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667 Cards in this Set
- Front
- Back
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What percentage of office visits are for derm complaints?
What percentage of derm complaints are treated by non-dermatologists? |
6%
60% |
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Primary vs secondary lesions in dermatology
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Primary lesions -- initial pathophysiologic alteration
Secondary lesions -- result from the evolution of the primary lesion |
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Macule
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Circumscribed flat area of discoloration
<0.5 cm Inflammatory -- vasodilation Intrinsic pigment -- freckle Extrinsic pigment -- tattoo |
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Patch
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Flat, circumscribed area of discoloration >0.5cm
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Papule
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Circumscribed, elevated superficial lesions, <0.5cm
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Plaque
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Circumscribed, elevated, superficial lesion > 0.5 cm
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Nodule
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Circumscribed, solid, palpable spherical or ellipisoidal lesion
Contains a superficial and deep component Typically >1 cm |
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Wheal
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Plaque subtype
Histamine response Edema, erythema, flare Transient Edema is bound |
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Vesicle
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Circumscribed collection of clear, free fluid <0.5cm
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Bulla
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Circumscribed collection of clear, free fluid >0.5cm
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Pustule
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Circumscribed collection of WBCs and fluid
Variable in size |
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Name some secondary lesions
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Scale
Crust Ulcer Fissure Scar Atrophy |
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Scale
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Excess dead epidermal cells (keratin)
Often produced by abnormal, rapid keratinization |
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Crust
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Collection of dried serum and cellular debris
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Erosion
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Focal loss of epidermis
Sometimes superficial tissue lost as well, but stays superficial |
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Ulcer
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Loss of epidermis and some degree of dermis
Variable in size, depth Heal with scar |
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Fissure
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Linear losses of epidermis/dermis
Sharply defined, abrupt walls |
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Scar
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Abnormal formations of connective tissue in response to damage
Dermal damage necessary Cicatrix |
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Types of scar
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atrophic -- thinned
hypertrophic -- keloid striae -- stretch mark |
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Atrophy
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Depression in the skin resulting from thinning of epidermis, dermis, or subcutaneous fat
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Excoriation
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Erosions caused by scratching
Often in fingernail distribution |
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Comedone
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Plugs of sebaceous and keratinous material lodged in openings of pilosebaceous glands
Closed (white head) or open (black head) |
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Milla
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Small, superficial keratin cysts
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Burrow
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Linear or curvilinear papule housing parasites (ie scabetic mite)
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Lichenification
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Areas of thickened epidermis
Increased prominence of skin lines Can also see scaling, some inflammation |
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Telangectasia
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Dilation of superficial blood vessels
Can have branching pattern, be linear |
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Petechiae
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Circumscribed deposits of blood or blood pigment in skin
<0.5cm Non blanching |
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Purpura
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Circumscribed deposits of blood or blood pigments in skin
>0.5cm Non blanching |
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Diascopy
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Test for blanching with pressure by finger or glass slide
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Complete skin exam
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Look at whole body
Remove make up Don't forget oral mucosa, scalp, nails |
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Derm exam report
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General appearance of patient
Distribution of lesions Arrangement of lesions Configuration or shape Primary lesions Secondary lesions Characteristics -- color and oozing, bleeding, infected, etc Involvement of the mucosa, nails |
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Shave biopsy
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Piece of skin removed with scalpel
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Punch biopsy
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Skin cored out with a punch tool
Cauterize and close with a stitch |
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Skin excision
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Scalpel is used to incise lesion in fusiform shape, down to panniculus, and then base is cut on a straight plane
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Flaps and grafts are used to...
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Close defects from excisions
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MOHS surgery
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Skin cancer excisions on the face
Margins examined immediately Reexcision in not clear |
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What kind of light is LASER used for derm procedures?
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Monochromatic and collimated
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What is LASER therapy used for in dermatology?
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Removal of pigmented lesions, warts, tatoos, cancer, hair, vascular lesions
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Botox
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Botulinum toxin
Prevents pre-synaptic ACh release Flaccid paralysis lasting 3-6 mos Reduces skin furrows caused by muscular contractions by facial muscles Cosmetic Blepharospasm |
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What separates the dermis and epidermis?
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Basement membrane
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Epidermis layers from basement membrane up
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Stratum basalis
Straum spinosum Stratum granulosum Stratum corneum |
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Keratinocytes fnc
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Barrier to prevent water loss, heat loss, infection
Also have role in immune response |
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Melanocytes
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Interspersed with keratinocytes in basal layer
Produce and transport melanin to other cells Stain with S-100 Have dark nucleus and clear cytoplasm |
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Langherans cells
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primary APCs of skin
located in the suprabasilar epidermis Contain Birbeck granule in cytoplasm (tennis racket on EM) Stain with S-100, CD1a HLA-DR positive Have a markedly folded nucleus |
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Aggregate of activated macrophages aka?
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Granuloma
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Apocrine glands
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Found in odor producing regions (axilla, groin)
and breasts, eyelids, ear canal Fnc other than body odor unknown |
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Eccrine sweat glands
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Major glands of temperature regulating sweat
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Sebaceous glands
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Holocrine glands
Uni/multilobular Produce sebum |
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Pilosebaceous unit
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Hair follicle
Erector pili muscle (smooth muscle) Sebaceous gland |
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Three portions of the hair follicle
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Lower
Isthmus Infundibulum |
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Five components of lower portion of hair follicle
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Dermal hair papilla
Hair matrix Hair shaft (medulla, cortex, cuticle) Inner root sheath (cuticle, Huxley, Henle) Out root sheath |
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Dermal microvasculature
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Superficial plexus and deep plexus
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Weibel - Palade body is found only in
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Endothelial cells
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Stratum corneum
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8-15 cell thick layer of
Dead, flat, polygonal cells, tightly packed together |
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Stratum granulosum characteristic
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Basophilic keratohyaline granules
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Stratum spinosum
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Appear to have spines (desmosomes) connecting cells
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Dermis
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Connective tissue layer containing collagen, blood vessels, lymph, nerves, pilosebaceous system, sweat glands
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Structure of dermis
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Papillary dermis
Superficial vascular plexus Reticular dermis |
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Papillary dermis
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Cellular
Each papillae going up to nourish epidermis contains capillary loop, lymph vessel, nerve fibrils plus connective tissue stroma |
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Reticular dermis
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Bulk of dermis
Large bundles of type I collagen, elastin Vertically running blood vessels connect subpapillary plexus with subcutaneous horizontal plexus |
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What's special about dermal blood vessels
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Thicker walls, more muscular than similarly sized vessels elsewhere
Blood can go through or bypass capillary bed |
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Autonomic innervation of the skin
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Cholinergic to eccrine sweat glands
Adrenergic to blood vessels, arrector pili muscles, apocrine glands |
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Where are nerve fibers in skin
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Most common in papillary dermis
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Histology of psoriasis
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Downgrowths of epidermis
Granular cell layer lost Infiltration of PMNs |
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Basal cell carcinoma histology
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Palasaiding cells from epidermis
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Bullous pemphigoid histology
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Subepidermal separation
Eosinophilic infiltrated |
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Pemphigus vulgaris histology
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Suprabasilar split
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Melasma
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Mottle brown hyperpigmentation
Usually in forehad, malar emminences, perauricular, areola Seen with pregnancy and OCPs May be permanent Either stimulation of MSH by estrogens or direct stim of melanocytes |
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Cells seen in skin during drug reaction?
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Eosinophils
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Sweet's syndrome
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Acute Neutrophilic Febrile Dermatosis
Associated with URIs, malignancy, AML Fever, leukocytosis, arthralgias red plaques, papillary dermal infiltrate of PMNs Pseudovesicular/juicy Often goes away with steroids |
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Mastocytosis
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Too many mast cells
Skin ones: Uticaria pigmentosum Teleangectasia macularis eruptiva persistans |
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Sarcoid granulomas
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Non-caseating
Naked- lacking swarm of lymphocytes |
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Vasculitis aka
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palpable purpura
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Vasculitis histology
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Inflammatory cells in vessel wall
Fibrinoid change |
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UV light: significance of wavelengths
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Large wavelength means deeper penetration but less energy
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UVC
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200-290 nm
Absorbed by ozone layer Germicidal Highest energy of UV |
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UVB
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290-315 nm
Sunburns, delayed suntan, cancer Much more tumorogenic than A |
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UVA
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315-400
95% of what reaches earth Not blocked by glass 340-400 UVAI 315-340 UVA II |
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Chromophore
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Light absorbing molecule
Wavelength dependent DNA is most important chromophore for UV light |
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Suntan
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Immediate -- UVA : oxidation and redistribution of existing melanin
Dealyed -- UVB : increase in melanocytes, melanin synthesis/delivery, thicker epidermis |
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Sunburn
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Immediate erythema -- UVA (not really a burn)
UVB - effects peak at 6-24 hours Dsykeratotic or dead keratinocytes on HandE |
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Skin phototypes
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Individuals tendency to burn vs tan
I- never tans, always burns VI- always tans, never burns |
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Skin aging is the result of
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Mostly UVA exposure because of its deep penetration
(so this can happen through glass) |
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Squamous cell cancer risk
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Long term psoralen/UVA therapy
Extensive, continuous sun exposure |
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Melanoma risk
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Blistering sunburns
Intermittent intense sun exposure Fair skinned people near equator |
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Photoxic reaction
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Direct tissue injury to skin
Photoxic chemical + UV exposure Phototoxics: furocoumarins (limes, lemons, celery), bergomot, tar, furosemide, naproxen, cipro, doxy, HCTZ, st john's wort |
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Polymorphus light eruption (PMLE)
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aka benign summer light eruption
Nonscarring, pruritic eruption in skin exposed areas (minutes to hours) F>M, 20-30s Worse in spring, improves over summer |
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Photoexacerbated dermatoses
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SLE
Herpes simplex Porphyria cutanea tarda Psorasis |
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Xeroderma pigmentosa
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Inherited defect in DNA excision repair mechanism
Easily sunburn Early onset skin cancer including melanoma |
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Erythropoietic porphyria
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Mild porphyria
Deficiency in ferrochetalase Photosensitive with itchying and burning sensation |
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Phototherapy
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UVA/UVB(narrow) light exposure results in reduced DNA synthesis and immune suppression
Used in: psoriasis, mycosis fungiodes, vitiligo, atopic dermatitis, graft vs host, pityriasis lichenoides, lymphomatoid papulosis, pruritis, others |
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Sunscreen
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Chemical -- work by absorbing the UV waves (UVB and UVA)
Physical sunscreen -- deflect light, works for A, B Protective clothing |
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UVB DNA damage
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thymidine dimers
pyrimidine/pyrimadone products ROS damage (indirect) Repaired by nucleotide excision repair pathway |
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UVA DNA damage
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Incorporation of oxygen atom in to DNA base
Repaired by base excision pathway |
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What causes intial ertheyma from sun?
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UVA (also B)
vasodilation |
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Tans providing protection from sunburn?
