unguium (onychomycosis) ddx

A

Psoriasis, lichen planus, contact dermatitis, traumatic onychodystrophies, bacterial infections

130
Q

Tinea unguium (onychomycosis) investigations

A

Microscopic examinations of KOH prep of scales from subungual scraping shows hyphae Culture of subungual scraping or nail clippings on Sabouraud’s agar PAS stain of nail clipping by patholog

131
Q

Tinea unguium (onychomycosis) management

A

Terbinafine (Lamisil) (6 wk for fingernails, 12 wk for toenails)

Itraconazole (Sporanox®) 7 d on, 3 wk off (2 pulses for fingernails 3 pulses for toenails)

Topical: ciclopirox (Penlac®); nail lacquer (often ineffective), Efinaconazole (Jublia®) (48 wk)

132
Q

Scabies clinical presentation

A
  • characterized by superficial burrows, intense pruritus (especially nocturnal), and secondary infection
  • primary lesion: superficial linear burrows; inflammatory papules and nodules in the axilla and groin
  • secondary lesion: small urticarial crusted papules, eczematous plaques, excoriations
  • common sites: axillae, groin, buttocks, hands/feet (especially web spaces), sparing of head and neck (except in infants)
133
Q

Scabies pathophysiology

A
  • scabies mite remains alive 2-3 d on clothing/sheets
  • incubation of 1 mo, then pruritus begins
  • re-infection followed by hypersensitivity in 24 h
134
Q

Scabies etiology

A
  • Sarcoptes scabiei (a mite)

* risk factors: sexual promiscuity, crowding, poverty, nosocomial, immunocompromised

135
Q

Scabies differential diagnosis

A

• asteatotic eczema, dermatitis herpetiformis, lichen simplex chronicus (neurodermatitis)

136
Q

Scabies investigations

A
  • microscopic examination of root and content of burrow and mineral oil mount for mite, eggs, feces
  • skin biopsy may sometimes show scabies mite
137
Q

Scabies management

A
  • bathe, then apply permethrin 5% cream (i.e. Nix®) from neck down to soles of feet (must be left on for 8-14 h and requires second treatment 7 d after first treatment)
  • change underwear and linens; wash twice with detergent in hot water cycle then machine dry
  • treat family and close contacts
  • pruritus may persist for 2-3 wk after effective treatment due to prolonged hypersensitivity reaction
  • mid potency topical steroids and antihistamines for symptom management
138
Q

Lice (pediculosis) clinical presentation

A
  • intensely pruritic red excoriations, morbilliform rash, caused by louse (a parasite)
  • scalp lice: nits (ie 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
139
Q

Lice (pediculosis) etiology

A
  • Phthirus pubis (pubic), Pediculus humanus capitis (scalp), Pediculus humanus humanus (body): attaches to body hair and feeds
  • can transmit infectious agents such as Bartonella quintana and Rickettsia prowazekii
140
Q

Lice (pediculosis) differential diagnosis

A

bacterial infection of scalp

seborrheic dermatitis

141
Q

Lice (pediculosis) diagnosis

A

lice visible on inspection of affected area or clothing seams

142
Q

Lice (pediculosis) management

A
  • permethrin 1% (Nix® cream rinse) (ovicidal) or permethrin 1% (RC & Cor®, Kwellada-P® shampoo)
  • comb hair with fine-toothed comb using dilute vinegar olution to remove nits
  • repeat in 7 d after first treatment
  • shave hair if feasible, change clothing and linens; wash with detergent in hot water cycle then machne dry
143
Q

Bed bugs (hemiptera) clinical presentation

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)

144
Q

Bed bugs (hemiptera) etiology

A

• caused by Cimex lectularius, a small insect that feeds mainly at night (hide in crevices in walls and furniture during the day)

145
Q

Bed bugs (hemiptera) differential diagnosis

A

dermatitis herpetiformis, drug eruptions, ecthyma, other insect bites, scabies

146
Q

Bed bugs (hemiptera) investigations

A

none required, but lesional biopsy can confirm insect bite reaction

147
Q

Bed bugs (hemiptera) management

A
  • professional fumigation
  • 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
148
Q

