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598 Cards in this Set
- Front
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Macule
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circumscribed, flat discoloration of skin up to 0.5 cm in size
Types: a. Inflammatory: produced by vasodilation of superficial vessels b. Intrinsic pigment deposition: Example is a freckle. c. Extrinsic pigment deposition: Example is a tattoo. |
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Patch
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circumscribed, flat discoloration of skin larger than 0.5 cm in size
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Papule
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circumscribed, elevated, superficial, solid lesion, up to 0.5 cm in size
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Plaque
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circumscribed, elevated, superficial, solid lesion larger 0.5 cm in size
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Maculopapule
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a hybrid term and one which has little to recommend it. Its use usually means that the examiner has not been able to determine the primary change and is confused. Avoid employing it.
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Nodule
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circumscribed, palpable, solid, round, or ellipsoidal lesion. Nodule refers to a growth that is both elevated above the skin surface and has a deeper component as well. Generally this refers to lesions larger than 0.5 cm, and most nodules are greater than 1cm and up to 4-5cm.
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Tumor
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implies proliferation of cells or tissues, either benign or malignant. Any of the other primary and secondary terms may be appropriate in the initial description of a tumor; e.g., nodule or plaque. A large nodule is often referred to as a tumor. There are no size specificities for tumor
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Wheal
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a special type of papule or plaque which is the response of the skin to histamine release and is characterized by the classic three features (triple response of Lewis) of edema, erythema, and a flare. The edema fluid is bound, which contrasts this lesion with the vesicle and bulla. A wheal is transitory or evanescent, seldom remaining in one location for more than 3 or 4 hours.
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Vesicle
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circumscribed collection of free clear, fluid up to 0.5cm cm. in size
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Bulla
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circumscribed collection of free clear, fluid more than 0.5cm. in diameter
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Pustule
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circumscribed collections of leukocytes and free fluid (pus) which are variable in size
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Scale
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(escale - husk): excess dead epidermal cells, i.e., keratin. Often produced by abnormal or rapid keratinization and shedding
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Crust
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(crusta - bark): collections of dried serum and cellular debris – “scab”
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Erosion
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focal losses of epidermis. Usually, some superficial dermal tissue loss as well, but superficial or thin in comparison to ulcers and heals without scarring
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Ulcer
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loss of epidermis plus variable degrees of the dermis. Variable in depth, size, and shape. Heal with scarring.
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Fissure
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linear losses of epidermis and dermis which have sharply defined, abrupt walls; a slit
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Scar
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abnormal formations of connective tissue replacing tissue lost or altered by some pathologic process. Always implies dermal damage. Cicatrix is a synonym
Types: a. Atrophic: thinned b. Hypertrophic (keloid) c. Striae: a stretch mark |
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Atrophy
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A depression in the skin resulting from thinning of the epidermis, dermis, or subcutaneous fat.
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Special lesions
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primary or secondary changes which could be described through the use of terms already given, but warrant special terminology
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Excoriation
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erosions caused by scratching. Often linear distribution or fingernail size.
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Comedone
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plugs of sebaceous and keratinous material lodged in the openings of the pilosebaceous follicles. The primary lesions of acne vulgaris. Commonly known as blackheads and whiteheads.
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Open comedo
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a “blackhead”- an open follicle stuffed with sebaceous and keratinous material.
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Closed comedo
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a “white head” follicular dilatation not as marked; skin appears to cover the follicular orifice.
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Milia
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small, superficial keratin cysts
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Burrow
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areas of thickened epidermis. The major sign of the thickening is increased prominence of the skin lines, although scaling and low grade inflammation are usually seen as well
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Telangiectasia
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dilations of superficial vessels. Often linear or branch-like
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Petechiae
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circumscribed deposits of blood or blood pigments less than 0.5cm but usually smaller, 1-2mm macules. Petechiae do not blanch with pressure (diascopy).
