Basement Membrane Zone (BZD) Genetic Protein EB Simplex (EBS) Keratin 5 Keratin14 Plectin

Mechanism AD: autosomal dominant Helix-initiation/terminiation region

Appearance Mechanobullous Pigment changes

Distribution Herpetiform Musocal Epidermal

Presentation

Treatment / Prognosis Heal with minimal scarring

Histology Epidermis (Basal layer)

+ Muscular dystrophy

Junctional EB

6 4 integrin BPAg2 Laminin 332

JEB (non-Herlitz)

Milder form

Mucosal Airway

+ Pyloric atresia

DermalEpidermal Junction (BZD) Severe: death

JEB (Herlitz) (does not adhere)

Most severeform

Systemic infection Airway obstruction High risk for sepsis More severe

Dystrophic EB

T7 collagen

Recessive (RDEB) = none Carriers normal

White papules Pruritis ³Mitten-sock´ Pseudosyndactyle

Scarring, Contracture, Deformity Squamous cell carcinoma (80%) Heals with scarring

Papillary Dermis (superficial)

Dominant (DDEB) = mutant Dominant negative effect Bullous Congenital IchthyosiformErythroderma (BCIE) Keratin 1 Keratin 2 Keratin 10 aka Epidermolytic Hyperkeratosis Blister Erythema Often inflamed (Extensive scaling) Appearance Vesicles / Bullae Tense Pruritus Urticarial base Can cross placenta into newborn! Vesicles / Bullae Tense Pruritus !!! Generalized Birth or early childhood

(Late childhood to adulthood) Distribution Extremities Axillae Groin Epidemiology Age > 60 Rarely in children Treatment Histology

Autoantibody Bullous pemphigoid (BP)

Protein BPAg1& BPAg2

Mechanism

Pemphigoidgestationis

BPAg2

Trunk

Pregnancy

Cicatricialpemphigoid

Laminin 332 ( 6 4 integrin) (BPAg2) T7 Collagen Bullae

Conjunctiva Oral mucosa Skin Heterogeneous Associated systemic diseases 1. IBS 2. RA 3. Multiple myeloma ³chronic bullous of childhood´

Scarring

EpidermolysisBullosaAcquisita (EBA)

Scarring Millia

Linear IgA Bullous Dermatosis (LABD) Phemphigus Vulgaris

BPAg2

Linear deposition of IgA

Vesicle / Bullae

Annular Arcuate Epidermis Oral mucosa

Desmoglein 3

Autoimmune (antibody to desmosome protein)

Heal without scarring Systemic corticosteroids

Acantholysis (spinous layer) = abnormal attach

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Herlitz Dystrophic EB Autoimmune Disease Bullous pemphigoid Ocular cicatricialpemphigoid Cicatricialpemphigoid EB acquisita *also known as BP180 or Type XVII collagen *EB = EpidermolysisBullosa Protein Xerosis (dry skin) Mechanism Less flexible stratum corneum 1. Malnutrition 6.non-Herlitz Junctional EB with pyloric atresia Junctional EB. Wetting-drying 3. hypoxia) Microchimerism with fetal cells Scleroderma Unknown Calcifications (dermis) Hardening Sclerodactyly Spotted pigmentation Loss of compliance &elasticity >fibroblast . CKD. Histamine (inflammatory) 2. Uncoordinated desquamation 3. HypoT4. Detergent 4. Decrease lipids 2. Arid environment 2. Medications (statins) Treatment / Prognosis Minimize exposure Emollient Keratolytics (urea or ammonium) Topical steroids Antihistamines Histology Dermis Protein Ehler-Danlos Syndrome (EDS) T5 Collagen T1 Collagen Mechanism (Type 1 and 2 EDS) Altered collagen fiber size & organization Skin Hyper-extensible Hypermobile joints Distribution Presentation Abnormal healing after trauma Gorlin sign (touch nose with tongue) Cigarette paper scars Vascular (aneurysms or rupture) Uterine rupture in pregnancy Swelling Papularurticaria Laxity Acral Bladder diverticula Hernias Corpulmonale Subsequent death can occur Corkscrew hairs Perifollicular hemorrhage Bleeding gums Loss of strength > collagen Loss of elasticity > elastin Summary Loss of strength > collagen T3 Collagen (Type 4: most severe) Cutis Laxa Elastin Acquired In some families (AD) Acral localized acquired ³Generalized elastolysis´ Fragmentation &lost dermal elastic fibers Scurvy Vitamin C Perifollicular hemorrhage b/c 1. Dehydration Prone to microfissure 1. Higher type 3 collagen in papillary dermis 2. TGF. More dependent on hydroxylation 3. Invasion Appearance Scaly Rough Pruritus Presentation Common (most by 60) During low ambient humidity Factors 1. Genetic 5.Lamellar Ichthyosis (NCIE) X-linked recessive Ichythosis BZD Summary Protein target BPAg2 6 4 integrin Laminin 332 Type VII collagen Epidermis TG1 (keratinocyte transglutaminase) Steroid sulfatase AR: autosomal recessive Defect in cornified cell envelope Scales (plate-like) Erythema Generalized aka Non-Bullous CIE Stratum corneum massively thickened (hyperkeratosis) Stratum corneum massively thickened (hyperkeratosis) Enzyme deficiency (ø cholesterol) Increased in keratinocyte lipids Decreased desquamation Scales (plate-like) No erythema Structural target Hemidesosome-anchoring filament complex Hemidesosome-anchoring filament complex Lamina lucida-lamina densa interface Anchoring fibrils Genetic Disease Junctional EB. Weaker in the absent of vitamin C Progressive fibrosis and vascular destruction Anti-fibrillin antibodies (Choctaw natives) Overstimulated fibroblast (cytokine.