Herpes simplex clinical presentation

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

• primary
■ 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

• secondary
■ 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

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

• two biologically and immunologically different subtypes: HSV-1 and HSV-2
■ HSV-1
◆ 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)
■ HSV-2
◆ 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

149
Q

Herpes simplex investigations

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
150
Q

Herpes simplex management 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

151
Q

Differential diagnosis of genital ulcers

A

Candida balanitis, chancroid syphilitic chancres

152
Q

Herpes simplex HSV 2 management

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 sexually-transmitted infections STIs
■ for active lesions in pregnancy, see Obstetrics

153
Q

Erythema Multiforme etiology

A

most often HSV or mycoplasma pneumoniae, rarely drugs

154
Q

Erythema multiforme morphology

A

macules/papules with central vesicles; classic bull’s-eye pattern of concentric light and dark rings (typical target lesions)

155
Q

Erythema multiforme management

A

symptomatic treatment (oral antihistamines, oral antacids)

corticosteroids in severely ill (controversial)

prophylactic oral acyclovir for 6-12 mo for HSV-associated EM with frequent recurrences

156
Q

Herpes zoster (shingles) clinical presentation

A
  • unilateral dermatomal eruption occurring 3-5 d after pain and paresthesia of that dermatome
  • vesicles, bullae, and pustules on an erythematous, edematous base
  • lesions may become eroded/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
157
Q

Herpes zoster (shingles) etiology

A
  • caused by reactivation of VZV

* risk factors: immunosuppression, old age, occasionally associated with hematologic malignancy

158
Q

Herpes zoster (shingles) differential diagnosis

A
  • before thoracic skin lesions occur, must consider other causes of chest pain
  • contact dermatitis, localized bacterial infection, zosteriform HSV (more pathogenic for the eyes than VZV)
159
Q

Herpes zoster (shingles) investigations

A

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

160
Q

Herpes zoster (shingles) management

A
  • compress with normal saline, Burow’s, or betadine solution
  • analgesics (NSAIDs, amitriptyline)
  • famciclovir, valacyclovir, or acyclovir for 7 d; must initiate within 72 h to be of benefit
  • gabapentin 300-600 mg PO tid for post-herpetic neuralgia
161
Q

Herpes zoster distribution

A

Herpes zoster typically involves a single dermatome; lesions rarely cross the midline

162
Q

Molluscum contagiosum clinical presentation

A
  • discrete dome-shaped and umbilicated pearly, white papul s caused by DNA Pox virus (Molluscum contagiosum virus)
  • common sites: eyelids, beard (likely spread by shaving), neck, axillae, trunk, perineum, buttocks
163
Q

Molluscum contagiosum etiology

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
164
Q

Molluscum contagiosum investigations

A

none required, however can biopsy to confirm diagnosis

165
Q

Molluscum contagiosum management

A
  • topical cantharidin (a vesicant)
  • cryotherapy
  • curettage
  • topical retinoids
  • Aldara® (imiquimod): immune modulator that produces a cytokine inflammation
166
Q

Manifestations of HPV infection

A

Verruca vulgaris (common warts)

Verruca plantaris (plantar warts) and verruca palmaris (palmar warts)

Verruca planae (flat warts)

Condyloma acuminata (genital warts)

167
Q

Verruca vulgaris (common warts) definition and clinical features

A

Hyperkeratotic, elevated discrete epithelial growths with papillated surface caused by HPV

Paring of surface reveals punctate, red-brown specks (thrombosed capillaries)

168
Q

Verruca vulgaris (common warts) differential diagnosis

A

molluscum contagiosum

seborrheic keratosis

169
Q

Verruca vulgaris (common warts) distribution

A

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

170
Q

Verruca vulgaris (common warts) hpv type

A

at least 80 types are known

171
Q

Verruca plantaris (plantar warts) and verruca palmaris (palmar warts) definition and clinical features

