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39 Cards in this Set

  • Front
  • Back
Atopic Dermatitis (Eczema) Associated diseases
Asthma in 50%
Allergic rhinitis in 50–80%
Atopic Dermatitis (Eczema) Pathogenesis
If filaggrin mutation –> barrier defect –> allergen entry
Langerhans cells stimulate cutaneous T–cells –> Th2 cytokines –> increased IgE production and eosinophilia
Generalized shift to Th2 immune response
Increased Staphylococcus aureus colonization
Atopic Dermatitis (Eczema) Clinical Manifestations
Symptoms and Signs
Itching
Scaling
Crusting
Oozing
PsoriasisAssociated Illnesses
Arthritis
Crohn’s disease
Obesity
Hypertension
Diabetes mellitus
Lymphoma
Psoriasis Clinical findings
Sharp borders
Silver scale
Underneath is red and glossy
Nail pitting
Koebner phenomenon = lesions at site of trauma
Auspitz sign = small blood drops when scraped
Psoriasis Pathophysiology
Shift to Th1 immune status
Activation of T–cells
Co–stimulation from cell–cell interactions
Shortened cell cycle of keratinocytes (36 hours vs. 311 hours)
Faster epidermis turnover time from basal cell layer to stratum corneum (4d vs. 27 days)
Acne Vulgaris: Pathophysiology
Follicular hyperkeratinization

Sebum production

Propionibacterium acnes

Inflammation
Follicular hyperkeratinization
refers to
Excessive keratinocyte proliferation –> narrowed follicular orifice
Propionibacterium acnes
Thrives in
in high triglyceride content of sebum
Converts triglycerides to free fatty acids
These lead to –>
Inflammation
Acne Vulgaris: Clinical Progression
1)Accumulation of sebum and keratin –>
2) Increased sebum –>
3) P. acnes replication –> inflammation –> rupture into dermis –>
1)Microcomedone
2)Closed comedone (whitehead)
Open comedone (blackhead)
3)Papules
Nodules
Cysts
Pustules
Intraepidermal Vesicle/Bulla microbes
Pemphigus vulgaris
Pemphigus foliaceus
Paraneoplastic pemphigus
Eczema (atopic dermatitis)
Subepidermal
Vesicle/Bulla Locations microbes
Bullous pemphigoid
Cicatricial pemphigoid

Dermatitis herpetiformis (bullous)
Bullous Pemphigoid characteristics
Elderly (> 60), no HLA association, M > F
Subepidermal bullous disease, ± dermal inflammation
Intense pruritus secondary to mast cell degranulation
Bullous Pemphigoid histology
Subepidermal blister
Eosinophilic, mononuclear and PMN infiltration
Bullous Pemphigoid Immunofluorescence
Anti–basement membrane IgG Ab against hemidesmosome
Binds to BP230 & BP180 antigens (BPAg1 & BPAg2)
BP180 Ag = collagen type XVII
Bullous Pemphigoid Pathogenesis
Complement mediated destruction of dermal–epidermal jxn
Mast cell degranulation –> itch
Bullous Pemphigoid Therapy
Glucocorticoids
Other immunosuppressants
Pemphigus Pathogenesis
IgG autoantibody against keratinocyte surface adhesion molecules DG1 or DG3 (DG = desmoglein)
Loss of cohesion –> acantholysis
Therefore: IF stains epidermal intercellular space
Pemphigus Clinical Manifestations
P. Vulgaris (vulgar = common)
Anti DG3 ± DG1 (if both more severe)
Acantholysis just above basal layer
Oral lesions at onset in 50%, eventual in almost all
Skin only in 10–15%
PemphigusTherapy
Glucocorticoids ± immunosuppressives
Dermatitis Herpetiformis Pathophysiology
Antibodies to:
Reticulin
Endomysium (transglutamase)
Granular IgA in dermis
BM deposition of IgA –> subepidermal blister
Granular deposition of IgA in dermal papillae
Dermatitis Herpetiformis Clinical Manifestations
Dermatologic
Multiform lesions
Urticarial plaques
Papules
Vesicles/bullae
Crusts
Symmetric
Uncommon
Mucous membranes
Hands and feet
Dermatitis Herpetiformis Associated Diseases
Celiac disease in 85%
Lymphoma
Autoimmune thyroid disease
Dermatologic Malignancies
Melanoma
Basal cell carcinoma
Squamous cell carcinoma
Basal Cell Carcinoma Epidemiology
Most common human cancer, COO = keratinocyte
From basal cell layer of epidermis
Caucasians, rare in persons of color
M > F, equatorial increase, increase with age
UV light, fair skinned, XRT, immunosuppression, Arsenic
Basal cell nevus syndrome
Basal Cell Carcinoma Clinical Presentation
Face (70%), trunk (15%)
Nodular (60%), superficial (30%), morpheaform (10%)
No precursor lesion
Rare metastases or mortality
Squamous Cell Carcinoma Epidemiology
Second most common human cancer, COO = keratinocyte
From epidermis, not at the basal cell level
UV light, age, Caucasian, XRT, immunosuppression
Chronic inflammation, arsenic, smoking
Xeroderma pigmentosa, albinism
Squamous Cell Carcinoma Clinical Presentation
Head and neck (55%), UE (20%), LE (15%)
80% from precursor actinic keratosis
Melanoma High Increased Risk
factors
Changing nevus
Familial melanoma w/ dysplastic nevi
> 50 nevi > 2 mm
Melanoma Moderate Increased Risk factors
Family member w/ melanoma
Past h/o melanoma
Sporadic dysplastic nevi
Congenital nevi
Melanoma:Mild Increased Risk
factors
Immunosuppression
Severe sunburn
Freckling
Melanoma Classic Locations
White men: back
Woman: legs and back
AA/Asians: feet, nails, mucosa
Melanoma Signs and Symptoms
Change in size and color of nevus (70%)
Itching (25%)
Late
Bleed, ulcer, pain, leukoderma
Melanoma Screening A, B, C, D, Es
Asymmetry
Border irregularities
Color variegation
Diameter > 6 mm
Enlargement/evolution
Color, shape, symptom change
Melanoma Types
Superficial Spreading

Nodular

Lentigo Maligna
Acral Lentiginous
Melanoma Superficial Spreading
Most common
30 – 50 years old
Radial growth
Melanoma Nodular
Second most common
> 60 years old
Rapid growth
Bleeds, ulcerates
Melanoma Lentigo Maligna
Less common
> 60 years old
Sundamaged skin (face)
Slow growing
Color variegation
Melanoma Acral Lentiginous
Rare
Markedly increased in persons of color
> 60 years old
Palms, soles, nails