MSS Skin intro Flashcards
What are the 4 layers of the epidermis?
Basal layer
Spinous layer
Granular layer
Cornified layer
Stratum basale
Bottommost layer of the epidermis attached to basement membrane
Contains Stem cells
Stratum Spinosum
Contains most of keratinocytes
Held together by desmosomes ( protein complexes that connect keratinocytes and kertain intermediate filament)
Stratum granulosum
Composed of flattened keratinocytes that are starting to lose their nucleus and cell organelles.
Keratohyalin granules: filled with proteins for formation of cornified envelope (profilaggrin).
Lamellar granules: (odland bodies): contains lipids (ceramides)
Stratum corneum
made up of anucleate cells (corneocytes)
held together by proteins and lipids (filaggrin and ceramides)
Where is the cornified layer the thickest? Thinnest?
Thickest: palms and soles
Thinnest: mucosal surfaces
Describe the process of keratinaization and recognize disorders of keratinization
Cornification: Process of keratinocyte migration and maturation. Starts with SC differentiation–> separation from basement membrane. Flattens out, forms lamellar and keratohyaline granules. Loses cellular organelles and releases granules.
Eventually becomes anucleate corneocyte in cornified envelope and is eventually shed.
Function of desmosomes
Protein complexes that connect keratinocyte and keratin intermediate filament
What layers do UVB and UVA penetrate?
UVB: epidermis and superficial dermis
UVA: penetrates into dermis
Interaction of UV and skin
UVB –> erythema and sunburn
UVA–> tanning and photoaging
Pharmacology of suncreen
Physical blockers: reflect UV radiation (zinc oxide/ titanium dioxide)
Chemical blockers: absorb UV radiation and convert it into heat ( PABA)
What makes up intermediate filaments? How do they assemble?
Keratins (alpha helical proteins) that make up IF. Keratin–> heterodimer–> tetramer–> protofilament–> IF
Pemphigus Vulgaris
Autoimmune blistering disease
Rare & affects elderly
Etiology: autoantibodies against desmosomes (desmoglein 1 & 3)
Sxs: flaccid blisters that turn into erosions
Sites: mouth, nose, genitalia, cutaneous site
Tx: immunosuppresion
Ichthyosis Vulgaris
Autosomal dominant
Etiology: mutations in profillagrin (defective cornified envelope)
Sxs: extremely dry skin, hyperlinear palms, large scales on body
Associated: atopic dermatitis, allergic rhinitis, food allergies, asthma
What is SPF?
Sun Protection Factor: measure of protection against UVB exposure and sunburns
Does NOT measure UVA protection
SPF= MED protected/MED unprotected
When is MED?
Minimal erythema dose: min. amout of UVB that causes skin redness at 24 hours.
What is the recommendation for sunscreen use?
At least SPF 30.
Apply 15 min before sun exposure. Need 1 oz to cover entire body. Reapply every 2 hrs. Avoid sun between 10-4p
Cells of the Dermis
Fibroblasts: Produce and secrete ECM
Macrophage
Endothelial cells: vascular network
Nerves
Sensory receptors
What are Meissner’s corpuscles? Where are they located?
Sense Light touch.
Located: concentrated in palms and soles in the dermal papillae ( under the epidermis)
What are pacinian corpuscles? Where are they located?
sense pressure
Located in weight bearing surfaces, lips, nipples, penis, clitoris (deep dermis and subcutaneous tissue)
Structural compotenents of dermis
Main component is ECM: collagen, elastic fibers and extrafibrillar matrix.
Role of Collagen in skin. What type is most abundant?
Provides structural integrity. Produced by fibroblasts. Type I collagen is most abudant.
When does the proportion of collagen III become more abundant in the skin?
Embryogenesis and wound healing
Role of Elastic fibers. What is it made up of?
Skin elasticity. Made up of fibrillin and elastin
What is the extrafibrillar matrix?