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Purpura
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circumscribed deposits of blood or blood pigments greater than 0.5cm. Do not blanch with pressure (diascopy).
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Systemic and orderly notation and description of the patient and his lesions is a prerequisite to complete an accurate diagnosis in dermatology. In your description, consider the following points in order.
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General description
Distribution of the lesions Arrangement of the lesions Configuration or shape Primary lesions Secondary changes Characteristics or quality of the lesions should be described in addition to the secondary changes Involvement of the mucous membranes and the hair and nails |
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Shave biopsy
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the shave technique is a tried and true, old but effective, quick and efficient way to obtain a skin specimen for histologic evaluation. After anesthesia, the skin lesion is simply cut with a scalpel blade or double edged razor, by sawing, back-and-forth, through the skin containing the lesion. This is especially good for removing small growth, tumors and nevi, as well as a small piece of skin for diagnosis.
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Punch biopsy
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the punch technique is also quick and efficient, good for obtaining skin for diagnosis of a rash, obtaining skin for special tests, such as immunofluorescence, and removal of small tumors and obtaining fat for evaluation. After anesthesia, the appropriate size punch tool is selected and rotated clockwise with firm pressure. Scissors help cut or remove the bottom of the specimen. Cautery may be necessary, and closure with a stitch is usually performed.
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Excision
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excision means to “cut out,” and simple excisions are used to remove larger pieces of skin, usually tumors, benign or malignant. After anesthesia, a scalpel is used to incise the lesion in a fusiform shape, down to panniculus, and the base of the lesion is cut or excised in a straight plane with the scalpel blade. The wound is cauterized to stop bleeding and sutured close. This basic technique is a large part of dermatology practice. The basics of simple excision are used for many other more complex plastic closures including flaps and grafts.
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Flaps and grafts
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these closure procedures will not be covered in this course, but you should know that dermatologists use them to close defects from excisions, usually from larger excision on the face, for skin cancer.
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MOHS MICROGRAPHIC SURGERY
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After excision of the tumor, a technician stains the removed tissue, marking the margins, ensuring complete removal of skin cancer before closure. If the first excision does not remove the entire tumor, another excision or layer is removed and stained, and margins examined while the patient waits. This is repeated until surgical margins are clear. Mohs is performed in an outpatient procedure room, under local anesthesia. The patient goes home knowing the cancer is completely removed.
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INCISION & DRAINAGE
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Many types of growths can become inflamed, tender, and infected. There are a few simple techniques used to relieve the effects of these conditions. Acne cyst and inflamed epidermal cysts are pesky, troublesome entities that are easily relieved by a few simple steps. After anesthesia, the cyst is incised with a #11 or #15 blade scalpel, and contents expressed with gentle palpation. Curettage of the central cyst may remove fixed or loculated debris. The wound can be left open or closed with suture.
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LASER
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There are a few constant principles and safety issues one needs to know about Light Amplified by Stimulated Emission of Radiation or “LASER” energy. Laser light is monochromatic and collimated. Beyond understanding the principles of laser energy, becoming familiar with lasers and their computers is as important when treating skin diseases. There are a variety of laser machines available for different skin treatments. Lasers can be used for unwanted vascular and pigmented lesions, for unwanted hair and tattoos, and for resurfacing wrinkled or scarred skin. Lasers can be used to destroy unwanted skin, warts, tumors and cancer. Another version of laser-like light is the intense pulsed light (IPL) machine which is adjustable and used for a variety of lesions.