Form continuous tract of pus Mechanism Forms isotonic (not hypotonic) excretion Overstimulation of SNS Skin Abscess-like Linear scars (sinus tract) Treatment Steroid injection Eccrine Cystic Fibrosis Hyperhidrosis Type ø CFTR Skin Distribution Presentation Chloride sweat test Treatment Excess sweating Palm Soles Distribution Presentation Nail Onychomycosis Type Mechanism Mechanical Trauma (manicure) Fungal infection (Trichophytonrubrum) Cuticle infection Skin Detachment Botulinum Toxin A (Botox®): inhibit mAChR Treatment Paronychia . face Unknown cause of irritation Autoimmune process (attack melanocytes) Skin Alopecia (thinning) Distribution Presentation 3 months post-delivery Androgenetic Alopecia ³Male Pattern´ ³Selective´ Alopecia Finasteride (Propecia®) -5AR inhibitor Areata (area) Totalis (scalp) Universalis (all) Distribution Axilla Anogenital Cerumen Breast Presentation Remove irritant Hair grows back usually Alopecia Areata Alopecia (selective) Apocrine HidradenitisSuppurativa Type ³Acne Inversa´ Mechanism Plug of unknown origin within hair follicle 1. pubis. Increased size and involve neighbor follicles 5. Hair loss 4. chest. Aprocrine cell swelling 3. Blocks apocrine gland secretion 2.Skin Appendages Sebaceous Acne Vulgaris Type Comedomal Mechanism Comedo (keratin plug in hair follicle) Block sebaceous glands secretion (antimicrobial) Inflammatory papule (build-up) Bacterial growth in sebum Rupture and cyst formation Skin Black head (open) White head (closed) Erythema Antibacterial&Anti-inflammatory Hormonal Distribution Presentation Comedolytics (thin epitheliumearly shed) Antisebocyte (shrink secretion) Inflammatory Treatment Tretinoiin (Retin-A®) Benzoyl Peroxide Isotretinoin (Accutane®) Benzoyl Peroxide Clindamycin Doxycycline (sub-dose) Spironolactone (offlabel) OCP (estrogen) Treatment Cystic Hair Follicle Telogen Effluvium Type ³Pregnancy´ Mechanism Increased hair thickness during pregnancy All hair enters cycle at same time Hair loss due to hair growth (shedding) 5-DHT (5 -reductase converts from testosterone) Paradoxical increase in axilla.