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Yes
Tanning bed tanns (UVA) not as good as natural tans |
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Chronic effects of UV radiation exposure
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Ephelides -- freckles
Solar lentigines Photoaging Skin Cancer |
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Cutis rhombiodalis nuchae
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Deep furrowing of skin on neck
Photoaging |
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Solar elastosis
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Thickened, wrinkled skin
Photoaging Result of build up of abnormal elastin |
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Favre-racouchot syndrome
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Nodules and open comedones from photoaging
Often under or lateral to eyes |
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Poikiloderma of Civatte
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Reticulated red/brown patches with telangectasias
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Photoallergy
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Antigen + UVR --> allergen --> Type IV hypersensitivity
Usually topical exposure Suncreens, fragrances, antibacterials, antifungals |
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Examples of chemical suncreens
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B -- PABA, salicylates, cinnamates
A - benzopenones, dibenzolymethanes, mexoryl |
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Determining SPF
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What is minimal does need for erthyma with/without applying
Assessed when apply 2 mg/cm2 |
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SPFs, is higher better?
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Yes, but
15 - 93% blocked 30 - 96% 50 - 98% |
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Functions of the dermis
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Barrier against water loss
Protection against abrasions, toxins Immune organ (innate and adaptive) Production of active Vit D Sensation Social communication |
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Cell populations in epidermis
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Stem cells -- at tips of rete ridges
Transient amplifying cells -rest of basalis Terminally differentiating cells |
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Desmosomes
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Intracellular adherence points between keratinocytes
Most in granulosum and spinosum |
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Hemidesmosomes
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Anchors at dermal/epidermal jct
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Biochemistry of keratin
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Intermediate filament
Basic and acidic heterodimerize Antiparallel associate yield tetrameric profilament Four of those form final 10 nm filament Give epidermis flexible strength |
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What do keratinocytes make?
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Keratin
Adhesion molecules Cytokines and growth factors |
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Merkel cell
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Neuroendocrine
Ectodermal origin Important in touch |
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T cells of the epidermis
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Dendritic (gamma-delta)
Essential to skin immunity |
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Proteins produced by basalis
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K5
K14 transglutaminase 2 bullbous pemphigoid antigen |
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Proteins in spinosum
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Envoplakin
Periplakin TG1 TG5 desmogleins 2,3,4 |
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Granular layer protein/feature
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Keratinohyaline granules and lamellar bodies
TG3 K1 K2e K9 K10 desmoglein-1 desmocollin-1 |
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Important proteins of the stratum corneum
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Loricin
keratins profillagrin trichohyalin involucrin small proline-rich proteins |
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Cornification
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Process of creating a stratum corneum
Basal layer makes cells, tonofilaments (keratin IFs) Spinosum -- desomosmes connect keratinocytes, tonofilaments become tonofibrils Granulosum -- keratinohyline, lamellar are made/extruded Corneum --dead cells with filaments connecting into matrix, thick membranes, surrounded by lipid layer |
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Keratin structure
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Coiled-coil triple helix
Cystein rich with disulfide bonds giving flexibility/elastic recovery |
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Fillagrin
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Causes aggregation of keratin filaments
Comes at least some from keratinohyaline granules |
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Stratum corneum cell envelope
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Loracrin based thick layer inside cell membrane
Most important linkage made by epidermal transglutaminase Necessary for stability of keratin IF and fillagrin network Involucrin is a connector between this and other proteins |
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Most important element of stratum corneum barrier?
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Lipid layer
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Epidermal kinetics
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Total turnover is 28 days
14 days from basal to corneum 14 days in corneum before shedding |
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Icthyosis vulgaris
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Disease of skin scaling
AD defect in filaggrin 1% of population Spares flexures, accentuate palmar creases Onset during childhood Scale retention is the problem, keratinocyte transit time is normal Associated with atopic states (50%) |
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X-linked icthyosis
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X-linked recessive
Steroid-sulfatase deficiency More severe that vulgaris Flexural areas spared Corneal opacifications - also seen in carrier 1/6000 |
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Icthyosis vulgaris biopsy
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Dense hyperkeratosis with loss of granular cell layer
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X-linked icthyosis biospy
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Dense hyperkeratosis with variable granular cell layer
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Lamellar icthyosis
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AR defect in transglutaminase
1 in 300,000 Thick scale Collodian baby Ectropian, eversion of lips Bacterial colonization common (smell) Rapid transit of keratinocytes Flexures, palms involved |
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Collodian baby
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Generalized erythema
Thick stratum corneum at birth shed shortly later |
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Epidermolytic hyperkeratosis
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AD, 1 in 100,000
Mutation in K1 and K10 Large areas of epidermis shed Formation bullae, vesicles Verrucous scale Rapid epidermal transit time |
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Biopsy in lamellar icthyosis
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Mild/moderate hyperkeratosis
Normal/large granular layer |
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Acquired icthyosis
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Drugs
Systemic disease Malignancy |
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Treating icthyoses
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Vulgaris/xlinked
Hydration Emolliants (petroleum) Keratinolytics (salicylic acid) Lamellar, epidermolytic: Lactic acid Retinoids Antibiotics to reduce infections Antiproliferative agents (methotrexate) |
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Epidermolytic ichthyosis biopsy
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Diagnostic
Marked hyperkeratosis w/ large basophilic keratohyalin granules in thicken granular layer Vaculoated cells in upper dermis |
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What kind of collagen is in dermis?
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Papillary dermis -- III
Reticular dermis -- I |
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Cells in dermis
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Fibroblasts
Mast cells Macrophages |
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Collagen formation
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Alpha chains made in ER
Hydroxylation Glycosylation Formation of trimer, triple heix Exocytosis Cleavage, assembly |
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Ehlers-Danlos syndrome
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Defects in collagen synthesis lead to
Hyperextensible skin, joints Atrophic scars Hyperpigmented plaques Gorlin sign + (touch nose w/ tongue) |
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Keloid
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Excessive scar formation
Spreads beyond confines of scar |
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Hypertrophic scar
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Excessive scar formation that stays within the confines of the scar
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Dermatofibromasacroma protuberans
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Low grade malignant proliferation of fibroblasts
Treat with WLE |
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Morphea
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Localized scleroderma
Indurated plaques |
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Elastin
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Single polypetide chain
B spiral fibril network Networks with fibrillin Allowing for stretch and recoil |
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Cutis Laxa
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Defect in elastin production
AD/AR, acquired Loosely hanging skin, prominent skin folds Hernias, diverticuli, emphysema |
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Pesudoxanthoma elasticum
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AD/AR
Yellow papules from degeneration of arterial elastic fibers leads to occlusion and rupture Seen on neck, flexures Can have ischemia/rupture of GI, urinary tract, cardiac vessels Eye exam - angiod streaks from rupture of Bruch's membrane |
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Grave's disease skin finding
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Pretibial mxyedema from excess mucopolysaccarides
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Histology for keloid
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Thick, cellular bands of collage
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Morphea histology
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Lymphocytes
Increased collagen (replacing fat) |
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Demosomes are made up of?
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Cell adhesion proteins -- cadherins, transmembrane proteins
Linking proteins -- attach to intracellular keratin |
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Desmoglein
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Cadherins
calcium dependent adhesion proteins 1 and 3 are restricted to stratified squamous epithelium Bind to each other to attach neighboring desmosomes |
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Distribution of desmogleins in epidermis
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Dsg 1 is mostly superficial
Dsg 3 is mostly deep |
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Acantholysis
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Breaking apart of keratinocytes
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Disruption of desmosome results in
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Acantholysis
Flaccid, intraepidermal bullae Usually ruptured easily |
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Basement membrane zone function
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Attaches dermis and epidermis
Permeability barrier Important for tissue repair |
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What keratins attach to basement membrane?
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5, 14
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What happens when hemidesmosome or basement membrane zone is disrupted?
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Blistering disease
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Antigen in paraneoplastic pemphigus
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BP180 -- a collagen
Located partially in hemidesmosome and partially in lamina lucida Also the major antigen in bullous pemphigus |
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Lamina lucida
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Most superficial part of basement membrane
Composed of anchoring proteins Weakest portion of basement membrane |
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Salt split test
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Localization of immune reactants in major immunolbulbous diseases
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Lamina densa
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Deep to lamina lucida
Basement membrane proper Type IV collagen |
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Sublamina densa
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Dermal portion of basement membrane zone
Anchoring proteins (type VII collagen) and anchoring plaques |
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Pemphigus vulgaris
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Autoimmune blistering disease
DSG 1 and 3 are antigens Always involves mucosa, 50% cutaneous also |
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Nikolsky
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Pushing on skin lightly results in erosion
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Pemphigus vulgaris epidemiology
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M=F
Any time, but typically 50-60s Jews/Mediterranean ancestry |
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Pemphgius vulgaris scarring?
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Heal with hyperpigmentation, not scarring
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Pemphigus vulgaris natural history
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Presteroids -- death w/in 5 years
Fluid loss Infection Poor nutrition from oral involvement |
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Pemphigus vulgaris histology
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Intraepidermal split
Acantholysis Tombstoning of basal cells |
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Diagnostic techiques for autoimmune bulous disorders
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Skin biopsy for HandE
Skin biopsy for immunoflorescence Serum for indirect immunoflorescence Rarely: salt split immunoflorescence, EM |
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What are you looking for with direct immunoflorescence in autoimmune bulbous disease
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IgM, IgG, IgA, C3
On perilesional skin of patient |
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Indirect immunoflorescence in autoimune bulbous disease
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Using patients serum and another tissue substrate
Like monkey esophagus |
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Diagnosing pemphigus vulgaris
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Direct IgG -- chicken wire pattern
C3 -- in areas of acanthocytosis Indirect -- 80-90% positive especially if advanced Reported as titer |
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Pemphigous vulgaris treatment
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High dose steroids
Immunosuppresants |
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Pemphigus foliaceus
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Superficial variant of pemphigus vulgaris
Antigen is DSG1 only Upper chest, scalp, rarely oral More benign course |
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Fogo Selvageum
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Endemic pemphigus foliaceous
Found in area of brazil ?environmenal allergen |
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Common causes of drug induces pemphigus
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Penicillamine
Captopril |
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Paraneoplastic pemphigus
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Classicaly seen in non-hodgkin's lymphoma, CLL
Usually mucosal |
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What is the most common autoimmune bulbous disorder?
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Bullbous pemphigoid
10x more than pemphigus |
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Bullbous pemphigoid
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Autoimmune
Tense bulae Flexural areas Elderly Itchy Negative Nikolsky |
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Absoe-Hansen sign
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Pressure on an intact bullae makes it expand
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Bullous pemphigoid histology
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Subepidermal blister w/ eosinophils
No acantholysis HandE not diagnostic Florescence shows C3, IgG in lamina lucida |
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Antigens in bullous pemphigoid
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Proteins of the hemidesmosome
BPAg1 and BPAg2 (Collagen XVII) |
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Serum titers in bullous pemphigoid
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Do not correlated with disease
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Treatment of bullous pemphigoid
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Topical steroids if limited
Oral steroids Immunosuppresives Usually clears in 5-6 years |
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Treating pemphigus foliaceous
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Topical steroid may be enough
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Mucous membrane pemphigoid or cicatrical pemphigoid
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Autoimmune against deep basement membrane proteins (laminin 5)
Oral/conjunctival 25% cutaneous Risks of scarring and blindness Treat with cyclophosphamide |
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Does bullous pemphigoid scar?