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BOTOX
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Botulinum toxin A or Botox blocks the release of presynaptic acetylcholine, thus causing significant temporary weakness or overt paralysis of muscles, lasting from 3 to 6 months. Botox can be used to remove chronic skin furrows caused by muscle contraction of facial muscles. Botox has been around for over 20 years, and is used in a variety of medical specialties and for many medical conditions, blepharospasm being the most common non-cosmetic use
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Collodion Membrane
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“Saran-wrap” covering at birth
Infants develop respiratory distress, cracks, fissures and temp. instability 85-90% have an identifiable underlying cause Diagnostic evaluation to exclude underlying cause Treatment is supportive |
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Diaper Dermatitis
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Red itchy rash in diaper area
Caused by urine combined with feces Creases are spared; secondary infection common Consider other causes if dermatitis is persistent Reduce skin wetness, treat secondary infection |
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How would you treat candida diaper dermatitis?
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either topical miconazole or oral nystatin if thrush is preasant too
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Infantile Seborrheic Dermatitis
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Scaly rash involving scalp, face and body folds; yellow waxy scale
Begins early in life; improves around 1 yr No firm cause established Consider HIV in severe cases DDx: AD, Psoriasis, LCH, Scabies, Tinea Treat with low potency CS, pimicrolimus, tacrolimus |
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Netherton Syndrome
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AR, atopic diathesis and hair abnormalities
Often seen in premature infants and FTT Caused by mutations in SPINK5 Eczema, erythroderma, ichthyosis, short hair Elevated IgE Consider CF and ectodermal dsyplasia Treatment similar to AD, systemic absorption with tacrolimus and pimicrolimus |
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Acrodermatitis Enteropathica
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Diarrhea, peri-orificial and acral vesiculobullous dermatitis, alopecia, and apathy
Inherited (AR) and acquired (more common) More severe in HIV and prematurity Irritability and FTT are prominent Low plasma zinc Consider biotin deficiency, CF, organic aciduria Symptoms improve quickly with oral zinc |
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Erythema Toxicum Neonatorum
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Benign, transient pustular eruption
More common in healthy term infants Rare on palms & soles; occurs in crops Lasts for first 2-3 weeks of life Smear of pustule shows eosinophils DDx: infection, infestation and TNPM Reassure parents Filled with eosinophils! Transient... goes away in 2 weeks. Usually don't see in premature infants |
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Is it easy to find scabies in lesions if you suspect them?
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NO. In fact if you do a scraping and find several live scabies and tons of eggs you are in trouble because it's much much much worse than what you see.
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Cutis Marmarata
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Transient mottling; resolves with warmth
Exaggerated vasomotor response Healthy infants Persistent mottling: Down syndrome, trisomy 18, hypothyroidism, neonatal lupus, septic shock 1 limb involved. CM is different than CMTC whatever the hell that means. |
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What might you see in neonatal lupus?
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the classic malar rash on the baby's face
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What might cause neonatal lupus?
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Typically maternal antibodies (mom has lupus) cross the placenta so it seems like the baby has lupus but that will pass. If the baby has cardiac abnormalities as a result of having lupus in utero then those are permanent even though the lupus is transient
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Henoch-Schonlein Purpura (HSP)
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Small vessel vasculitis; seen mostly in children
Often follows a respiratory illness IgA immune complexes in post-capillary venules Palpable purpura, joint and abdominal pain, glomerulonephritis LE involved; lesions occur in crops Can have multiple organs involved Must rule out infection NSAID for joint pains, systemic corticosteroids for GI and renal complications |
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Urticaria Pigmentosa
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A form of cutaneous mast cell disease
Itchy brown spots that blister with rubbing Commonly begins between 3-9 mo of age Can involve liver, spleen, GI tract, bones Must distinguish from cancer Patients must avoid non-immunologic mast cell degranulators Anti-histamines to control symptoms Typically: mom or dad might notice a lesion and then as wash it in the tub it gets much worse When rubbed mast cells degranulate... bad news. |
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Pyogenic Granuloma
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Bleeding exophytic dome-shaped papules
Important factors: trauma and hormones Common on head and neck and fingers Rapid growth, fall off, re-grow Biopsy before treatment Treated with ED&C |
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Neurofibromatosis Type I (NF1)
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AD; café-au-lait macules, axillary freckling, numerous neurofibromas, iris hamartomas
1:3000-4000; new mutation in 50% Diagnostic criteria NF1 gene – tumor suppressor - neurofibromin Optic glioma, long bone dysplasia, scoliosis, learning disabilities (unlike tuberous sclerosis) hypertension, macrocephaly DDx: AD café-au-lait macules, McCune-Albright syndrome |
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Tuberous Sclerosis Complex
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AD; multiple hamartomas
Tumor suppressor genes: TSC1 (harmatin) and TSC2 (tuberin) Hypopigmented macules, angiofibromas, connective tissue nevi, sub/periungual fibromas Can involve CNS, eyes, kidneys, heart and lungs DDx: Basal cell nevus syndrome, Cowden syndrome |
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When might you see adenoma sebaceum?