Cytokine overproduction Loss of barrier defense Xerosis (dry skin) Crust (infection) Pruritis Vesicular Lichenification Pigment Symmetric Skin folds (antecubital) (popliteal) Flexures Face Elbow Knee Scalp Trunk Atopic Triad (associated with) 1. Host (GVHD) Drug Eruption Tumor (CD4+ Th2) Mycosis fungiodes (classic) Sezary syndrome (erythrodermic) De novo (tumor only stage) Patch-Plaque-Tumor Red Scale Pruritus Macule / Papule Blistering Erythema Papular Erythema Purpura White patches Irregular shape Wheal Erythema Edema Pruritus Progression Diffuse High CD8/CD4 better prognosis (CD8 has antitumor effect) Monoclonal T cells Abnormal lymphocyte Epidermotropism Transplant Donor CLA+ T cells Cyclosporine Polyclonal T cells Normal lymphocyte Many Erythema multiforme (EM) Toxic epidermal necrolysis Cutaneous vasculitis Melanocytes destroyed Generalized Trauma area Vitiligo Autoimmune Urticaria (³hives´) Mast cell Mast cell degranulation Histamine release Lasts less than 24 hours Non-cellular infiltrate Dermis .Skin Immune System Immune Allergic Contact Dermatitis (ACD) Stimulus Allergen (mild chemical) Hapten (binds proteins to make antigenic) Chemical Mechanism Delayed-Type Hypersensitivity 1. Proliferate in situ (re-exposure) Direct cellular injury No immunologic memory Appearance Vesicles Papule/Plaques Erythema Edema Pruritus Distribution Geometric! Linear (ivy) Nickel jewel Generalized Presentation Often no reaction at first exposure Delayed reaction Severe: general cutaneous reaction Treatment / Prognosis Histology Spongiolysis (Epidermis) = fluid accumulation Irritant Contact Dermatitis (ICD) Atopic Dermatitis (AD) Local Reaction at first exposure Immediate (minutes to hours) Dose related Spongiolysis (Epidermis) Often inherited: øfilaggrin ³eczema´ ³itch that rashes´ Th2 predominant (IgE. Sensitization(LC and CLA-T) 4. Tacrolimus. Pimecrolimus 2.S. CD4. Allergic rhinitis Common onset in childhood Higher risk of cutaneous infection (HSV. IL-23: self-proliferation Streptococcus A infection Plaques Scale (hyperkeratotic) Salmon-color Erythema Demarcated Ustekinumab (ø IL-23 receptor) Cyclosporine BMT for other reason (curative) Acanthosis (Epidermis) Parakeratosis (hyperkeratosis) Bacilli in dermis Foamy macrophages Leprosy (Hansen¶s) M. molluscumcontagiosum) 2% world population Nail involvement common Arthritis in 5% Other:guttate/pustular/erythroderma Constitutionally ill Leonine facies Immigrants to U. Toxic shock toxin (TSST-1) 3. Asthma 2. CLA. CD45RO+. No atrophy Spongiolysis (Epidermis) Psoriasis Minor trauma (Koebner) Th17 1. Superantigens stimulate T cells 2. IL-5. Elicitation (Memory T) 5. Histamine 2. Block T cells 3. IL-22: keratinocyte proliferation 2. IL-10 Systemic immunosuppressants Calcineurin Inhibitors 1.CD8Th2: IL-4. leprae Intracellular MHC I Lepromatous: Th2 (antibodies) Widespread Face Few Tuberculoid: Th1 (cell-mediated) Resistance Cutaneous T-Cell Lymphoma (CTCL) Graft vs. Armadillos in the South Often indolent Early CD8+ antitumor response CD3. eosinophils) Staphylococcusaureus 1. Th1 predominance 3.