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No
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Gestational pemphigoid
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Pruitic uticarial wheals on trunk
AKA herpe gestationalis Onset 2 or 3 trimester or postpartum Autoimmune bullous disease |
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Pigmentation development stages
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I - Neural crest cells migrate to skin at 3-8 weeks, remain in basal layer with dedrites extending to 30 keratinocytes
II - Production of melanin begins in last trimester III - |
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Melanosomes
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Small membrane bound-spheres full of melanin
Mature (darken) in cyoplasm |
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Eumelanin vs pheomelanin
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Each melanosome can make either
Made by oxidation of phenylalanine Pheo -- red hair As people age, more more eumelanin |
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Apocopation
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Direct transfer between cells
How melanosomes are transfered into keratinocytes |
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Melanosome grouping in keratinocytes
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After transfer melanosomes are group
Small, grouped together -- fair skin Large, not grouped -- dark skin |
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Melanocytes with aging
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Fewer
But skin color does not change Are remaining ones working harder |
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Non-genetic changers of skin tone
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UVA/UVB -- temporarlity stimulate melanosomes
Hormones - MSH, estrogen |
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Hair pigments?
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Melanocytes of hair follicle
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Congenital Dermal Melanosis
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Sacral spot
Dark area on buttocks Biopsy shows larger number of normal appearing melanocytes in DERMIS Most resolve in childhood Disorder of established epidermal melanin unit |
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Nevus of Ota
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Dermal meloncyte trapping in one of the CNV dermatomes
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Nevus depigmentosus
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Absence of pigment because of failure of melanocytes to aggregate and transfer appropriately
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Piebaldism
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Localized albinism
Rare, congenital patchy absence of pigmentation Associated with heterochromic iridies, deafness, MR |
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Tinea versicolor hypopigmentation
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Fungus produces azaleic acid
Inhibits tyrosinase, a step in the production of melanin |
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Hansen's disease
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Lack of pigmentation is due to decreased melanin production by melanocytes
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Occulocutaneous albinism
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Inherited generalized hypopigmentation
Defect in tyrosinase Photophobia, visual defects, nystagmus common |
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Pityriasis alba
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White excema
Disruption of melanosome transfer |
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Psoriasis and pigmentation
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Can get hypopigmentation if turnover is high
Not enough time for melanosome transfer |
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Lentigenes
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Liver spot
Hyperpigmentation Increase in melanocytes |
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Junctional nevus
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Increase in number of melanocytes in basal epidermis in a localizd area
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Process of hair graying
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Loss of melanocytes from hair follicles
Influenced by age, genetics, sress |
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Chemical leukoderma
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Selective destruction of melanocytes by toxic agents leave hypopigmented patches
Ex hydroquonone derivatives |
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Vitiligo
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Sponatneous loss of melanocytes
Often periorifical areas Treat w/ topical steriods, melanocytes transfer If extensive consider destroying remaining cells |
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Post-inflammatory pigmentation
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Inflammatory dermatoses can stimulate melanogenesis
Dermal macrophages can take up pigment Usually mottle hyper/hypo More common with dark skin Often resolves with time |
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Ephelides
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Freckles
Increased number of melanosomes produced locally Melanocyte number constant |
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Addison's and skin
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Hypocortisol results in increased ACTH and MSH
Diffuse or Blotchy hyperpigmentation with increase in palamar creases, scar pigmentation, mucous membranes, sun exposed skin |
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Idiopathic guttae hypomelanosis
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Multiple drop-like areas of hypopigmentation
Related to sun damage? |
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Treating vitiligo
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Psoralens and light exposure
Psoralens increase size of melanosomes, increase typrosinase activity, promote transfer 50% success at best |
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Vogt-Koyagani Harda
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Acquird uveitis, vitiligo, alopecia, poliosis (white lashes, brows), decreased hearing
Usually in adults (30s) preceeded by viral illness (fever, HA, photophobia) |
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Only permanently regenerating organ?
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Hair
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Where are hair stem cells?
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In the bulge
Along hair stem |
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Layers of hair from inside to out
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Matrix
Medulla Inner sheath (cuticle, Huxley, Henle) Outter sheath |
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Hair/skin angle
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Normally at an oblique angle
Layering effect = protection Facilitates transport of sebum, debris, apocrine sweat Can be changed by arrector pili muscle -- under adrenergic control |
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Three types of hair
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Terminal -- greater than 1 cm
Vellus - less than 1 cm, most abudant Lanugo -- mostly gone at birth, sign of anorexia nervosa |
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Shape of hair shaft
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Round = straight hair
Oval = wavy hair Ellipsoid = curly Triangular = kinky |
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What's different about African American hair?
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Curved hair follicle
Commonly a spiral shaped hair shaft Increased number of melanosomes |
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Hair follicle growth cycle (scalp)
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Anagen -- growing phase - 3-6 year
85% of hair Catagen -- involution phase, lower follicle collapses - 2-3 weeks 3% Telogen -- resting phase, club hair is produced -- 3 months 12% Generally: grows for 3 years, involutes for 3 weeks, rests for 3 months |
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How fast does scalp hair grow?
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0.4 mm/day
1/2 inch/mo |
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How does hair on eyebrows, extremities, trunk
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Grow for 6 months
Rest or 3 weeks |
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Why is hair different lengths on different parts of the body?
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Different lengths of time spent in anagen
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Potential causes of alopecia
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Hair style/care products
Hyperandrogenism Diet Severe illness General anesthesia Hereditary Toxin exposure |
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What to look for on physical exam with alopecia
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Pattern of loss
Inflammation/infection Scarring Condition of remaining hairs |
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Causing of scarring (cicatricial) alopecia
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Primary
SLE Linchen planopilaris Acne keloidalis Dissecting cellulitis Secondary Trauma (burns/xrt) |
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Causes of non-scarring alopecia
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Alopecia areata
Androgenic alopecia Trichotillomania Telogen effluvium Anagen effluvium Secondary syph Loose anagen syndrome Hair shaft disorders |
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Alopecia areta
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Non-scarring alopecia
Well demarcated, patchy loss of hair Autoreactive T cells to hair follicle keratinocytes/melanocytes Variable, spontaneous remissions M=F, children and adults |
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Alopecia totalis
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Alopecia areta variant involving whole scalp
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Alopecia universalis
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Alopecia areta variant involving all hair bearing areas
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Poor prognostics in alopecia areta
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Childhood onset
Widespread involvement Acute onset Ophiasis pattern (wave circumfrentially around head) Onychodystrophy Atopic dermatitis |
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Residual hairs in alopeica areta can look like
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exclamation points
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Androgenic alopecia
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Most common hair loss type in both men and women
Androgen dependent, genetically mediated form of hair loss Increased 5alpha reductase and androgen receptors in scalp leads to miniaturization of hair follicles Hair thinning, decreased density |
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Treatment of androgenic alopecia
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5-alpha-reductase inhibitors (finasteride)
topical minoxodil (rogaine) -vasodilator can stabilize process Hair transplant Scalp reduction |
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Anagen effluvium
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Toxic insult disrupts mitotic and metabolic hair processes
leads to shaft thinning, breakage, failure of formation Shedding 2-4 weeks later Toxins: radiation, chemo, drugs Often total, comes back after cessation |
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Telogen effluvium
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Premature entry to telogen phase
Results in hair loss 3-5 months later Positive hair pull Inciting events: childbirth, fever, diet, surgery, drugs Spontaneous growth in a few months |
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Nutritional causes of telogen effluvium
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Protein/calorie deprivation
Deficiency in biotin, zinc, fe, essential fatty acids |
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Medication causes of telogen effluvium
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Cessation of OCPs
TCAs Anticoagulants (comadin) Betabockers Retinoids Lithium |
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Anatomy of nail
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Free edge
Hyponychium Onchydermal band Nail plate Lunula Eponychium (cuticle) Proximal nail fold |
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What is deep to proximal nail fold?
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Nail matrix
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Nail plate growth
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Synthesized by nail matrix
Thickness proportional to size of matrix Fingernails 0.1mm/day -- 6 mos to grow out Toes -- 0.05 mm/day -- 12 mos to grow out |
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States of increased nail growth rate
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Childhood
Pregnancy Warm weather |
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Onychodystrophy
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Changes in nail plate shape that result in malformed nail
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Nails in psoriasis
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Nail pitting
Oil spots Distal onchyolysis |
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Nails in lichen planus
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Longitudinal ridging and fissuring
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Nails in Darier's disease
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Candy-cane nails
V shaped nicking |
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Clubbing of nails is an indicator of
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Aortic aneurysm
Bronchogenic ca others |
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Yellow nail syndrome is an indicator of
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Lymphedma
Chronic bronchitis Bronchiectasis |
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Lindsey's nails indicate
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Half and half nails
Indicate renal disease |
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Terry's nails indicate
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Mostly white with coloration at top
Cirrhosis |
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Periungal telangectasias indicate
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Autoimmune disease
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Proximal subungual onychomycosis is a sign of
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HIV
Immune suppression |
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Aldrich-Mee's lines are an indicator of
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Midnail horizontal lines
Heavy metal intoxication |
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Beau's lines are an indicator of
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Midnail, horizontal fissures
Toxic insult/chemo |
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Onychomycosis define and pathogens
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Fungal infection of the nail
Pathogens: trichophytum rubrum, epidermophyton floccosum, trichophytom mentagrophytes, scopulariopsis brevicaulis, Aspergillus Fusarium Candida |
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Onychomycosis appearance
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Onycholysis - nail plate/bed separation
Subungual debris Thick Brittle Yellow |
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Types of onychomycoses
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Distal subungual
Proximal subungual -- HIV related White superficial |
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Pigmented stripes on nail could be from
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physiologic variant
often in multiple nails nevus melanoma |
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Hutchinson's sign
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Pigmentation at base of nail with stripe in nail -- melanoma
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Longitudinal melanonychia
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Physiologic stripe of hyperpigmented nail
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Psoriasis
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Immune malfunction causes rapid proliferation of skin cells
Excess cells build up on surface Scaly plaques : itching, discomfort, pain, bleeding |
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Plaque (stable) psoriasis
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Raised, scaly lesions on extensor surfaces
80% of cases |
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Guttate psoriasis
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Small dot-like lesions
Strep infection related |
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Erythrodermic psoriasis
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Intense redness
Inflammation Some scaling Often medication or infection related Can cause loss of water, skin |
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Pustular psoriasis
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Pus filled lesions with some scaling
Often on palms and soles |
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Scale
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abnormally thick, flaky stratum corneum
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Characteristic lesions of psorasis
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Pink lesions with scaly tops
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Psoriasis nail findings
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Pitting
Oil spotting Dystrophy |
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Auspitz sign
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In psoriasis
Pinpoint bleeding where scale is removed 2/2 dilated capillaries and thin epidermis |
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Treatment of psoriasis
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Usually lifelong, so need to rotate between different modalities
Topicals Phototherapy Systemic therapy |
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Topicals used in psoriasis
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Coal tar - toxic to epi cells, anti-inflammatory to PMNs, lymphs
Anthralin Steroids Vitamin D Retinoid |
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Phototherapy in psoriasis
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UVB -- 3-5x week, risks include sunburn, photaging/cancer unlikely
Psoralens + UVA (PUVA) - effective SE: SCCs, photaging Combining with acitretin make more effective |
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Systemic therapy in psoriasis
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Methotrexate
Slows down fast dividing cells Helps with the arthritis too Potential liver tox Cyclosporine Il-2 production inhibitor Renal tox Acitretin Oral retinoid Liver, teratogen, alopecia |
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Biologic options for psoriasis treatment
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Anti-T cell
alefacept, ustekinumab Anti- TNFalpha |
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Enteracept
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TNFalpha inhibitor
Plaque psoriasis, psoriatic arthritis, JIA |
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Alefacept
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T cell inhibitor, bind CD2
Used in plaque psoriasis |
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What is assesed when looking at psoriasis severity?