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typical finding for someone with tuberous sclerosis
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How would a thyroglossal duct cyst present and how should thye be treated?
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In the midline of the throat.
Might have thyroid tissue in it (in fact may be the only thyroid tissue) so need to do some evaluation before just simply removing it. |
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How would a dermoid cyst present?
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Lateral face often right above the brow.
Won't go away on their own so need to be removed. Can present centrally but if htat's true you need to check to make sure it isn't connected to the CNS before it is removed. |
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What is Psoriasis?
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Common, chronic, inflammatory genodermatosis
Etiology incompletely understood Abnormal T cell function and communication May affect skin, nails, joints Immune system malfunction causes skin cells to multiply too quickly 7 to 12 times faster than normal Excess cells build up on surface of skin Scaly plaques may result in itching, discomfort, pain, and bleeding |
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Types of Psoriasis
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Plaque
Most common, 80% of all cases Raised, red scaly lesions Guttate Small, dot-like lesions Erythrodermic Intense redness, inflammation, some scaling Pustular Pus-filled lesions, some scaling; often localized to palms and soles |
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Chronic Psoriasis appearance
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Spots are very well define and have a very characteristic color: ham pink. May have various amounts of scale but the color is the same/ very characteristic of it.
pitting of the nail. Could also get lifting, oil spotting etc of the nail. due to psoriasis in the nail matrix which causes cell death and leaves pits |
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Cause of Guttate Psoriasis
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Usually due to Strep
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Erythrodermic Psoriasis
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HURTS
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Pustular Psoriasis
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Either hand and foot or full body. Associated with cigarette smoking… current or past
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Psoriasis Treatment Options3 Primary Treatment Methods
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Topicals
Medications applied to surface of skin Phototherapy Treatment of the skin with natural or artificial ultraviolet light Systemics Medications given orally (by mouth) or by injection |
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What is rotating order of psoriasis treatments? (would be drawn out potentially in a circle)
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UVB phototherapy-> biologics -> methotrexate -> cyclosporine -> Acitretin -> PUVA phototherapy
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Psoriasis Topical Therapy
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Most commonly prescribed treatments
Typically used for mild to moderate psoriasis (< 5% BSA) Creams, ointments, lotions, solutions, foams, gels, baths, shampoos Typically applied twice per day Coal Tar Anthralin Topical steroids Calcipotriene/ calcipotriol (vitamin D) Tazarotene (retinoid) |
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Psoriasis Phototherapy
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Light unit or lasers direct specific wavelengths
of ultraviolet light For moderate to severe psoriasis, localized areas of stubborn plaques May require 1-5 weekly treatments |
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Ultraviolet B (UVB) Tx for Psoriasis
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Effective:
Use 3 to 5 x/week Risks: Acute photoreaction (sunburn) Activation of herpes virus Photoaging, skin cancer very unlikely Combinations increase efficacy: Coal tar, anthralin, tazarotene, and calcipotriene Acitretin Biologics |
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Psoralens + Ultraviolet A (PUVA) as Tx for psoriasis
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Effective
Side effects: Risk of acute photoreactions and chronic photoaging of skin Increased risk of SCC (with > 200 PUVA sessions) Possible increased risk of melanoma Can be used for maintenance Combination with acitretin more potent |
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Psoriasis Systemic Therapy: Methotrexate
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Originally a chemotherapy drug
Folate antagonist Slows fast-dividing cells Potential liver toxicity Effective for psoriatic arthritis |