Ground substance: composed of water, electrolytes, plasma proteins and proteoglycans (protein+GAG)
Function of dermis
Provides skin with structure and flexibility, vascular support for skin, immunologic protection, nerve sensation
Collagen structure and synthesis
Triple helix of alpha chains. Gly-X-Y with glycine and proline or hydroxyproline)
RER translation–> modification ( OH, glycosyl), folding–> cleavage of N and C terminals–> assembly and cross-linking with other collagens
Ehlers-danlos
Etiology: mutation that interferes with structure, production, processing or assembly of collagen
Sxs: fragile skin that is very elastic and prone to scarring. Extremely flexible joints, severe scoliosis
Associations: collagen in blood vessels –> rupture of blood vessels, intestines and uterus
Marfan syndrome
Etiology: Mutation in fibrillin (autosoma dominant)
Signs: Tall and thin, long limbs, scoliosis, flexible joints, nearsigtedness, ectopia lentis, striae, arotic dilation or aneurysm, mitral valve prolapse
Would healing
Hemostasis: vasoconstriction
Inflammation: erythema, heat, edema, pain
Proliferation: fibroblasts proliferate and synthesize collagen and MMP
Maturation: inflammatory cells are cleared. Collagen undergoes resorption and deposition to remodel
Structural components of subcutaneous fat
Below dermis ( derived from mesoderm)
Adipocytes: synthesize and store lipids in cytoplasm
Erythema nodosum
Acquired disorder
cause is usually idiopathic but infectious cause is common (Strep), Oral contraceptives, sarcoidosis, IBD, maliganacy can also trigger
Sxs: tender, red nodules that arise on shins that starts as crops that involute)
Morphea
Localized scleroderma: autoimmune acquired disease
Characteristics: sclerosis (thickening of collagen)
Sxs: erythematous; indurated plaques
Associations: more common in females
Systemic Sclerosis
Acquired autoimmune disease
Characteristic: sclerosis
2 types: limited and diffuse systemic sclerosis
Limited: CREST syndrome (Calcinosis cutis, Raynaud, esophageal dysmotility, sclerodactyly, telangiectasia)
Systemic: widespread sclerosis, w/ pulmonary fibrosis, renal failure, GI disease, cardiac disease
Direct Immunofluorescence
Helps detects Ig and C3 ON biopsy specimens. Sample from PERI-lesional skin.
Indirect Immunofluorescence
Detects CIRCULATING antibodies against BMZ in SERUM. Serum is applied to human skin. Antibody complexed to fluorescein conjugated antibody and visualized
Structure of BMZ
Hemidesmosomes
Lamina Lucida
Lamina densa
Sublamina densa
Hemidesmosomes (important proteins)
Attach cell to ECM
BP 230 (BP1)
BP 180 (BP2)= Type 17 collagen: connect basal keratinocytes and cytoskeleton to dermal collagen Type 7 (via laminin 332)
Lamina Lucida
thin, translucent layer
Lamina Densa
Composed of type 4 collagen and laminins 332 (laminin 5): binds to hemidesmosome (integrin a6b4) and to type 7 collagen (NC-1)
Sublamina Densa
Type 7 collagen: anchoring fibrils
Necessary to maintain epidermal-dermal cohesion ( binds to both type I and type IV collagen)
Bullous Pemphigoid (BP)
Autoimmune Bullous dermatosis–> antibodies to BP1 and BP 2 causes subepithelial blisters
Association: primary in eldery
Sxs: TENSE blisters with serous fluid
DIF: linear deposits of IgG and C3 on BMZ
IIF: staining of epidermal side
Mucous Membrane Pemphigoid (MMP)
Autoimmune–> antibodies to BP180 (BP230, integrin B4, laminin 332)
DIP: linear deposits of IgG and C3 in BMZ
IIF: epidermal/dermal staining, dermal side (anti-laminin 332)
Epidermolysis Bullosa Acquisita
Autoimmune bullous dermatosis against Type VII collagen
Sight trauma–> blistering and erosion
Characteried by fibrosis of hands and feet
DIF: IgG and C3 along BMZ
IIF: dermal side
Epidermolysis Bullosa
Mutations in genes of BMZ proteins
Simplex: Keratins 5 and 14
Junctional: laminin 332 and BP180 in BMZ
Dystrophic: Type VII collagen of dermis