Topical or systemic antifungal Yeast / Buds Pseudohyphae Bacterial Cellulitis Organism Staph. aureus Strep. pyogenes (GAS) + other strep species Peaud¶orange Fever Lymphadenopathy Systemic antibiotics Recurrence (destroyed lymphatics) Superficial dermis Erythrasma Corynebacterium Groin Coral-red fluorescence (Wood lamp) Odor Topical antibiotics (erythromycin) TrichomycosisAxillaris Underarm hair MicrococcusKyptococcus Altered cool dry surface +sweat: methane thiol (CH3 SH) Unimpressive host response Direct toxicity Interfere with blood flow Tissue breakdown Toxin cleaves desmoglian 1 Infection at distant site Toxin cleaves desmoglian-1 Exfoliative dermatitis Pits Sulci / Erosions Sole (foot) Rule out tinea with KOH prep Odor Topical antibiotics (clindamycin) Pitted Keratolysis Necrotizing Fasciitis Strep.aureus Not scarring . pyogenes (GAS) Presentation Fever Lymphadenopathy Treatment / Prognosis Systemic antibiotics Histology Deep: Dermis / Fat Erysipelas Strep.Infections Fungal Tineacorporis Organism Dermatophyte Mechanism Keratinases for invasion Manninsdecrease desquamation Appearance Pink-Red-brown Scaly Annular Demarcated Distribution Pedis (feet) Cruris (groin) Scalp Face Presentation Complex toe-web space infection Treatment / Prognosis Topical or systemic antifungal Histology Hyphae on KOH Tineaversicolor Malassezia furfur Hypo/Hyperpigment Papules / Plaques White scale (scrape) Erythema Plaque Beefy red Satellite pustules Mechanism Appearance Red Hot Tender Un-raised Poor demarcation Red Plaque Raised-Indurated Warmth Edema Demarcated Altered cool dry surface Red-Brown Plaque Face Leg Distribution Often in the summer Can be hypopigmented afterwards (substance that bleaches melanin) Topical ketoconazole Topical selenium ³SpaghettiMeatball´ on KOH Cutaneous Candidiasis Candida spp. pyogenes (GAS) MRSA Erythema Vesicles / Bullae Purpura Eschar Bullae Erythema Desquamatization Rapid progression and spread Systemic symptoms Febrile Shock Also produces staph scalded skin Fever Usually infants and young childrenRarely adults with renal disease Antibiotics Surgical debridement High mortality (20%) Subcutaneous tissue Bullous Impetigo Scalded Skin Staph.aureus Staph.

Abscess MRSA Nodules .

Viral Herpes simplex Eczema Herpeticum Organism HSV-1/-2 Mechanism Appearance Vesicles Erythematous base Distribution Grouped Presentation Pain Treatment / Prognosis Anti-virals (acyclovir) Histology Acantholysis Defects in antimicrobial defense due to eczema allow rapid spread of herpes Drug (Common) HSV M. pneumonia Herpes Zoster Poxvirus (MCV) Papules Umbilicated Erythema Dermatome Genitals Trunk Common in children Destructive therapies Inclusion bodies (gram-stain) Acanthosis akaStevens-Johnson Syndrome Erythema multiforme Shingles Molluscum Warts HPV *thrombosed capillaries Papules / Plaques Verrycous Black dots * Biopsy to rule out cancer Destructive therapies Acanthosis .

teeth.g. acne) Hormonal Pan-HypoPituitarism Addison¶s Disease Appearance Chalky-white Hypopigmentation Bronze Hyperpigmentataion Distribution Presentation Secondary adrenal insufficiency Treatment / Prognosis Histology Diffuse Melasma Destruction Vitiligo Mutation Appearance White to pink Depigmentation Appearance Silver-Blue Distribution Patchy Presentation Mouth/Eye/Nose/Hands/Genitals Associated with thyroid disorders Presentation Treatment / Prognosis Light (UV) Histology External Argyria Mutation Silver Mechanism Ingestion of silver Distribution Treatment / Prognosis Histology Around eccrine glands Minocycline Antibiotic Tetracycline antibiotic Blue-Black Scars Black thyroid.Pigmentation Migration Dermal Melanocytosis Mutation (Mongolian spot) Mechanism Arrested melanocyte migration Stuck in dermis AD: autosomal dominant Stem cell factor receptor Critical in melanocyte migration Melanoblast proliferation Melanoblast migration Appearance Blue/Black Hyperpigmentation Distribution Lumbosacral Presentation At birth African and Native American (90%) Can be confused with bruising White forelock of hair (85-90%) At birth Treatment / Prognosis Lighten and disappear with age Histology Piebaldism C-Kit gene White Depigmentation Skin Hair Persist and unchanged with age Waardenburg Syndrome Pax 3 MITF Sox 10 Depigmentation Deaf Heterochromic eyes White forelock Associated with Hirschprung disease Distribution Skin Eyes Hair Presentation Nystagmus Photophobia Diminished visual acuity Increased risk of skin cancer Mental deficiency Epileptic seizures Presentation Immunodeficiency Tyrosine rich diet Low phenylalanine diet Treatment / Prognosis Histology Treatment / Prognosis Histology Production Oculo-cutaneous Albinism (OCA) Mutation I: Tyrosinase II: P-protein III: TRP-1 Mechanism Appearance No Pigment AR: autosomal recessive Lack or reduction of pigment AR: autosomal recessive Lower tyrosine Lower melanin Mechanism AR: autosomal recessive Impaired melanosome transport Fumbled transfer Engulfed by melanophages Mechanism Decreased melanin production Decreased glucocorticoids Adrenal insufficiency Pituitary overcompensation Melanin synthesis increased By estrogen and progesterone Mechanism Autoimmune Destruction of melanocytes Reduced Pigment Minimal Pigment Pale skin Blue eyes Blond-white hair Appearance Hypopigmentation Silvery hair Hyperpigmentation Phenyl-ketonuria (PKU) Transfer Griscelli Syndrome Phenylalanine hydroxylase Mutation Myosin-Va gene RAB27A Inflammation (secondary) Mutation MSH ACTH MSH ACTH Pregnancy Skin Eyes Hair Distribution Diffuse Post-Inflammatory (e. bones. sclera .