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Psoriasis Systemic Therapy: Cyclosporine
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Originally an organ transplant drug
Inhibits IL-2 production/ release Nephrotoxicity The FDA recommends continuous cyclosporine treatment be limited to one year at a time |
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Psoriasis Systemic Therapy: Acitretin
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Synthetic retinoid
Long half-life Teratogenic Potential liver toxicity Potentiates other treatment modalities Side Effects: Dose-dependent retinoid side effects include alopecia Start with low doses, increase if needed & tolerated Very limited drug interactions Follow LFT’s, triglycerides Gemfibrozil (Lopid) 3-600 mg BID, if needed Teratogenic & long half-life Shouldn’t give blood after taking acitretin |
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Psoriasis Biologics:
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Anti T-cell Therapies:
Alefacept (Amevive) Efalizumab (Raptiva) – off market 2009 Ustekinumab (Stelara) Anti TNF-α Therapies: Adalimumab (Humira) Etanercept (Enbrel) Infliximab (Remicade) |
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Psoriasis Treatment OptionsBiologics: RaptivaTM (efalizumab)
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Approved 10/2003
humanized monoclonal to CD11a chain of LFA-1 Blocks T cell trafficking into skin Self-administered SC Injection once per week Progressive multifocal leukoencephalopathy Pulled by FDA 2009 |
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Psoriasis Treatment OptionsBiologics: EnbrelTM (etanercept)
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Indicated for plaque psoriasis and psoriatic arthritis
Has pediatric indication for JRA Soluble TNF alpha inhibitor - hydrid of human TNF type I receptor and human IgG1 Fc region Can be used in combination with methotrexate Self-administered SC Injection twice per week |
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Psoriasis Treatment OptionsBiologics: AmeviveTM (alefacept)
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Indicated for plaque psoriasis
Hydrid of human LFA-1 and IgG1 Fc region, binds CD2 Can be used in combination with other systemic agents and/ or phototherapy In office administered IM injection once per week for 12 weeks May be repeated or used in longer course |
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Psoriasis Area and Severity Index (PASI) Score
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The Psoriasis Area and Severity Index (PASI) score is calculated from the severity and surface area of psoriasis in 4 body regions: head, trunk, arms, and legs.
The severity of disease in each body region is determined by examining the parameters of erythema, induration (thickness), and scaling. Each parameter is given a score in each body region. The PASI score is calculated by combining these elements according to the formula shown below, which accounts for the percentage of body surface area that each region occupies. |
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PASI
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GOLD STANDARD FOR EFFICACY IN PSORIASIS
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Seborrheic Dermatitis
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Common papulosquamous disorder
Etiology related to Pityrosporum yeast Clinical presentations differ in adults vs. infants |
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Seborrheic Dermatitis: Adults
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Moist, transparent to yellow, greasy scaling papules
Distribution favors areas where the concentration of sebaceous glands is maximal scalp margins, central face and presternal areas eyebrows, the base of eyelashes, nasolabial folds and paranasal skin, and external ear canals Flexural skin may be similarly involved Adults tends to have a chronic course with remissions and exacerbations scales just come right off and rarely occurs on the face except in someone with HIV |
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Seborrheic Dermatitis: Infants
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Yellow greasy adherent scale “cradle cap”
Minimal underlying redness Scale may become thick and adherent Diaper area and axillary skin with redness > scaling Usually a self-limited condition often not requiring treatment |
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Pityriasis Rosea
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Common, self-limited, usually asymptomatic, clinically distinctive papulosquamous disorder
More than 75% of patients are between 10 and 35 years of age Many patients report a mild prodrome Seasonal clustering of cases Starts with 1 and then BAM hudnreds and hundreds of spots… could be post viral skin reaction. Coincides with cold season |
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What does pityriasis rosea look like?