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Area involved
Erythema, thickness, scaling |
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Pathogenesis of psoriasis
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Proliferation and Inflammation
Proliferation of epidermis with abnormal maturation and keratinization --mitosis above basal layer, short transit time, short cell cycle Vasodilation, increase in mononuclear cells in dermis and epidermis, migration of PMNs form microabscesses |
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Course of psoriasis
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Onset at any age, but biomodal around 20s and 50s
Relapsing course for rest of life |
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Drugs that aggravate psoriasis
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Lithium
Antimalarials Beta blockers Steroid withdrawl Trazadone Terbinafine |
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Seborrheic dermatitis
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Papulosquamous disorder
Related to pityosporum yeast? Facial redness, dandruff |
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Seborrheic dermatitis increased severity with
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Head trauma
Spinal cord injury Parkinsons Stroke HIV |
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Seborrheic dermatitis in adults
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Moist, transparent/yellow greasy scaling papules among red patches and plaques
Scalp margins, central face, presternal, eyelids, paranasal Not well circumscribed Chronic course with season variation |
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Seborrheic dermatitis in infants
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Yellow, greasy, adherent scale
cradle cap Minimal underlying redness Diaper area and axillary are more red Usually self-limiting |
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Pityriases Rosea
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Herald patch
oval, salmon plaque 1-2 cm thin collar of scale inside border 1-2 weeks later numerous similar but smaller lesions with christmas tree pattern Usually clear in a month or two w/o scarring (some hypopigmentation in darker skin) |
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Who gets pityriasis rosea?
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10-35 year olds
After a mild prodrome, URI |
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Treating seborreic dermatitis
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Mild antifungal topically
Anti-dandruff shampoo |
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Lichen planus
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Purple polygonal pruritic papules and plaque
Inflammatory disease of unknown etiology Wickham striae - lacy reticulated Keobner phenomenon -- lesions develop in areas of injury Skin, nails, hair, mucus membranes |
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Koebner phenomenon
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Lesion develop in areas of trauma
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Does lichen planus itch?
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Sometimes
But instatiably |
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Risk with severe oral lichen planus
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3% risk of degeneration of squamous cell cancer
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Lichen sclerosus
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Inflammatory skin disease
Ivory white atrophic lesions Anogenital skin often Women >> Men Increased risk of squamous cell cancer |
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Davener's dermatosis
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Trauma to lower back during payer
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Nevus of ota
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Pigmented lesion around eye that looks blue
Can involve sclera More common in asians |
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Infundibulofolliculitis
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Small papules pierced by hair
Pinpoint papules More common in darker skin Not concerning Typically around trunk |
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What is different about darker skin
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Thicker epidermis
Hair follicle at acute angle More melanosomes, larger melanosomes |
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Skin types
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1-6
Based on reaction to light (not baseline color) |
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How does inflammation look on dark skin?
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Ashy white or gray
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How does redness look on darker skin?
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Purple
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Sarcoid of the skin appearance
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Red-brown "apple jelly" change
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Tinea capitis
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Scalp and hair shaft infection
Person to person transmission Patchy hair loss, scale, broken hairs "Black dots" -- broken hair shafts Kerion - thick scale -- overreaction to tinea |
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How to diagnosis tinea capitis?
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PIuck a hair from affected area and KOH it
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Keloids are more likely in?
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People with darker skin
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Pomade acne
|
Comedones and pustules on temple and forehead
Curved hairs Occurs when pomade drinks onto face |
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Traction alopecia
|
Localized hair loss from braiding, etc
Mechanical loosening of follicles Scarring |
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Dermatosis papulosa nigrans
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Flat, waxy brown papules on cheeks
Variant of seborrheic keratosis Blacks and Asians |
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Pigmented nail bands
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Dark linear banks
More common in darker skin Can be caused by trauma, UV light Must be distinguished from melanoma |
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Erythema multiforme
|
Acute, self-limited eruptive reaction
Targetoid macules but other morphologies possible Infections and medication reactions Spectrum of severity |
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Erythema multiforme histology
|
Inflammation at dermal/epidermal jnc
Dying keratinocytes a few is okay many is a sign of internal organ necrosis |
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Spectrum of erythema multiformae disease
|
Erythema multiforme minor
EM major SJS - not a real thing Toxic epidermal necrolysis |
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Erythema multiforme minor
|
Little or no mucosal involvement
Few systemic signs |
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Most common cause of reccurent erythema mutliforme minor
|
Herpes simplex virus
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Erythema multiforme major
|
Always has mucosal involvement
(stoma, genitals, eys) Widespread skin involvement Systemic symptoms (fever, anorexia, malaise) Labs with hepatitis, nephritis, eosinophilia Often due to meds: anticonvulsants, bactrim/pen multiple treatments |
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What does blistering erythema mutliforme indicate?
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Necrosis of skin--->necrosis of other organs
Need for hospitalization |
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Toxic epidermal necrosis
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Full thickeness epidermal necrosis
Generalized redness with tense bullae, vesicles Thick sloughing of skin Any organ may be affected 5-40% mortality rate |
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Toxic epidermal necrosis pathophysiology
|
Cytoxic T cell mediated
Cell death is apoptotic and mediated by Fas/FasL interactions Perforin and granzyme also involved |
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How to treat toxic epidermal necrosis
|
Admit
Stop any offending drugs ? steroids, probably IVIG Burn unit if there is significant skin sloughing |
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Plamar plantar hyperpigmentation
|
Polymorphus macules or patches
Sharp or indistinct borders Common in black skin |
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Acne keloidis nuchae
|
Chronic progressive keloid scarring
Foreign body reaction Sinus tracts and purulent discharge Nape of neck Much more common in darker skin Excision is treatmetn |
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Pseudofolliculitis Barbare
|
Inflammed pustules, papules, scars
Mechanical irritation Secondary infection Shaving makes worse |
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|
Which skin cancer is more common in darker skinned individuals in the US?
|
Squamous cell
Also acral melanoma |
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Necrobiosis lipodica diabeticorum
|
Red-orange atrophic plaques
Bilateral shins May be painful/ulcerate Associated with DM Treat topcially |
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Granuloma annulare
|
Firm red-violet annular plaques
No scale -- dermal process Dorsal hands and feet Assymptomatic, associated w/ DM Can recur Can make individual lesions go away with injection of steroids |
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Porphyria cutanae tarda
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Inherited blistering disease
Deficiency of uroporphyrinogen decarboxylase Sun sensitive Fragile skin, bullae, erosions Hypertrichosis Urine florescent with woods lamp |
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|
What makes porphyria cutanae tarda worse?
|
Hep C
Alcohol Drugs OCPs |
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What makes prohyria cutane tarda better?
|
Phlebotomy
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Pyoderma gangrenosum
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Inflammatory not infectious
Begins as a small pustle, grows into an ulcer Rolled or undermined border Associated with IBD, gammopathy, RA, lymphoma/leukemia Treat with systemic immunosuppression Often on bilateral legs |
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|
Pruitic uticarial papules and plaques of pregnancy
|
PUPPP
"Itchy stretch markers" Begins as striae --> generalized puritic eruption (abdomen, breasts, buttocks) Third trimester, First pregnancy, resolves with delivery Treat with steroid cream |
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Herpes gestationalis
|
Uticaria --> vesicles/ bullae
Begins in second trimester Can lead to prematurity, fetal demise Immunflorescence shows C3 at basement membrane Can recur with subsequent pregancies |
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|
Acrodermatitis enteropathica
|
Kids
Worsening rash Growth retardation, diarrhea Zinc deficiency Rash is diaper area, face -- patchy red scale, exudate, crust Alopecia |
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When do kids get acrodermatitis enteropathica?
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Neonatal -- if mom's milk is zinc deficient
Weaning -- baby has inborn abnormal zinc absorptoin |
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Pruitic papular eruption of AIDS
|
Dry, red, pruitic papules
Can see eosinophilia on biopsy |
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Skin manifestations of AIDS
|
Many
Papular eruption of AIDS Xerosis Drug eruptions Seborrheic dermatitis Tinea Molluscum Condyloma accuminata Herpes simplex, zoster Thrush Eosinophilic folliculitis Kaposi's sarcoma Bacillary angiomatosis Oral Hairy Leukoplakia |
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Risk factor for developing toxic epidermal necrolysis
|
AIDS
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Colloidian membrane
|
Saran-wrap covering at birth
Respiratory distress, cracks, fissure, temperature instability Idiopathic in 15% Treatment is supportive |
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Harlequin baby
|
Colloidan membrane 10x severity
Almost always fatal |
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Features associated with colloidian membrane?
|
Ectropian - pulled open eyes
Ectlabium -- pulled open mouth |
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Diaper dermatitis
|
Red, itchy rash in diaper area
Caused by irritant: urine and feces Creases are spared, secondary infection common Treat by reducing wetness, toilet training ASAP |
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Infantile seborrheic dermatitis
|
Yellow waxy scale -- involving scalp, face, body folds
Improves by age 1 Concern for HIV when severe Treat with low potency immunosuppresion |
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|
Does infantile seborrheic dermatitis increase risk of adult form?
|
Nope
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|
|
Netherton syndrome
|
Autosomal recessive
Atopic diathesis and hair abnormalities SPINK5 mutations More often in premature/FTT infants Ezcema, erythroderma, icthyosis, short hair Elevated IgG Treat with tacrolimus, pimicrolimus |
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Erythema Toxicum Neonatorum
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Benign, transient pustular eruption
Full term infant Last 2-3 weeks Eosinophilia on biopsy Usually spares palms/soles More common with darker skin Reassurance |
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Neonatal Candidiasis
|
Erythema, pusules
Maternally transmitted Usually just a skin infection Can also be hepatosplenomegaly, microcephaly |
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|
How to treat neonates with scabies?
|
Vasoline occulsive treatment only
|
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|
Cutis marmarata
|
Transient mottling that resolves with warm
Exaggerated vasomotor response Seen in healthy infants If mottling persists -- downs, trisomy 18, hypothyroid, neonatal lupus, spetic shock |
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|
Henoch-Schonlein Purpura
|
Small vessel vasculitis
Usually in kids following a URI IgA complexes in post-capillary venules Palpable purpura, joint and abdominal pain, glomerulonephritis |
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|
Treating Henoch-Schonlein Purpura
|
NSAIDs for joint pain
Corticosteroids for renal, GI |
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Urticaria pigmentosum
|
Cutaneous mast cell disease
Itchy brown spots Blister with rubbing 3-9 month onset Can involve liver, spleen, GI tract, bone Antihistamines can help |
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|
Pyogenic granuloma
|
Bleeding exophytic dome-shaped papules
Proliferation of capillaries in response to trauma Head, neck, fingers Rapidly grown, fall off, regrow Treated with excision |
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|
Adenoma sebaceum
|
Reddish papules on face in butterfly distribution - angiofibromas
Features of tuberous sclerosis |
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|
Why do you not just excision thyroglossal cyst?
