Exam 3 - Dermatology Flashcards
Fitzpatrick Skin Types
1 - Never tans, always burns 2 - Hardly tans, usually burns 3 - Average tanning, sometimes burns 4 - Easily tans, rarely burns 5 - Very easy to tan, very rarely burns 6 - Never burns
Dark skin (Melanosome distribution and melanin type)
Melanosomes larger
Distributed throughout cytoplasm of keratinocyte
Eumelanin: black to brown pigment
Light skin (Melanosome distribution and melanin type)
Melanosomes smaller
Distributed in clusters above nucleus of keratinocyte
Pheomelanin: yellow to red/brown pigment
Vitiligo
Autoimmune attack against melanocyte
Acquired depigmentation
Absence of melanocytes
Hemidesmosomes
Keratinocyte attachment to dermal border
Dermal-epidermal junction
Dz: EB, Bullous Pemphigoid
Desmosomes
Keratinocytes attachment to other keratinocytes
Stratum spinosum (epidermis)
Dz: Pemphigus Vulgaris
Recessive Dystrophic Epidermolysis Bullosa
Defect in collagen VII at DEJ (congenital) Pseudosyndactyly (mitten hand deformity) Flexion contractures Increased risk of SCC Infection
Bullous Pemphigoid
Aquired blistering of DEJ Antibodies to BP 230 and BP 180 Tense blister (hemidesmosomes) No MM (No des3) Often on flexor surfaces Linear on IMF along BM
Pemphigus Vulgaris
Antibodies to desmoglein 1 (skin) and 3 (MM)
Flaccid bulla (intraepidermal blisters)
Desmosomes
Not linear on IMF (obliterated epidermis)
Epidermolysis Bullosa Simplex
Defect in keratin 5 and 14
Blisters on hands, feet, and extremities
Manage with age
Icthyosis Vulgaris
Filaggrin mutation - NMF loss
Defective skin barrier
Large white scaly appearance
Epithelial Zones
Stratum corneum
Stratum granulosum
Stratum spinosum
Stratum basalis
Dermal Zones
Papillary dermis - interlocks with epidermal rete, thin collagen bundles
Reticular dermis - visible elastic fibers, thick collagen bundles
Major Components of Dermis
Collagen - strength
Elastic fibers - resilience
Ground substance - facilitates diffusion
Solar elastosis
Acquired disorder of elastin
Pseudoxanthoma Elasticum
Congenital disorder of elastin
Hair phases
Anagen - growing (3 years)
Catagen - transition (3 weeks)
Telogen - resting (3 months)
Seborrheic Dermatitis
cradle cap - scalp Malassezia furfur (fungus)
Stasis dermatitis
lower extremity edema
bilateral
Numular Dermatitis
Excess use of soap and dry skin
Red scaly patches
Minimize soap, moisturize, topical steroids
Types of Hypersensitivity Reactions
Type I - Anaphylactic rxn (immediate)
Type II - Cytotoxic rxn
Type III - Immune complex rxn
Type IV - Delayed type hypersensitivity rxn
Type I HS
Immediate
IgE to antigen
Histamine release
Ex: urticaria and angioedema
Type II HS
Cytotoxic
IgG bind and lysis (activates complement)
Ex: ABO mismatch
Type III HS
Immune complex
Organ and vessel deposition
Activation of complement - inflammatory damage
Ex: serum sickness
Type IV HS
Delayed
Langerhans cells are APC
Local rxn w/out antibodies
Ex: Drug eruptions, allergic contact dermatitis
Allergic contact dermatitis
Delayed type IV rxn
Dx w/ patch testing
Psoriasis
Increased risk of CVD
Extensor surfaces
May include arthritis over joints
Atopic Dermatitis
Filaggrin mutation - NMF loss
Defective skin barrier
Flexor surfaces
Associated with asthma and allergic rhinitis
Erysipelas
aka St. Anthony’s Fire
Strep pyogenes
Common on face (cliff drop border, non-pitting, pain)
Lymphadenopathy
Impetigo
Non-bullous (80) and bullous (20) High humidity Cutaneous carriage Poor hygine Honey colored crust
Non-bullous impetigo
Face followed by extremities