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First lesion or herald patch
Oval plaque of 1–2 cm, salmon color thin collarette of residual scale inside the border 1–2 weeks later numerous similar but smaller lesions, “Christmas Tree” pattern usually clear spontaneously in 4–12 weeks, without scarring post-inflammatory hyperpigmentation may take months to resolve in darker-skinned people |
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Lichen Planus
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uncommon, inflammatory papulosquamous disorder of unknown etiology
Skin, nails, hair and mucus membranes may be affected Rare in children aged under 5 More common in women than in men 10% of patients have a positive family history 5 “P’s”: purple polygonal pruritic papules and plaques Wickham's striae - lacy reticulated Koebner phenomenon - lesions develop in areas of injury Clinical course variable and unpredictable Itching is variable, but is usually intermittent and insatiable Severe oral lichen planus may degenerate to squamous cell in an estimated 3% of cases. |
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Lichen Sclerosus: what is it?
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uncommon chronic papulosquamous disease of unknown etiology
affects both skin and mucosal surfaces predilection for the anogenital skin female to male ratio is 10 : 1 more common in women over 60 years of age, but can occur at any age |
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Lichen Sclerosus: clinical presentation
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Affected women complain of chronic vulvar pruritus, dysuria or dyspareunia
Men have persistent balanitis which, if untreated, tends to progress to phimosis. Squamous cell carcinoma develops in 3% of mucosal lesions Consider lichen sclerosus to be a pre-cancerous condition Skin lesions are often asymptomatic Might see pores clogged with keratin (blackheads). You may see a lilac color around the lesion |
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EMu
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Epidermal melanin unit
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SKIN COLOR
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The result of a cooperative effort between units of melanocytes and adjacent keratinocytes
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Function of the EMU
Three Phases |
I – Establishment of Peripheral Pigment “Factories” (EMUs) during neonatal period
II – Ongoing Production of Pigment within melanocytes III – Ongoing Transfer of melanin to adjacent keratinocytes |
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What are melanocytes derived from?
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neural crest cells
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Establishment of EMUs
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Melanbolasts originate in the NeuralCrest and migrate to the Skin at 3-8 weeks
Melanocytes remain in the basal layer of the epidermis; dendrites extend to 30-36 epidermal cells |
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Pigment production within melanocytes
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Pigment production begins during the last trimester
Melanin is produced within small membrane-bound spheres known as melanosomes |
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Two forms of melanin can be produced in the same cell
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eumelanin and pheomelanin
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What are eumelanin and pheomelanin products of?
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oxidation of phenylalanine
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Melanosome Transfer
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Once Melanosomes are formed they migrate to the tips of dendrites
Melanosomes are then transferred directly to adjacent keratinocytes (via apocopation) Details of the transfer process not yet completely understood |
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What produces hair pigments?
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melanocytes in the hair bulb
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The EMU is a stable unit
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Melanocytes remain in the lower epidermis, providing melanin to keratinocytes as they mature
One melanocyte transfers pigment to 30-36 keratinocytes |
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Pigment disorders can be related to the steps in the pigmentation process (4 steps):
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I - Establishment of the EMU
II- Melanin Synthesis III - Melanin Transfer IV - Loss or Destruction of the EMU |
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Disorders Related to the Establishment of EMUs
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Sacral spot (Congenital Dermal Melanosis)
Nevus of Ota (Oculodermal Melanocytosis) Nevus depigmentosus (Congenital Pigment Loss) Partial albinism (Piebaldism) |
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Disorders Related to Melanin Production
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Decreased Pigmentation:
Tinea versicolor Hansen’s Disease Oculocutaneous Albinism Increased Production of pigment: Tanning Melasma Addison’s Disease |
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Tinea versicolor
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Azaleic acid, a metabolite of the fungus, inhibits tyrosinase activity
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Hansen’s Disease
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Decrease in melanogenic activity within melanocytes
aka leprosy |
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Occulocutaneous Albinism
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Most common inherited disorder of generalized hypopigmentation
Frequency 1:20,000 4 Types of OCA In Africa an important cause of skin cancer and melanoma |
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Does UVB or UVA radiation stimulate melanogenesis?