A

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

172
Q

Verruca plantaris (plantar warts) and verruca palmaris (palmar warts) differential diagnosis

A

May need to scrape (“pare”) lesions to differentiate wart from callus and corn

173
Q

Verruca plantaris (plantar warts) and verruca palmaris (palmar warts) distribution

A

Located at pressure sites: metatarsal heads, heels, toes

174
Q

Verruca plantaris (plantar warts) and verruca palmaris (palmar warts) hpv type

A

commonly HPV 1, 2, 4, 10

175
Q

Verruca planae (flat warts) definition and clinical features

A

Multiple discrete, skin coloured, flat topped papules grouped or in linear configuration

Common in children

176
Q

Verruca planae (flat warts) differential diagnosis

A

Syringoma, seborrheic keratosis, molluscum contagiosum, lichen planus

177
Q

Verruca planae (flat warts) distribution

A

Sites: face, dorsa of hands, shins, knees

178
Q

Verruca planae (flat warts) hpv type

A

commonly HPV 3, 10

179
Q

Condyloma acuminata (genital warts) definition and clinical features

A

Skin-coloured pinhead papules to soft caulflower like masses in clusters

Often occurs in young adults, infants, children

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

180
Q

Condyloma acuminata (genital warts) ddx

A

Condyloma lata (secondary syphilitic lesion, dark field strongly +ve), molluscum contagiosum

181
Q

Condyloma acuminata (genital warts) distribution

A

Sites: genitalia and perianal areas

182
Q

Condyloma acuminata (genital warts) hpv type

A

Commonly HPV 6 and 11

HPV 16, 18, 31, 33 cause cervical dysplasia, SCC and invasive cancer

183
Q

Condyloma acuminata (genital warts) investigations

A

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

184
Q

Condyloma acuminata (genital warts) complications

A

fairy-ring warts (satellite warts at periphery of treated area of original warts)

185
Q

Treatment for warts

A

• first line therapies
■ salicylic acid preparations (patches, solutions, creams ointments), cryotherapy, topical 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

• other viruses associated with skin changes, such as measles, roseola, fifth disease, etc.

186
Q

Candidiasis etiology

A
  • many species of Candida (70-80% of infections are from Candida albicans)
  • opportunistic infection in those with predisposing factors (e.g. trauma, malnutrition, immunodeficiency)
187
Q

Candidal paronychia clinical presentation

A

painful red swellings of periungual skin

188
Q

Candidal paronychia management

A

topical agents not as effective; oral antifungals recommended

189
Q

Candidal intertrigo clinical presentation

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

190
Q

Candidal intertrigo predisposing factors

A

obesity, DM, systemic antibiotics, immunosuppression, malignancy

191
Q

Candidal intertrigo management

A

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

192
Q

Why is oral Terbinafine not used for candidiasis intertrigo

A

Oral Terbinafine (Lamisil®) is not effective because it is not secreted by sweat glands

193
Q

Pityriasis (tinea) versicolour clinical presentation

A
  • asymptomatic superficial fungal infection with brown/white scaling macules
  • affected skin darker than surrounding skin in winter, lighter in summer (does not tan)
  • common sites: upper chest and back
194
Q

Pityriasis (tinea) versicolour pathophysiology

A
  • microbe produces azelaic acid → inflammatory reaction inhibiting melanin synthesis yielding variable pigmentation
  • affinity for sebaceous glands; require fatty acids to survive
195
Q

Pityriasis (tinea) versicolour etiology

A
  • Pityrosporum ovale (Malassezia furfur)
  • also associated with folliculitis and seborrheic dermatitis
  • predisposing factors: summer, tropical climates, excessive sweating, Cushing’s syndrome, prolonged corticosteroid use
196
Q

Pityriasis (tinea) versicolour investigations

A

clinical dagnosis but can perform microscopic examination, KOH prep of scales for hyphae and spores