Photo-oxidation 2. Cytokines (IL-1. Melanosome number 2. Kinins 3. tans deeply Photo-aggravated Idiopathic Pigmentation . TNF ) 2. Histamine. prostate. Melanin synthesis (new) 3. darker. Redistribution of melanin Delayed (Main) 1.Disease Sunburn Mutation UVB Mechanism Weak epidermal attachment Vessel dilationand permeability 1. altitude Associated colon. MSH Alteration of elastin Reduced collagen Increased T3:T1 collagen Essential for calcium metabolism Mechanism Accumulate and diffuse in dermis Photoactivated by UV AR: autosomal recessive DNA nuclear excision repair Appearance Redness Swelling Pain Blisters Distribution Presentation Treatment / Prognosis Aspirin Indomethacin Histology Necrotic keratinocyte Epidermis UVA Tanning UVA Hyperpigmentation Occurs within minutes UVB Thickening 48-72 hours Photo-aging UVA Tough-Leathery Wrinkles Pigmentation Risk in elderly. Eicosanoids Direct effect on vessels Immediate (Meirowsky) 1. breast CA Presentation Retinoic acid can inhibit MMP (prevent and reversal of aging) Rickets Osteomalacia Photosensitive Porphyria Vitamin D Deficiency Mutation Porphyrin Appearance Blisters Distribution Subepidermal Treatment / Prognosis Histology XerodermaPigmentosa UV Nodules Tumors Sun spots Photo-aging Skin cancer Exogenous UV absorption Sulfonamide Thiazide Lime Lupus CTD Rosacea HSV Polymorphous light eruptions Solar urticaria Vitiligo Albinism Skin Type: I ± always burns. NO. never tans VI ± never burns.

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Risk in fair skin. Hair follicle 2. scaly White. scaly patch Indurated nodule Excision Curettage Radiation Crowding Precancerous Full thickness atypia . Risk in family history 5. nevi) CDKN2A(INK4A) -p16 -p14ARF Melanocyte A: asymmetry B: border irregularity C: color varied D: diameter large E: evolving Amelanotic melanoma Risk of metastasis Survival 99% if early diagnosis Survival 15% if metastasis Third common (3. Risk in organ transplant (decreased immunity andHPV) Locally destructive Very low metastasis risk Mortality rare Palmar / plantar pits Skeletal abnormalities Calcification of falxcerebri Precursor Cancer Second common (20%) 1.Skin Cancers Cancer Basal Cell Carcinoma Precursor lesion None Precursor Cell Progenitor cells 1. Slight M > F 2.5%) 1. Interfollicularepithelium Appearance Pearly papule Telangiectasia Ulcerated-Crusted Pigmented Pink. Risk in organ transplant (decreased immunity and HPV) Low risk of metastasis (5-30%) Malignant Melanoma Multiple (de novo. Most common cancer in 25-29 2. ill-defined Distribution (classic) Presentation Most common (80%) 1. light 3. Risk if many nevi 4. red hair. Heavy UV exposure Excision GDC-0449 (in trial) PTCH (tumor suppressor) Treatment / Prognosis Excision Curettage Radiation Histology (ulceration) (pigmented) (superficial) (subtle) Basal Cell nevus syndrome Squamous Cell Carcinoma PTCH AD: autosomal dominant BCCs Actinic keratosis Keratinocyte Pink. Primarily in Caucasians 2. Median age 68 3.

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