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Both stimulate melanogenesis
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Melasma
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Stimulation of pigment production by hormones
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Addison’s Disease
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Adrenal failure results in an increase of melanotropic hormones
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Disorders in Related to Defects in Melanin Transfer
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Pityriasis alba
( Disruption of pigment transfer in eczema) |
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Psoriasis
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Rapid turnover of keratinocytes inhibits pigment transfer
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Disorders Related to Reconfiguration or Loss of Melanocytes
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Increase in EMUs
-Lentigines (Liver Spots) - Junction Nevi Loss of EMUs -Gray Hair -Chemical Leucoderma -Vitiligo |
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Lentigenes
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An increase in the number of melanocytes/ surface area
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Junction Nevus
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An increase in the number of melanocytes in the basal epidermis
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Graying of Hair
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Loss of melanocytes from the Hair Bulb
Influenced by Age, Genetics, and Possibly Stress |
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Chemical Leukoderma
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Selective destruction of melanocytes by toxic agents (eg hydroqunone derivatives)
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Vitiligo
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SpontaeousLoss of Melanocytes: Cause Unknown
Often in Periorificial Areas |
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Vitiligo Therapy
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Topical Steroids
Melanocyte transplantation If greater than 50% of skin, consider destruction of remaining melanocytes |
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Non-melanin pigmentation
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Tattoo pigmentation
Drug deposition ( e.g. Minocycline) |
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Vitiligo is due to a..
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loss of melanocytes
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What is the rate limiting enzyme in melanin production?
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tyrosinase
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What pigment is present in red hair?
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pheomelanin
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Papillary dermis
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Type III collagen
Cellular Horizontal vascular plexis |
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Reticular dermis
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Bulk of dermis
Type I collagen Vertical vessels |
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Cells of the dermis
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Fibroblasts
Control CT matrix Near collagen and elastic fibers Macrophages Bone marrow Antigen presentation Wound healing Mast Cells Cytoplasmic granules Histamine Heparin Peptidases Measure tryptase |
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Ehlers–Danlos syndrome
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defect in the synthesis of procollagen
Multiple types 3 most common Hyperextensible skin Atrophic scars (typically look like cigarette paper and are secondary to trauma Might see the atrophic fibrotic hyperpigmented irregularly shaped plaques on the face and positive Gorlin sign (ability to touch nose with tongue tip) |
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Collagen and Dermis
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Most abundant protein in mammals
Alpha chains form in RER Hydroxylation Glycosylation From trimers, triple helix Cleavage, assembly |
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Collagen disorders- keloids and hypertrophic scars
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Keloids and hypertrophic scars
Excessive scar formation Hypertrophic: within confines of scar Keloid: spread beyond confine of scar |
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DFSP
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Low grade malignant proliferation of fibroblasts
Wide local excision collagen disorder |
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Morphea
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Localized scleroderma
Etiology unknown Indurated plaques collagen disorder |
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Elastic fibers
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Stretch and recoil
Elastin Single polypeptide chain B spiral fiber network Desmosine/ isodesmosine Fibrillin Forms microfibrils framework for elastin |
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Cutis Laxa
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Elastic fiber disorders
AD/AR, acquired Loosely hanging skin Defective elastin production Note the loose lax skin with prominent skin folds may also have severe diarrhea and failure to thrive |
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Pseudoxanthoma elasticum (PXE)
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Elastic fiber disorders
AD/AR Yellow papules Degeneration of arterial elastic fibers leads to occlusion and rupture Angioid streaks from rupture of Bruch’s membrane symmetric confluent yellow papules and redundant skin folds characteristic “plucked chicken” skin changes occurring on the neck of patients with pseudoxanthoma elasticum. |
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Mucopolysaccharides
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Polysaccharide linked to protein
Maintain tissue salt and water balance Various types involved in skin |
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Pretibial myxedema
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Disorder of mucopolysaccharides
Ass. With Grave’s disease Anterior tibia May progress Excessive amounts of MPSs |
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BASIC SCIENCE OF DARKER SKIN COLOR
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THICKER EPIDERMIS
HAIR FOLLICLE AT ACUTE ANGLE NORMAL MELANOCYTE NUMBER GREATER MELANOSOME NUMBER LARGER MELANOSOMES |
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What are some of the basic appearance differences in darker skin than fairer skin?