Strep pyogenes or staph aureus
Bullous impetigo
Anywhere on body
Staph aureus ONLY
Cellulitis
Extremities (unilateral) Painful erythemia WTT Lymphatic streaking Regional lymphadenopathy Septic danger (staph a, strep p, h. flu)
KOH Examination of skin
Used with fungal infections
Hyphae/arthrospores = Tinea
Pseudohyphae/yeast = Candidiasis
Short hyphae/yeast (spaghetti/meatballs) = Tinea versicolor
Fungal culture test
Dermatophyte Test Medium (DTM)
Sabouraud agar
Fungal biopsy stain
PAS w/ diastase
Gomori methenamine silver (GMS)
Tinea Versicolor
Warm/humid, post pubertal patients
Food: follicular lipids
Hyper/hypopigmented macules/patches on chest
Scabies
Webspace, flexures, waist, axillary, genital
Night, hot bath
Burrows and genital nodules
Seborrheic Keratosis
“Barnacles of Life”
Stuck on appearance
Leser-Trelat sign - indication of internal malignancy
Malignant Melanoma ABCDE
Asymmetry Border irregularity Color variation Diameter >6mm Evolution The ugly duckling
Skin defenses against UV
DNA repair
Apoptosis of cells with damage
Defenses against ROS
Melanin
Actinic keratosis
Common precancer
1/1000 will go on to cancer in a year
Usually becomes SCC
Basal cell carcinoma
Most common (2nd in IS/IC patients)
Pearly and shiny
Not usually fatal
Squamous cell carcinoma
2nd most common (1st in IS/IC patients)
More invasive than BCC
FAMM syndrome
Familial atypical moles and melanoma
Malignant melanoma in 1 or more 1/2 degree relatives
Numerous atypical nevi
148x risk (biggest RF)
UVA
Longer wavelength
Penetrates deeper
Dark patches, wrinkles, loose skin
DNA damage
UVB
Shorter wavelength Penetrates more shallow Vitamin D synthesis Sunburns Eye problems DNA damage
6 UV effects on skin
Damage to DNA, RNA, lipids, proteins Pro-inflammatory Immunosuppressive Induction of innate defense Induction of apoptosis Vitamin D synthesis
3 Photodermatoses
Lupus Erythematosus
Dermatomyositis
Mixed Connective Tissue Disease
4 dermatomyositis clinical signs
Heliotrope leading to periorbital edema
Samitz sign = ragged cuticles
Gottron’s papules=extensor lichenoid papules/poikiloderma
Shawl sign
Dermatomyositis and malignancy
Adult onset is sign of internal malignancy (10-50%)
Neurofibromatosis Type I criteria
- > 6 cafe au lait
- > 2 neurofibromas or >1 plexiform neurofibroma
- Crowe’s sign (axillary/inguinal freckling)
- Optic glioma
- > 2 Lisch nodules
- Osseous lesion, sphenoid wing dysplasia, cortex thin
- 1st degree relative with dz
Tuberous Sclerosus
Adenoma sebaceum
Hypomelanotic macules
Shagreen patch
Kaposi’s Sarcoma
Indication of immunocompromise
Triggered by HHV-8
Pyoderma Gangrenosum
Neutrophil overreaction
Large skin wound - AVOID I&D = more trauma
Usually have underlying AI Dz
Lichen Planus
Purple, polygonal, pruritic papules
Wickham’s striae - overlying lace like pattern
Concern for hepatitis C
Acanthosis Nigricans signs and mech
Velvety dark patch
Usually neck, axillae, dorsal hands
Epid keratinocyte and D fibroblast proliferation
Acanthosis nigricans associations
Familial Obesity Diabetes Endocrinopathies (Cushing's) Drugs (rare) Malignancy (look for weight loss)
4 drug factors that affect skin absorption
Drug concentration
Molecular size
Lipophilicity
Vehicle composition
4 patient factors that affect skin absorption
Barrier disruption
Anatomic location
Skin hydration (up=up)
Occlusion
Classifications of topical steroids
Class 1 to Class 7
More to less potent
Examples of topical steroids
Class 1: Clobetasol
Class 4: Triamcinolone
Class 7: Hydrocortizone