197
Q

Pityriasis (tinea) versicolour management

A
  • ketoconazole shampoo or cream daily
  • topical terbinafine or ciclopirox olamine bid
  • systemic fluconazole or itraconazole for 7 d if extensive
198
Q

Syphilis clinical presentation

A
  • characterized initially by a painless ulcer (chancre)

* following inoculation, systemic infection with secondary and tertiary stages

199
Q

Syphilis etiology

A
  • Treponema pallidum

* transmitted sexually, congenitally, or rarely by transfusion

200
Q

Primary syphilis clinical presentation

A

Single red, indurated, painless chancre, that deveops into painless ulcer with raised border and scanty serous exudate

Chancre develops at site of inoculation after 3 wk of incubation and heals in 4-6 wk; chancre may also develop on lips or anus

Regional non-tender lymphadenopathy appears <1 wk after onset of chancre

201
Q

Primary syphilis investigations

A

CANNOT be based on clinical presentation alone

VDRL negative – repeat weekly for 1 mo

Fluorescent treponemal antibody-syphilis (FTA-ABS) test has greater sensitivity and may detect disease earlier in course

Dark field examination – spirochete in chancre fluid or lymph node aspirate

202
Q

Primary syphilis management

A

Penicillin G, 2.4 million units IM, single dose

203
Q

Primary syphilis ddx

A

chancroid (painful), HSV (multiple lesions)

204
Q

Natural history of untreated syphilis

A
  • Inoculation
  • Primary syphilis (10-90 d after infection)
  • Secondary syphilis (simultaneous to primary syphilis or up to 6 mo after healing of primary lesion)
  • Latent syphilis
  • Tertiary syphilis (2-20 yr)
205
Q

Secondary syphilis clinical presentation

A

Presents 2-6 mo after primary infection (patient may not recall presence of primary chancre)

Associated with generalized lymphadenopathy, splenomegaly, headache, chills, fever, arthralgias, myalgias, malaise, photophobia

Lesions heal in 1-5 wk and may recur for 1 yr

3 types of lesions:

  1. Macules and papules: flat top, scaling nonpruritic, sharply defined, circular/annular rash (DDx: pityriasis rosea, tinea corporis, drug eruptions, lichen planus)
  2. Condyloma lata: wart-like moist papules around genital/perianal region
  3. Mucous patches: macerated patches mainly found in oral mucosa
206
Q

Secondary syphilis investigations

A

VDRL positive

FTA-ABS +ve; –ve after 1 yr following appearance of chancre

Dark field +ve in all secondary

207
Q

Secondary syphilis management

A

same as primary syphilis

208
Q

Tertiary syphilis clinical presentation

A

Extremely rare 3-7 yr after secondary

Main skin lesion: ‘Gumma’ – a granulomatous nontender nodule

209
Q

Tertiary syphilis investigations

A

As in primary syphilis, VDRL can be falsely negative

210
Q

Tertiary syphilis management

A

Treatment: penicillin G, 2.4 million units IM weekly x 3 wk

211
Q

Latent syphilis

A

70% of untreated patients will remain in this stage for the rest of their lives and are immune to new primary infection

212
Q

Gonococcemia clinical presentation

A
  • disseminated gonococcal infection
  • hemorrhagic, tender, pustules on a purpuric/petechial background

common sites: distal aspects of extremities

  • associated with fever, arthritis, urethritis, proctitis, pharyngitis, and tenosynovitis
  • neonatal conjunctivitis if infected via birth canal
213
Q

Gonococcemia etiology

A

Neisseria gonorrhoeae

214
Q

Gonococcemia investigations

A
  • requires high index of clinical suspicion plays because tests are often negative
  • bacterial culture of blood, joint fluid, and skin lesions
  • joint fluid cell count and Gram stain
215
Q

Gonococcemia management

A
  • notify Public Health authorities
  • screen for other STIs
  • cefixime 400 mg PO (drug of choice) or ceftriaxone 1 g IM

Dermatology (11 decks)

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