|
Make sure that's not all the thyroid tissue someone has
|
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Nevus
|
Benign circumscribed overgrowth of cells that are normal components of the skin
|
|
|
Indradermal nevus
|
Raised, flesh colored nevus
Melanocytes in nests Only in dermis Typically on head/neck |
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Compound nevus
|
Raised brown lesion
Melanocyte necests in dermis and deep epidermis Typicall on trunk |
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|
Junctional nevus
|
Melanocytic nests found in epidermis only
Flat, dark lesion Typically on legs |
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|
Lentigo
|
Small circular to oval brown macule
Elongation of rete with increased pigmentation No melanocyte nesting Not a nevus |
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|
Halo nevus
|
White halo around nevus
2/2 infiltrating lymphocytes Most often idipathic But increased in frequency if there is malignant melanoma present, vitiligo Common in teenagers on back |
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|
Spitz nevus
|
Spindle and epitheloid cell nevus
Pink and brown papules Common on head and neck Benign vs uncertain malignant potential |
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Blue nevus
|
Solid blue macule or papule
Due to spindle shaped cells in dermis |
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|
Dermal melanocytosis
|
Blue babies
Ribbon like melanocytes trapped in dermis because of migration problem Usually regresses by age 3-5 More common in darker skinned |
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|
Congential melanocytic nevus
|
More likely to have hair growing out of it
|
|
|
Hemangioma of infancy
|
Vascular nevus
Red Present in first days of life, grows for 12 months, stable for 1-2 years, then starts to involute 5x more common in girls |
|
|
Where are hemangiomas of infancy usually?
Where is worrisome? |
Head and neck (80%) also liver
Worry in beard area (swallowing), eye |
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|
What distinguishes hemangiomas from vascular malformations genetically?
|
Glut-1 positivity
|
|
|
PHACES syndrome
|
Posterior fossa malformation
Hemangioma of cervicofacial region Arterial abnormalities Cardiac abnormalities, coarction of aorta Eye abnormalities Sternal or supraumbilical raphe |
|
|
PELVIS syndrome
|
Perineal hemangioma
External genital malformation Lipomyelomeningocele Vesico-renal abnormalities Imperforate anus Skin tag |
|
|
Vascular malformations
|
Anomalies of blood/lymphatics 2/2 abnormal devo
Classified by vessel type/flow Do not spontaneously resolve |
|
|
Sturge Weber syndrome
|
Sporadic
V1 capillary malformation Seizures Glaucoma Developmental delay |
|
|
Nevus araneus
|
Spider angioma
Failure of sphincteric muscle around a cutaneous arteriole Dot is arteriole, spider legs are small veins In childhood--resolve spontaneously Also in high E states: OCP, pregnancy, liver disease |
|
|
Cherry angioma
|
aka de Morgan spots, cherry hemangioma
Benign proliferation of capillaries Do not blanch Increase in no, size w/ age Eruptive -- may signal internal malignancy |
|
|
Epidermal nevus
|
Hamartomas characterized by hyperplasia of epidermis, adnexal structures
Linear epidermal nevi follow Blaschko's lines |
|
|
Nevus sebaceus
|
Yellowish plaques of increased sebaceous glands
Scalp and face Present at birth, grow and become verrcous at puberty, can develop tumors in adulthood Syringocystadenoma papillferum, basal cell carcinoma |
|
|
Becker's nevus
|
First appears as irregular pigmentation (by age 20)
Gradually enlarges, becomes thickened and hairy Upper arm, torso Men |
|
|
Life cycle of a nevus
|
Active growth : birth through young adult (n=12-20)
Mature phase -- adulthood Regression -- old age Expect changes during puberty and pregnancy, but be vigilant |
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Seborrheic keratosis
|
Proliferation of keratinocytes
Etiology unknown Occur with aging If symptomatic electrocautry, freeze, excise |
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Achrochordon
|
Skin tag
Common benign skin polyp Usually in intertriginous areas Increased in pregnancy, obesity |
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Epidermal inclusion cyst
|
Occluded pilosebaceous unit
Cyst filled by the production of keratin Completely excise I and D if secondarily infected |
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Gardner's syndrome
|
AD
Multiple epidermal inclusion cysts Intestinal polyps with high malignant potential prophy colectomy |
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Pilar cyst
|
Nodular lesion of scalp
Derived from follicular cells Strong familial tendency Treat symptomatic lesions with excesion, particularly if proliferating |
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Dermatofibroma
|
Firm papule
Overlying erythema or hyperpigmentation Dimple with palpation May arise from trauma, insect bite Usually benign, excise if symptomatic, or watch |
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Actinic keratosis
|
Premalignant skin lesion
Most common in sun exposed areas Treat with superficial destruction liquid N2, 5FU, curettage |
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Squamous cell CIS
|
AKA Bowens
Erythema , scaling, thin plaque Histologic changes limited to epidermis |
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Squamous cell cancer in situ on trunk possible etiology?
|
Arsenic exposure
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Squamous cell cancer of the skin
|
Arises from keratinizing epidermal cells
UV light exposure is primary etiology Metastatic potential is worse greater than basal cell but less than melanoma Worse prognosis in immunocompromised |
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Squamous cell cancer of the skin presentation
|
Single enlarging nodule
Frequently painful Patient > 60 |
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Squamous cell cancers with higher metastatic potential?
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Lips and Ears
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Keratoacanthoma
|
Low grade squamous cell cancer
Rapid growth but low metastatic potential In sun damaged skin Dome shaped, volcano appearance with central plug |
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Basal cell carcinoma
|
Arise from stem cells (basal cells) of epidermis
Stroma dependent Rarely metastasize Local destruction UV damage is key to pathogenesis both in DNA damage and allowing tumor growth |
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Basal cell carcinoma risk factors
|
Genetics:
Fair skin Defects of genetic repair Basal cell nevus syndrome Sun Xray Arsenicals ingestion Chronic inflammation |
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Basal cell appearances
|
Nodular
Pearly, telangiectasic papule May have pigment Superficial Erythematous, scaly, thin plaque Morpheaform/sclerosing Whitish, scar like Cystic Translucent, gelatinous papule |
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Treatment of basal cell carcinoma
|
Depends on the type
Excision Radation Cryo MOHS for big lesions in sensitive areas |
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Melanoma incidence is ...
|
Increasing
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Risk of developing melanoma in lifetime
|
Males: 1 in 37
Females: 1 in 56 |
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Melanoma Risk for African Americans and Hispanics
|
1/10 of caucasians, but still a risk
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Most common cancer in women 25-29?
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Melanoma
Second most common in 30-34 |
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Who finds the melanoma?
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Patient - 50%
Family member - 25% MD - 25% |
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ABCDEs of melanoma
|
Assymetry
Border irregularity Color variation Diameter > 6 mm Evolution -- change in lesion |
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Colors of melanoma
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Red -- inflammation
White -- focal regression Blue -- deep melanin pigment |
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Non-ABCDE suspicious factors for thinking this might be a melanoma
|
Inflammation around nevus
- little red riding hood Bleeding or crust in the absence of trauma Ulceration Pain or itch Heightened awareness of lesion |
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Clinical patterns of melanoma
|
Superficial spreading - 70%
Nodular 10% Lentingo maligna Acral lentiginous Amelanocytic -- 2% |
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Superficial spreading melanoma
|
Radial growth phase prior to invasion
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Nodular melanoma
|
Rapid growth from the outset
Most common in 60s |
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Lentigo maligna melanoma
|
Long horizontal growth phase
Sun exposed skin of the elderly |
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Most common site of melanoma in women and men?
|
Women - legs
Men - trunk |
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forgotten melanoma sites
|
Periungual
Mucosal Ocular |
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Melanoma predisposing factors
|
Fair skin
Sunburns in childhood Acute, intermittent exposure to UV Cumulative sun exposure Tanning salon use Treatment with UVA/Psoralen Higher socioeconomic status Family/personal history of melanoma Many nevi, large nevi Immunosuppression |
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How many melanomas arise out of pre-existing nevi?
|
One of four
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Risk with large congenital nevi (>20 cm)
|
Lifetime risk of melanoma 5-20%
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Genes implicated in the pathophysiology of melanoma
|
CDKN2a (INK4a/ARF)
Tumor suppressor gene encoding two cell cycle regulating proteins p16, p14ARF Associated with familial melanomas, nevi syndrome BRAF, NRAS, MC1R |
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When to think a patient with melanoma might have a p16 mutation?
|
Numerous large, irregular nevi
Strong family history of melanoma and pancreatic cancer |
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What do you do if you suspect something is an melanoma?
|
Excise the whole thing
No biopsying |
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Breslow depth
|
measured from granular layer to deepest invasion of melanocytes
Prognostic |
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Treatment success in melanoma
|
Appropriate surgical excision will cure 90% of Breslow <1mm cancers
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Treating melanoma
|
Surgical excision with margins
(1 cm if 1 mm deep, 2-3 if deeper) Sentinal node Chemo -- not great Immunotherapy INF alpha |
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Percentage of adults with acne?
|
12% of women, 3% of men
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Percentage of 12-24 year olds with acne?
|
85%
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Four factors in acne pathogenesis
|
Hyperproliferation/abnormal differentiation of keratinocytes
Increased sebum production Infection with Propionobacterium acnes Inflammation |
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What's wrong with keratinocytes in acne?
|
Abnormal desquamation
-- usually shed into follicular lumen and extruded, in acne are retained and accumulate in upper portion of follicle |
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Process of acne inflammation
|
Comedo expansion 2/2 keratinocyte accumulation and expansion
Comedone wall rupture from increased force Inflammatory rxn to extruded immungenic sebum and keratin |
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Propionobacterium acnes
|
Gram pos, non-motile rods
Found deep w/in sebaceous follicles Inflammatory response via TLR2 Makes lipase which helps comedone rupture |
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Hormonal influence on acne
|
Hormones control the secretion of sebum
T and DHT (more), DHEAS |
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Clinical features of acne vulgaris
|
Non-inflammatory or inflammatory
Non: open and closed comedones Inflammatory: papules, pustles, cysts Graded mild-mod-severe |
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How long does it take for acne treatment to work?
|
6-8 weeks and it can get worse before it gets better
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Topical retinoids
|
Comedolytic -- promotes normal desquamation
Anti-inflammatory -- inhibits WBCs, release of pro-inflam cytokines, immunomodulation Helps other agents penetrate |
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SEs of topical retinoid
|
Irritation
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What are some topical retinoids
|
Tretinoid
Adaplene Tazarotene |
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Benyzol peroxide
|
Topical anti-acne
Antibacterial Antiinflammatory --use w/ antibiotics (limits resistance) SE: drying, itching |
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Topical antibiotics for acne
|
Clindamycin
Erythromycin Antibacterial and anti-inflammatory Well tolerated for mild-mod inflammatory acne Don't use alone because of resistance |
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When to use systemic treatment for acne?
|
Mod/severe
Inflammatory disease w/ failure of topicals Chest, back, shoulders Scarring lesions |
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How long to treat with systemic in acne?
