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39 Cards in this Set
- Front
- Back
Atopic Dermatitis (Eczema) Associated diseases
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Asthma in 50%
Allergic rhinitis in 50–80% |
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Atopic Dermatitis (Eczema) Pathogenesis
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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 |
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Atopic Dermatitis (Eczema) Clinical Manifestations
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Symptoms and Signs
Itching Scaling Crusting Oozing |
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PsoriasisAssociated Illnesses
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Arthritis
Crohn’s disease Obesity Hypertension Diabetes mellitus Lymphoma |
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Psoriasis Clinical findings
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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 |
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Psoriasis Pathophysiology
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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) |
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Acne Vulgaris: Pathophysiology
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Follicular hyperkeratinization
Sebum production Propionibacterium acnes Inflammation |
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Follicular hyperkeratinization
refers to |
Excessive keratinocyte proliferation –> narrowed follicular orifice
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Propionibacterium acnes
Thrives in |
in high triglyceride content of sebum
Converts triglycerides to free fatty acids These lead to –> Inflammation |
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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 |
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Intraepidermal Vesicle/Bulla microbes
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Pemphigus vulgaris
Pemphigus foliaceus Paraneoplastic pemphigus Eczema (atopic dermatitis) |
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Subepidermal
Vesicle/Bulla Locations microbes |
Bullous pemphigoid
Cicatricial pemphigoid Dermatitis herpetiformis (bullous) |
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Bullous Pemphigoid characteristics
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Elderly (> 60), no HLA association, M > F
Subepidermal bullous disease, ± dermal inflammation Intense pruritus secondary to mast cell degranulation |
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Bullous Pemphigoid histology
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Subepidermal blister
Eosinophilic, mononuclear and PMN infiltration |
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Bullous Pemphigoid Immunofluorescence
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Anti–basement membrane IgG Ab against hemidesmosome
Binds to BP230 & BP180 antigens (BPAg1 & BPAg2) BP180 Ag = collagen type XVII |
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Bullous Pemphigoid Pathogenesis
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Complement mediated destruction of dermal–epidermal jxn
Mast cell degranulation –> itch |
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Bullous Pemphigoid Therapy
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Glucocorticoids
Other immunosuppressants |
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Pemphigus Pathogenesis
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IgG autoantibody against keratinocyte surface adhesion molecules DG1 or DG3 (DG = desmoglein)
Loss of cohesion –> acantholysis Therefore: IF stains epidermal intercellular space |
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Pemphigus Clinical Manifestations
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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% |
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PemphigusTherapy
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Glucocorticoids ± immunosuppressives
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Dermatitis Herpetiformis Pathophysiology
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Antibodies to:
Reticulin Endomysium (transglutamase) Granular IgA in dermis BM deposition of IgA –>subepidermal blister Granular deposition of IgA in dermal papillae |
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Dermatitis Herpetiformis Clinical Manifestations
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Dermatologic
Multiform lesions Urticarial plaques Papules Vesicles/bullae Crusts Symmetric Uncommon Mucous membranes Hands and feet |
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Dermatitis Herpetiformis Associated Diseases
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Celiac disease in 85%
Lymphoma Autoimmune thyroid disease |
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Dermatologic Malignancies
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Melanoma
Basal cell carcinoma Squamous cell carcinoma |
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Basal Cell Carcinoma Epidemiology
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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 |
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Basal Cell Carcinoma Clinical Presentation
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Face (70%), trunk (15%)
Nodular (60%), superficial (30%), morpheaform (10%) No precursor lesion Rare metastases or mortality |
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Squamous Cell Carcinoma Epidemiology
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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 |
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Squamous Cell Carcinoma Clinical Presentation
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Head and neck (55%), UE (20%), LE (15%)
80% from precursor actinic keratosis |
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Melanoma High Increased Risk
factors |
Changing nevus
Familial melanoma w/dysplastic nevi > 50 nevi > 2 mm |
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Melanoma Moderate Increased Risk factors
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Family member w/ melanoma
Past h/o melanoma Sporadic dysplastic nevi Congenital nevi |
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Melanoma:Mild Increased Risk
factors |
Immunosuppression
Severe sunburn Freckling |
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Melanoma Classic Locations
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White men: back
Woman: legs and back AA/Asians: feet, nails, mucosa |
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Melanoma Signs and Symptoms
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Change in size and color of nevus (70%)
Itching (25%) Late Bleed, ulcer, pain, leukoderma |
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Melanoma Screening A, B, C, D, Es
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Asymmetry
Border irregularities Color variegation Diameter > 6 mm Enlargement/evolution Color, shape, symptom change |
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Melanoma Types
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Superficial Spreading
Nodular Lentigo Maligna Acral Lentiginous |
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Melanoma Superficial Spreading
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Most common
30 – 50 years old Radial growth |
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Melanoma Nodular
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Second most common
> 60 years old Rapid growth Bleeds, ulcerates |
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Melanoma Lentigo Maligna
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Less common
> 60 years old Sundamaged skin (face) Slow growing Color variegation |
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Melanoma Acral Lentiginous
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Rare
Markedly increased in persons of color > 60 years old Palms, soles, nails |