Dermatologic Inflammatory Disease
Psoriasis
Chronic, inflammatory disease of skin and/or joints that causes rapid turnover of skin cells. Will see periods of intense flares in which there is pain, itch, or persistent warmth and swelling around a joint.
Clinical features
Plaque: Red plaques with thick white/silver scales. Favors extensor elbows, knees, scalp, lower back
Guttate: Small lesions favoring the trunk and upper extremities. Typically in children, young adults
Erythrodermic: Fully body redness/erythema
Pustular: Focal/diffuse sterile pustules on erythematous base
Nail changes : Defective keratinization of proximal nail fold (forming pits), or discoloration and oily material in nail bed
Pathogenesis
Environmental triggers activate keratinocytes, which stimulate inflammatory messengers.
Key cell types
- Dendritic cells
- Mast cells
- TNF-alpha proteins
- IL-17, IL-12/23
Histology
- Epidermal thickening (acanthosis)
- Parakeratosis (nuclei retained in stratum corneum)
- Loss of granular cell layer
- Dilated capillaries
- Neutrophil recruitment
Treatment
- Topical creams: Salicylic acid to shed the outer layer of skin, as well as moisturizers
- Vitamin D derivates and coal tar to slow skin growth
- Light therapy (narrow band UVB)
- Injectables which mimic natural body function and inhibit immune cytokine pathways implicated in disease development (TNF-alpha, IL-12/23, IL-17, etc.)
Corticosteroids
The most common treatment. Has classes of strength, 1 being the strongest and 7 being the weakest. Long term use can lead to atrophy, neovascularization, and steroid acne. Can also suppress natural hormone production.
High potency: Clobetasol
Medium potency: Triamcinolone
Lowest potency: Hydrocortisone
Atopic Dermatitis
Chronic pruritic inflammatory skin disease with a wide range of severity. Periods of remission and exacerbation.
A type of eczematous dermatitis, but not synonymous with eczema.
Clinical features
Tends to spare areas around nose due to being sebum-rich. Erythematous papules can form erythematous plaques that may display weeding, crusting or scaling.
Distribution varies by age
- Infants: Cheeks, forehead, scalp, extensor surfaces
- Adolescents: Flexural areas
- Adults: Lichenification in flexural regions, extremities and face
Pathogenesis
Part of the atopic triad: Asthma, atopic dermatitis, allergic rhinitis.
Treatment
Long-term use of emollients and topical steroids for acute flares. Antihistamines for pruritis and sleep issues.
Acne
Clinical features
Usually in areas with abundant sebaceous glands, beginning with clogged pores (comedones).
Pathogenesis
Increased sebum production and keratin, sebum plug the pore. Finally, Cutibacterium acnes proliferates in the sebaceous follicle and stimulates pro-inflammatory cytokines.
Morphology
Open comedones: Blackheads
Closed comedones: Whiteheads
Nodulocystic acne will lead to scarring.
Treatment
Often fails due to lack of adherence, as results generally take 2-3 months.
Mild: Topical retinoid or benzoyl peroxide
Moderate (inflamed lesions): Topical retinoid and benzoyl peroxide, plus potentially a topical antibiotic
Severe (extensive inflamed lesions and scarring): Oral antibiotics, topical retinoid and benzoyl peroxide
Hormonal therapy (in females) or isotretinoin may be considered if the response is inadequate.
Topical
- Retinoids (Vitamin A derivatives): Normalize desquamation of follicular epithelium and prevents new comedone formation. Can cause dryness, redness, or photosensitivity.
- Benzoyl peroxide: Has antibacterial and comedolytic properties and generates free radicals that oxidize C. acnes cell wall
Oral
- Antibiotics: Reduce C. acnes colonization of skin/follicles. Usually doxycycline.
- Spironolactone: Affects androgen receptors in sebaceous glands for decreased sebum production. Can block testosterone effects, so only used in cis-women women and trans-women.
- Isotretinoin (Accutane): Retinoic acid derivative that targets all four pathophysiologic factors involved in acne. Only used in severe cases and is teratogenous (to the extent that women have to pledge to be using two forms of contraception if prescribed).
Drug Rashes
Clinical features
Immediate reactions occur less than an hour after consumption. Urticaria, angioedema, and anaphylaxis are common co-occurrences.
Delayed reactions can occur weeks or months after consumption.
Exanthematous eruptions
Type IV hypersensitivity reaction occurring 7-10 days after consumption. Often caused by antibiotics or anticonvulsants. Fully resolves a within a week after stopping the medication.
Erythematous macules and mild lesions initially appear on trunk then spread centrifugally to the extremities. May also see pruritus and mild fever.
Systematic reactions
Stevens-Johnson Syndrome (SJS) or Toxic Epidermal Necroylsis (TEN). Dermatologic emergencies that involve extensive necrosis and detachment of the epidermis and mucosal surfaces. They differ in severity based on extent of body surface area covered.
Typically begins within 8 weeks after starting drug. Begins with erythematous, irregularly shaped, red to purpuric macules that coalesce. Lesions evolve to flaccid blisters, which spread and break easily (positive Nikolsky sign).
Can have permanent sequelae, such as blindness.
Introducing the best acronym ever for SJS/TEN associated drugs
Sulfa- antibiotics
Allopurinol
Tetracyclines
Anticonvulsants
NSAIDs
Pemphigus Vulgaris
Clinical Features
Flaccid bullae and erosions and positive Nikolsky sign. Involvement of mucus membranes. Older age of onset (50+ years old).
Pathogenesis
IgG antibodies against cell surface of keratinocytes in a net-like distribution.
Biopsy findings
- Intraepidermal blister above the basal layer
- Tombstoning
- Acantholysis (keratinocytes falling apart)
Treatment
High dose systemic glucocorticoids and then transitioning to biologic attacking pathogenic B cells.
Bullous Pemphigoid
Clinical features
Tense, pruritic bullae and urticarial lesions (erythematous, inflamed plaques). Negative Nikolsky sign. Older age of onset (60+ years old).
Pathogenesis
IgG antibodies against hemidesmosomes.
Biopsy findings
- Band-like/linear deposition of IgG and C3 at the dermo/epidermal junction
- Subepidermal blister with eosinophilic fluid
Treatment
Systemic or topical glucocorticoids depending on extent of disease and transition to “steroid sparing agent” for more severe cases.