|
3-6 months
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Systemic antibiotics for acne
|
Tetracylcine (cheap, but on empty stomach), minocylcine (penetrates better), doxycylcine
--Sun sens, GI upset, staining of teeth, gums, scars, Erythromycin, clindamycin, trimethoprim/sulfamethoxazole |
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Isotretinoin
|
Treatment of severe acne
Prohibits maturation of basal cells in sebaceous gland -- 90% reduction in sebum (no P acnes can live, keratinization normalizes) |
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|
Isotretinoin SEs
|
Dry skin, lips, mucosa
Teratogenic Hepatotoxic -- avoid alcohol |
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Isoretinoin efficacy
|
At 3 years after treatment
40% clear skin 18% topicals 25% oral abx 20% isoretinoin |
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Acne variant treated with isoretinoin
|
Gram neg folliculitis
Inflammatory rosacea Acne fulminans Hidradenitis supperativa |
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Clues that this might be hormonal acne
|
Flare around menses
Chin, lower cheek involvement Signs of excess androgens |
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Diet and acne? What to avoid?
|
High glycemic index
Milk |
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|
Acne complications
|
Scars
Hyperpigmentation |
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Neonatal acne
|
20% of healthy newborns
Facial papules or pustules Cheek and nose Causes: maternal hormones? Malessezia? Resolves within months |
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Infantile acne
|
Persists beyond neonatal period or starts after 4 wks
More comedonal than neonatal Resolves by 1-2 Treat with topicals or orals |
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Childhood acne
|
Continued from infantile or starts >2 years
M>F Papules, pustules, comedones, nodules Positive family history |
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Acne fulminans
|
Rare type of severe cystic acne
Abrupt onset -- more shoulders, back than face Systemic: fever, leukocytosis, polymyalgia, erosive arthritis, osteolytic bone lesions (clavicle, sternum) Teenage boys |
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Acne fulminans treatment
|
Aggressively
Prednisone 4-6 weeks Isotretinoin Intralesional steroids |
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Acne conglobata
|
Eruptive severe nodulocystic acne without systemic symptoms
Back, buttocks, chest, face, anterior shoulders Often adolescent males Treat with steroids, then isotretinonin |
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Acne mechanica
|
Secondary to repeated mechanical obstruction of pilosebaceous outlet
Helmet acne |
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Acne excoriee
|
Picker's acne
Young women Typical acne is compulsively excoriated Leads to scaring Sign of depression, anxiety, OCD Treat: SSRI, behav mod |
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|
Drugs that induce acne
|
Androgens
Corticosteroids Phenytoin Corticotropin Lithium Isoniazid Iodides Bromides EGFR- inhibitors |
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Gram negative folliculitis
|
Occurs in pts with inflammatory acne treated with long term tetracyclines
Pustules from nares or deep lesions Culture for Klebsiella, E Coli, Enterobacter, Proteus |
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|
Treating gram neg folliculitis
|
Isotretonin
Amoxicillin if not tolerated |
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Hidradenitis suppurativa
|
Acne inversa
Recurrent sterile abscess formation Painful red nodules that can rupture and scar Axilla, inguinal, perineal W>M |
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Hidradenitis suppurativa etiology
|
Nothing proven causative
Friction, smoking, obesity, irritants, immunologic dysfunction |
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Hidradenitis suppurativa treatment
|
Cure is rare
Drainage not helpful Treat with topical antibiotics, steroids Isoretinoin Infliximab, finasteride Surgical excision is best at not recurring |
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Rosacea
|
Persistant erythema +/- acneiform papules on central face
Telangectasias, flushing, erythematous papules, pustules Cheeks/nose>brow/chin |
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Rosacea etiology
|
Vascular hyperreactivity
Hyperirritable skin Teleangectasia and fibrosis are 2/2 chronic vasodilation, edema, lymphatic compromise |
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Who gets rosacea?
|
Light skinned women 30-50
Rhinophymatous changes-- men |
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Rosacea -- erythematotelangectatic
|
Prolonged flushing >10 min
Reacts to stimuli (stress, alcohol, spices, exercise, cold, hot) Burning or stinging sensation common |
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Rosacea -- papulopustular
|
Striking red face with erythematous papules and pinpoint pustules
Flushing, but not much irritation |
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Rosacea - glandular/phymatous
|
Edematous papules, pustules, nodulocystic lesions
Rhinophyma is most common Less flushing, but persistant edema Men history of adolescent acne |
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Ocular rosacea
|
Ocular involvement occurs in 50%
Can be first sign Gritty, stinging, burning, foreign body sensation Can cause blepharitis, conjunctivitis, chalazion, keratitis, iritis, episcleritis |
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Treating ocular rosacea
|
Tetracycline antibiotics
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Treating papulopustular rosacea
|
Topical metronidazole, sulfa, azelaic acid, benzyol peroxide
Oral tetracylcines |
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Treating erthyematotelangectatic
|
Pulse dye laser
Foundation |
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Treating glandular rosacea
|
Topical metronidazole, clindamycin, sulfa, azelaic acid, benzyol peroxide
Oral tetracylcines Isotretinoin for severe cases |
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Periorificial dermatitis
|
Acniform papules and pustules around eyes, mouth
Burn, but do not itch Associated with inhaled or topical steroid use Treat with tetracyclines, stop steroids, non-steroid topicals |
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Eczematous dermatitis
|
Immunologic response of skin to antigens
Mainly type IV Involve T and B cells interacting Vasoactive factors released have inflammatory, destructive, proliferative effects on skin |
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Clinical appearance of acute contact dermatitis
|
Erythema
Edema Vesicles Oozing |
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Pathologic appearance of acute contact dermatitis
|
Separation of epidermal cells by serum (spongiosus)
Dilated superficial capillaries Bound serum in dermis Serum reaching the surface of epidermis |
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Clinical appearance of subacute contact dermatitis
|
Crust
Scale |
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Pathologic appearance of subacute contact dermatitis
|
Dried serum, cellular debris on surface of epidermis
Excess keratin |
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Clinical appearance of chronic contact dermatitis
|
Thickening (lichenification)
Hyper or hypopigmentation |
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Pathologic appearance of chronic contact dermatitis
|
Epidermal thickening (acanthosis) w/ elongation of rete ridges
Stimulation/inhibition/destruction of melanocytes |
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|
Allergic contact dermatitis
|
Cell damage resulting from cellular (type IV) immune reaction to an antigen
Acquired through exposure |
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|
Allergic contact dermatitis risk factors
|
Increased with pressure, heat, H20 with exposures
Decreased wtih atopy |
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|
Allergic contact dermatitis occupational importance
|
30% of occupational skin disease
|
|
|
Refractory period in contact dermatitis
|
Time from first exposure to sensitization begins
Highly variable |
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|
Incubation period in contact dermatitis
|
Time from beginning of immunologic response to allergen to first clinical manifestation of allergy
10-30 days usually |
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Reaction time (eliciation) in contact dermatitis
|
Time from contact of allergen w/ sensitized skin to reaction
4-24 hours |
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Persistance of sensitivity in contact dermatitis
|
Usually for life
No known way to desensitize from this type of allergy |
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|
Keratinocyte involvement in contact dermatitis
|
Stimulation of their toll-like receptors results in inflammatory mediators, necessary second signals
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|
What does contact dermatitis look like?
|
Initial erthyema progresses to intense inflammatory rxn with papules and vesicles
Usually pruritic Pattern is indicative of exposure |
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|
Severity of reaction in contact dermatitis determined by?
|
Concentration and length of exposure
|
|
|
Treating contact dermatitis
|
Avoidance
Cold compresses Topical/systemic steroids Antihistamines Barrier creams |
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Irritant dermatitis
|
Cell damage develops on any exposure of sufficient concentration and duration
|
|
|
Risk factors for irritant dermatitis
|
Cold, windy weather
Low humidity High heat, sweat Friction/injury Atopy Biomodal age Fair skin |
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|
Irritant dermatitis occupational impact
|
70% of occupational skin complaints
|
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|
Pathophysiology
|
Reactions induced by binding to TLRs of keratinocytes
|
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|
Clinical picture in irritant dermatitis
|
Early dry skin w. fissure
Red papules, vesicles with oozing and crusting Lichenification and further fissuring if chronic |
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|
Differentiating between irritant and contact derm?
|
Patch test negative in irritant
Both are ezcematous dermatitis |
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|
Treating irritant dermatitis
|
Protection from irritant
Compresses for acute relief Topical/system steroids, immunosuppressants, antihistamines for pruritis |
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|
Contact vs Irritant in immune system
|
Contact -- most adapative, small doses of antigen
Irritant -- innate, large doses of antigen, skin barrier break is the initiator |
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|
Type of antigen in contact dermatitis
|
Low molecular weight
Lipid soluble Chemical reactivity Hapten |
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|
Keratinocytes effect on Langherans cells
|
Chemical stimulus activates keratinocytes
They make: TNFalpha - encourages migration of langerhans cells Il1, GMCSF -- maturation of langerhans cells |
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|
Baboon butt
|
Initial skin desensitization
Subsequent oral exposure Weird pattern of erythema -- perianal, axilla, drawers pattern |
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|
Skin features of SLE
|
Malar rash
Discoid rash Photosensitivity |
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|
Cutaneous lupus
|
Acute - 90% have systemic disease
Subacute - 50% Chronic - 10% |
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|
Acute cutaneous lupus
|
Malar rash
Most common rash in setting of lupus Flare of skin disease may represent general disease flare Often photosensitive anti-dsDNA |
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|
Subacute cutaneous lupus
|
Widespread scaly rash on arms, chest, upper back, sometimes face
Marked photosensitivity anti-Ro, anti-La 50% with systemic involvement Can be drug induced: HCTZ, NSAIDs, terbinafine, diltiazem |
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|
Chronic cutaneous lupus
|
"discoid lupus"
Skin disease Risk of progression to SLE - 5-10% Favors face, scalp Scarring is a problem |
|
|
Treating cutaneous lupus
|
Hydroxycloroquine
risk for retinal tox Sun protection Topical steroids Systemic immunosuppression Retinoid Thalidomides |
|
|
Skin lesions in dermatomyositis
|
Heliotrope rash
Purple facial rash that does not spare eyelids Joint rashes in hands: Gottron's papules small violaceous flat papules on extensor hands Gottron's sign: Symmetric, scaly, erythematous rash over extensor hands Erythema and hyperkeratosis in hands (mechanics hands) Peri-ungual telangectasias Photosensative scaly rash Vasculitis/calcinosis in kids |
|
|
Severity of rash in dermatomyositis
|
Does not correlate with severity of muscle involvement
Rash can be a sign of recurrence in cancer patients |
|
|
Treating skin in dermatomyositis
|
Topical corticosteroids
Antimalarials |
|
|
Morphea
|
Skin limited scleroderma
Inflammatory lesion that expands Initially lilac or hyperpigmented Then sclerotic, white May involve fat w/ loss of subq Involvement of joints may impair fnc |
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|
Treating morphea
|
Does not usually work
Disease uses progresses for several years then regresses Try: steroids, PUVA, VitA and D, immunosuppression |
|
|
CREST
|
limited sclerodera
Calcinosis cutis Raynaud's Esophageal dysmotility Sclerodactyl Telangectasias anitcentromere antibody |
|
|
Skin symptoms of systemic scleroderma
|
Diffuse hyperpigmentation
Skin thickening Teleangectasias Sclerodactaly Digital ulcers Raynaud's Diffuse skin involvement carries a worse prognosis |
|
|
How to treat systemic scleroderma skin disease
|
Poorly responsive
Try immunomodulation Calcium channel blockers for Raynaud's IV alprostadil (PGE1) for refractory Reynaud's |
|
|
What used to kill people with scleroderma? and now?
|
Renal crisis used to, but ace inhibitors have improved that
Now its more likely pulmonary |
|
|
Amyopathic dermatomyositis
|
Skin features of dermatomyositis without the muscle involvement
|
|
|
Most common skin pathogens in the immunocompetent?
|
Staph and Strep
|
|
|
What precedes most skin infections?
|
Breech of skin barrier
|
|
|
Appropriate antibiotics for most skin infections?
|
First generation cephalosporins
Penicilliase resistant penicillins |
|
|
Normal skin flora
|
Helps keep other infections away
Staph epidermidis Corynebacterium -- intertrignious areas Propionibacterium - sebaceus glands Gram negs -- axilla, groin Yeasts (Pityrosporum sp) on skin rich in sebaceous glands (chest, upper back) |
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|
Impetigo
|
Most common skin infection kids
Staph aureus, group A strep Nonbullous and bullous Heat, humidity, overcrowding predispose Direct contact, autoinnoculation (nares) |
|
|
Impetigo clinical appearance
|
Honey colored crusts on erythematous base
Often around nose and mouth May be preceeded by skin trauma Systemic symptoms rare |
|
|
Impetigo and atopic dermatitis
|
Secondary impetigo is a common complication
--abnormal skin barrier Staph can act as a superantigen and worsen the atopic dermatitis |
|
|
Bullous impetigo
|
Large, flaccid bullae
Blisters leaving shallow erosions Result of staph exfoliatin |
|
|
Treating impetigo
|
Mild cases-- topical muprocin
More severe -- first gen ceph or penicillinase resistant penicillin Culture for resistant strains |
|
|
Treating recurrent impetigo
|
Mupirocin for nares
Body bath with chlorhexidine or bleach baths |
|
|
Complications of impetigo
|
Usually none
If untreated can progress deeper Staph scalded skin syndrome Glomerulonephritis can complicate group A strep impetigo (w/o regard to treatment) |
|
|
Staph scalded skin syndrome pathogenesis
|
Most cases caused by Staph aureus, phage group II
Exotoxin (exfoliatin A and B) Split the skin a superificial granular layer |
|
|
Staph scaled skin syndrome clinical picture
|
Kids <6, immunosuppressed
Site of impetigo may not be obvious Prodrome of malaise, fever, irritability Tender skin Symmetrical erythema around facial orifices, neck, flexures Superifical blisters, sloughs leaving most skin, scales Heals w/o scar in 10-14 days |
|
|
Prognosis of staph scalded skin syndrome
|
Good in kids mortality 3%
Bad in adults 50% mortality, they all have underlying disease |
|
|
Folliculitis
|
Superficial Infection of hair follicle
Usually caused by staph Also some gram negs, yeast |
|
|
Hot tub folliculitis
|
Pseudomonas aeruginosa
Usually larger lesions than the typical folliculitis Treat w/ ciprofloxacin |
|
|
Factors predispositing for folliculitis
|
Trauma
Maceration Occlusion Immunosuppresion |
|
|
Furuncle
|
Infection of entire follicle and surrounding tissue
|
|
|
Carbuncle
|
Multiple coalescing furuncles, deep tissue
|
|
|
Treating folliculitis, furuncles, carbuncles
|
Topical muprocin for superficial folliculitis
Abscesses require inscision and drainage Antibiotics for: widespread lesions, critical areas, immunsuppressed, valvular heart disease, non responsive to local therapy, cellulitis |
|
|
Very pain, virulent furuncle
|
Think MRSA
|
|
|
Treating MRSA skin infections
|
Sulfonamides
Tetracylcines Topical muprocin Clindamycin sometimes |
|
|
Cellulitis
|
Infection of deep dermis and subcutaneous tissues
Staph aureus, strep pyogenes Immuno competent -- skin break Immun compromised -- bloodborne route Lymphatic damage may predispose |
|
|
Clinical appearance of cellulitis
|
Red
Warm Painful Swollen Ill-defined Can blister Associated with fever, chills, malaise common |
|
|
Erysipelas
|
Superficial cellulitis with significant lymphatic involvement
Strep pyogenes Rapidly progressive painful erythema, usually on face Peau d'orange Penicillin 10-14 days |
|
|
Treating cellulitis
|
Oral antibiotics
If systemically ill, consider IV |
|
|
Complications of strep cellulitis
|
Glomerulonephritis
Lymphadenitis Lymphatic scarring Endocarditis |
|
|
Streptococcal perinal disease
|
Recurrent bright red erythema in children
|
|
|
Necrotizing facitis
|
Life threatening, rapidly progressive infection of subcutaneous tissue, fasica
Presents as exquisitely painful, normal appearing skin |
|
|
Necrotizing facitis bugs
|
Usually polymicrobial staph, e coli, bacteroids, clostridium
Sometimes strep A, dermatonecrotic exotoxin |
|
|
Necrotizing facitis progression
|
Normal appearing, painful skin
Necrosis in 1-2 days w/ blue-gray skin, blisters, thin water discharge Can be profoundly ill Usually on extremities |
|
|
Predisposing to necrotizing facitis
|
Alcoholism
DM Vascular disease Cardiac disease |
|
|
Necrotizing facitis treatment
|
Extensive surgical debridement
Broad spectrum IV antibiotics ?hyperbaric oxygen |
|
|
Necrotizing facitis prognosis
|
20-40% mortality
Complications high: deformity, toxic shock syndrome |
|
|
Lyme disease
|
Borrelia bergdorferi
Tick bite Erythema migrans rash expands Bells palsy, arthritis, myocarditis, meningioencephalitis |
|
|
Treating lyme disease
|
Doxycline
Amoxicillin for pregnant women |
|
|
Atopic diseases
|
Atopic dermatitis
Allergic asthma Urticaria Type I drug reactions Migraines |
|
|
Atopic dermatitis epi
|
10% of infants
15-20% during lifetime 85% have onset <5, most have improvement, resolution by adolescence Can recur Familial, autosomal dominant with highly variable penetrance |
|
|
Atopic dermatitis pathophysiology
|
Genetically determined abnormal skin reaction
Bone marrow important (cured by BMT) |
|
|
Cutaneous features of atopic dermatitis
|
LOF in fillagrin:
Increased keratinizaiton icthyosis, palmar linearity Defective water binding Lower irritation threshold Lower itch threshold (not histamine driven) Sweat retention Loss of antimicrobial peptides |
|
|
Immunologic features of atopic dermatitis
|
T cell dysfunction
Increased IgE (perhaps because of t/b imbalance) |
|
|
Neurovascular features of atopic dermatitis
|
Increased peripheral vasomotor tone
---white dermographism delayed blanching to cholinergics Reduced cAMP, throws off immune signalling |
|
|
Clinical features of atopic dermatitis
|
Chronic and fluctuating
Itchy Superimposed bacterial infection Dry, scaly skin Facial pallor Cool extremities Extra folds in lower lid - Dennie's lines Hyperpigmentation of lower lids -- atopic shiners |
|
|
Keratosis pilaris
|
Chicken skin
|
|
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Atopic dermatitis in lifespan
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Infancy: acute, generalized eczematous dermatitis
Kids/teen: subacute, chronic predominantly flexural Adults: irritant hand and foot dermatitis Senescence: dry skin eczematous dermatitis |
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What must you have to get diagnosis of atopic dermatitis?
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Pruitis
Eczematous dermatitis |
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Things that aggravate atopic dermatitis
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Antigens in foods, inhalants
Sweating Excessive drying Clothing -- wool Infection -- staph mostly Pityrosporon yeast Horomones Stress |
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Labs in atopic dermatitis
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Moderate eosinophilia
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Complications of atopic dermatitis
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Exfoliative dermatitis -- total body redness and scaling
Premature cataract formation Increased susceptibility to viral, fungal, bacterial infections no smallpox vaccines HSV can be severe Short stature if severe |
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Treating atopic dermatitis
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Reduce aggravators (bathing, sweating)
Lubricate Antihistamines Topical corticosteroids Brief use of compresses Immunosuppression (tacrolimus topical, cyclosporin oral) Interfereon UV light Mast cell stabilizer Leukotrient receptor antagonist TNF alpha inhibitior |
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Why doesn't atopic skin adhese properly
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Balance between adhesion proteins and proteases in skin is off
Overactive caspase |
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Scabies pathophysiology
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Caused by mite: scaroptes scabei
Female burrow between stratum corneum and stratum granulosum Lays eggs, which hatch in 3-5 days Sensitization is necessary for reaction Th1 mediated rxn |
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Scabies transmission
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Prolonged close physical contact
Veneral is possible Increased at time of overcrowding |
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Scabies clinical appearance
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Classic lesion in burrow
usually an excoriated, crusted, papule Pruitic, especially at night Affects genital, flexor wrists, finger and toe webs, buttocks, breasts, waistline Secondary infections (impetigo, ecthyma, cellulitis) |
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Nodular scabies
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Persistent red-brown prutitic nodules
Genital, intertriginous skin Prolonged hypersensitivity phenomenon |
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Crusted/Norweigan scabies
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Infestation with huge numbers of mites
Hyperkeratotic, crusted ezcematous or papulosquamous dermatitis Widespread distribution Senile, MR, immunocompromised |
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Scabies treatment
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Gamma benzene hexachloride (Lindane) lotion over whole body
Crotamiton lotion for pregnant, infants Permethrin, precipitated sulfur, benzyl benzoate, malathion Treat all close contacts |
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Pediculous capitus
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Head lice
Live on hair, feed on blood Biting releases a mild toxin that causes pruitic response and irritation 1 month lifespan, eggs hatch form nits in 7 days |
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Pediculous capitus epi
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Infestations in school children common
Less common in blacks Transmitted by close contact, shared hair tools/hats |
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Pediculosis capitus physical findings
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Itchy scalp
Lice in occipital, temporal regions Nits attached to hair shafts Erythematous papular bites on periphery/neck -- often crusted Region adenopathy -- secondary to pyoderma |
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Treating pediculous capitus
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Lindane shampoo
Malathion lotion Fine toothed comb removal of nits Treat family, clean clothes, hats, etc |
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Pediculosis corpis
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Body lice
Caused by pediculus humanus, corpis Disease of unlaundered clothing Major vector for typhus, relapsing fever, trench fever |
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Pediculosis corpis pathophysiology
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Lice live in clothes, lay nits in clothes
Feed off human blood Sensitization is part of disease process Nits can remain viable on clothes for 1 month |
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Pediculosis corpis physical findings
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Louse bites start are red macules w/ central punctum
Quickly develop into papules Excoriated Shoulders, upper back, trunk, butt Chronic -- crusted ezcematous dermatitis, thickened, dry, hyperkeratotic, hyperpigmented skin |
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Pediculosis corpis treatment
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Must treat clothes
DDT/lindane or sterilized and put in bags for 30 days Pyrethums spray |
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Pediculosis pubis
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Pubic lice
Phthirus pubis -- smallest louse Transmitted by close physical/sexual contact, can be on bedding Symptoms from excoriation |
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Pediculosis pubis physical findings
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Pubic itch
Excoriation, erythematous papules, maculae cerulae Brownish organisms on skin |
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Demodex folliculorm
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Hair follicle mites
Not pathogenic |
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Scabies in babies
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More palms and head involvement
More pustular |
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What test to see scabies
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Scraping of burrow into mineral oil
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How do viruses affect skin?
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Epidermal degeneration (cytolysis)
Epidermal proliferation (cytoproliferation) --warts Dermal inflammation -- RNA virus |
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Warts
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HPV related
Usually self-limited Hyperplastic response to virally infected cells |
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HPV strains associated with common warts
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1,2, 4
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HPV strains associated with plantar warts
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1, 2, 4
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HPV types associated with plane warts
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3, 10
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HPV types associated with genital warts
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6, 11
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Clearing of warts
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Immunologic response
Mostly cell mediated Does not necessarily mean infection has been cleared Difficult/impossible in immunocompromised patients |
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Verucae vulgaris
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Common warts
Flesh colored to whitish-gray Papules Rough, hyperkeratotic surface Uniform papillary structure with capillaries Punctate microhemorrhages |
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Verucae plantaris
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Initially a callus or corn-like lesion with painful hyperkeratosis
Normal surface lines are interupted May become confluent with other warts -- moasic |
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Do plantar warts need to be treated?
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If they are painful
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Filform of digitate wart
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Hyperkeratotic, elongated, projecting papule
Often on face or neck |
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Plane or flat wart
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Verucae plane
Smooth, slightly elevated, keratotic papules Flesh to reddish brown Usually multiple: dorsum of hands, elbows, knees, shins Difficult to eradicated |
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Condyloma acuminata
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Genital warts
Moist, soft papillary projections Sometimes producing cauliflower like growths on genital mucosa and skin |
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Histology of warts
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Hyperkeratosis
Thickening of epidermis Vacuolated cells in upper epidermis with basophilic inclusions |
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Treating warts
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Common and genital
N2 cryotherapy Electrodessication (scarring) Chemocauterants -- multiple Rx Surgical excision Imiquomid for genital |
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Molluscum contagiosum
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Molluscum contagiosum virus -- pox
Discrete pink/flesh colored dome shaped papules with central, whitish umbilicated area Usually 2-5 mm and multiple |
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Molluscum contagiosum epi
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Spread by close physical contact
Kids, wrestlers, lovers |
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Molluscum contagiousum pathophys
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DNA virus
Replicates within infected cell Epidermal hyperplasia in response |
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Mollucsum contagiousum histology
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Hyperplastic epidermis
Infected cells showing intracytoplasmic dense inclusion bodies displacing nucleus to one side |
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Treatment of mollucusum
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liquid N2
curettage Imiquimod |
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Numbered viral exanthums
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First - Measles
Second - Scarlet fever Third - Rubella Fourth - Duke's disease - ECHO virus Fifth - B19 Sixth - roseola infantum - HSV6 |
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Hand foot and mouth
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Cosackie A virus
Vesicles appear in mouth, on hands and feet Sporadic and epidemic |
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HSV 2 in someone who has HSV1
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less severe symptoms of initial HSV2 infection
fewer kids are getting hsv1, so first hsv2 infection is having more severe symptoms |
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How many Americans have HSV2
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1 in 5
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When does most HSV transmission occur?
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Asymptomatic shedding
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Sexual transmission of HSV is more likely
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From a male to female
African Americans are more susceptible to infection than whites |
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Factors triggers HSV recurrence?
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Sunlight
Skin trauma Cold/heat Stress Menstruation Concurrent infection |
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What keeps HSV at bay?
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Cell mediated immunity
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Incubation period of HSV2
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6 days
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Physical finds of primary infection with HSV
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Majority are asymptomatic
Widespread painful vesicles and erosions of the Oral area Vulva/vagina/cervix Perianal region Penile region Non mucosal Regional lymphadenopathy, fever, malaise Resolve in 2 weeks |
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Recurrent HSV infections
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Localized, grouped, umbilicated vesicles on an erythematous base
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Neonatal HSV
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Infection via birth canal
Untreated disease leads to disseminated or CNS infection in 70% 65% mortality Highest transmission rates if mother as primary asymptomatic infection during pregnancy |
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Eczema herpeticum
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Cutaneously disseminated herpes
Usually in patients with atopic dermatitis, other widespread dermatoses |
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Culturing/PCR for HSV
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Should be done form new lesions, at base
Can ID 1 vs 2 |
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Histology of HSV infection
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Multiloculated vesicles in epidermis
Acantholysis Multinucleated giant cells |
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Prodrome of recurrent herpes
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Tingling, itching, pain
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Treating herpes
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Uncomplicated recurrence : keep lesion dry, OTC balm
Penciclovir for recurrent oral Acyclovir for immunocompromised, disseminated, neonates Eye- trifluridine Suppression of recurrence - acyclovir, valcyclovir, famiciclovir |
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Zoster
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Reactivation of herpes zoster virus
Necrotizing ganglionitis Cutaneous re-infection limited by dermatome |
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Zoster course
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Pain or hyperesthesia (1-7 days)
Grouped, umbilicated vesicle with erythematous base in dermatomal pattern Crusting and healing in 2-3 weeks Neuralgia can persist Dissemination can occur in immunocompromised |
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Chicken pox
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Herpes: varicella zoster
10-20 day incubation Prodrome of fever of malaise Pink papules/macules --> vesicles with erythematous halo Can occur on all cutaneous surfaces including mucosa Adult disease may be complicated by pneumonia |
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Biopsy of Varicella zoster infeciton
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Mutlinucleated giant cells
Vesicles |
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Treating Varicella zoster
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Chicken pox - symptomatic, avoid secondary infection
Consider acyclovir in adults Zoster - Flexible collodian may limit hyperesthesia Systemic steroid may limit neuralgia Acyclovir et al may decrease severity |
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Varicella zoster vaccination
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Chicken pox vaccine recommend
- decreased incidence and severity Zoster vaccine can decrease incidence of shingles by >50% |
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Undersurface of wart
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Smooth projection into dermis
No roots |
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Is this a plantar wart or trauma?
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Does in interupt skin lines?
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Pearly penile papules
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Angiofibromas
Normal variant, not wart |
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What to order in presexual couples screening
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HIV
RPR HSV Hep CT/GC |
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What to think if a molluscum bump is inflammed?
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Its going away
Inflammation spontaneously clears |
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Evolution of a herpes lesion
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Vesicle
Umblicated pustule Crust |
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What is the most prevalent STD?
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Herpes
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What causes syphilis?
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Treponema pallidum
spirochete Form and motility corkscrewing Visible using dark field microscopy only |
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Primary syphilis
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21 day incubation
Chancre -- clean, painless, hard scars Lymphadenopathy If untreated, 75% resolve |
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Chancre of chancroid
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dirty
painful soft |
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Secondary syphilis
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Begins 6 weeks after chancre
Flu-like Hepatomegaly Generalized adenopathy Condyloma lata Mucocutaneous lesion - polymorphic Rash on palms |
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Gonorrhea
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Gram neg diplococci
Arthritis-dermatitis syndrome Fever and joint/tendon pain/swelling Few hemorrhagic pustules |
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Lymphogranuloma venereum
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C. trachomatis
Inclubation 5-21 days Vesicles erode, ulcerate, heal rapidly Headache, fever, arthralgia Lymphadenopathy, buboes Groove sign Labial edema |
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Chancroid
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H. ducreyi - gram neg rod
Painful, soft ulcer, dirty chancre Ulcers are high infectious Supperative regional adenopathy with potential for node breakdown |
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Granuloma inguinale
Donovanosis |
C. granulomatis - gram neg rod
Painless red, beefy lesions Pseudoelephantisis of labia Long incubation Rare to have nodal involvement Australia, India |
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Tinea versicolor on KOH
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spores and hyphae
Spaghetti and meatballs |
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Tina versicolor
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Malassezia furfur
Thrives on lipid -- back and chest Inherited susceptibility to disease, as we are all colonized Fine, grainy scale Carboxylic acid production inhibits melanin -causing hypopigmentation |
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Treating tinea versicolor
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Topical antifungal
Ketoconazole orally in severe cases - does have SE Selineum shampoo |
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Tinea
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Targetoid lesions
Described by location Caused by fungi |
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Where to skin fungi live?
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Corneum
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Kerion
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Exaggerated immune response to a tinea infection
Usually a boggy, annular lesion of the scalp See in kids -- response of an immature immune system to fungus |
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Oncomycosis
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Common and hard to treat
Recurrence rates high Terbinafine is only antifungal that penetrates nails, has SEs |
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Tinea uguium
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Fungal infection under the nail
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Green nail?
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Pseodomonas infection
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Sources of fungus
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Kittens
Puppies Farm animals Pets |
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Majocchi's granuloma
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Follicular tinea
Fungus in follicle causes granuloma formation Classically on legs of women after shaving |
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Dermatophyosis generally
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Fungal infection of skin
Inherited susceptibility Immune variability Acquired immunity important |
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Appearance of tinea
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Red pink annular scaly patches
Inflammatory advancing border Trailing scale Central clearance |
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Tinea incognito
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Loss of normal fungal patterns of infection because of steroids
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Tinea imbricata
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Superficial fungal infection of polynesia
Full body infection sign of power |
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Candida on KOH
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Spores and psuedohyphae
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Difference between tinea and candida in appearance
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Yeast has:
Satellite lesions More erythema Less central clearing Production of white, masserated stuff |
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Thrush
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Candida in oral cavity
Self-limited in babies Can be bad in immunocompromised adults |
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Where is candida albicans?
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Its a normal skin inhabitiant
Infection occurs in skin folds, mucous membranes In obesity, pregnancy, steroids, immunocompromised |
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Sporotrichoisis
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Sporothrix schenckii
Soil organism Innoculation through skin -- thorn Papule forms week later Lymphadenopathy spreading up the arm Immunoflorescence is only lab test |
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Chromobastomycosis
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Deep fungal infection
Phialophora, cladosporium, fonescaea Soil organisms Warty plaques Vegetating ulcers Draining sinuses Feet and legs |
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Mycetoma/Madura foot
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Deep fungal infection
Allescheria and others Soil organisms Papules, pustules, ulcers, sinus tract Difficult to treat No previous skin injury necessary |
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Disorders predisposing patients to chronic fungal infection
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Atopic dermatitis
DM Immunodeficiency syndromes Cancer Corticosteroid use Transplant patients AIDS |
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Tinea barbare
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Often a zoophilic species
Usually vigorous inflammatory Secondarily infected with bacteria Can lead to scarring |
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Tinea on KOH
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Hyphae
Crisscrossing lines |
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Id reactions
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Fungal-like inflammatory responses
During a fungal infection Not at site of infection Will resolve with treatment of fungal site |
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Griseofulvin
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Systemic anti-fungal against dermatophytes
--not candida or tinea versicolor |