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RED IS MORE VIOLACEOUS/PURPLE
HYPERPIGMENTATION COMMON HYPOPIGMENTATION DRAMATIC INFLAMATION IS ASHY WHITE OR GRAY |
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TINEA CAPITIS
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SCALP & HAIR SHAFT INFECTION
PERSON-TO-PERSON SPREAD MORE COMMON IN BLACK CHILDREN? BRAIDING AND POMADE PATCHY HAIR LOSS, SCALE, BROKEN HAIRS “BLACK DOTS” |
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KELOIDS
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SCAR-LIKE PLAQUE EXTENDING BEYOND THE AREA OF TRAUMA
ACNE, BURNS, BITES, PIERCING, TRAUMA, SURGERY PRURITIC OR TENDER UPPER TRUNK, SHOULDERS, EAR LOBES INTRALESIONAL STEROIDS SURGICAL EXCISION MAY LEAD TO RECURRENCE |
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POMADE ACNE
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COMEDONES AND PUSTULES
CURVED HAIRS FOREHEAD AND TEMPLES AVOIDANCE |
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SARCOIDOSIS
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MULTISYSTEM GRANULOMATOUS DISEASE
MORE COMMON IN BLACKS PERINASAL, PERIORBITAL, NASOLABIAL FOLDS MANY CLINICAL VARIANTS NON-CASEATING GRANULOMAS DIFFICULT TO TREAT |
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In what disease would you find apple jelly like lesions around the mouth, nose, and eyelids?
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sarcoidosis
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TRACTION ALOPECIA
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PROLONGED TENSION OF SCALP HAIR
LOCALIZED HAIR LOSS MECHANICAL LOOSENING OF HAIR FOLLICLES FOLLICLE INFLAMATION SCARRING |
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DERMATOSIS PAPULOSA NIGRA
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BLACK AND ASIAN SKIN
VARIANT OF SEBORRHEIC KERATOSIS FLAT WAXY BROWN PAPULES ON CHEEKS COSMETICALLY TROUBLESOME |
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PIGMENTED NAIL BANDS
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DARK LINEAR BANDS
50% IN BLACK NAILS TRAUMA AND ULTRAVIOLET LIGHT THUMB AND INDEX FINGER DRUG-INDUCED, ADDISION’S , PEUTZ-JEHGERS MUST DISTINGUISH FROM MELANOMA |
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PALMAR PLANTAR HYPERPIGMENTATION
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COMMON IN BLACK SKIN
POLYMORPHOUS MACULES OR PATCHES SHARP AND INDISTINCT BORDERS |
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ACNE KELOIDALIS NUCHAE
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CHRONIC, PROGRESSIVE, KELOIDAL SCARRING
NAPE OF NECK (NUCHAL) CURVED HAIR, INFLAMATION, ELIMINATION FOREIGN BODY REACTION AND SCARRING SINUS TRACTS AND PURULENT DISCHARGE EXCISION |
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PSEUDOFOLLICULITIS BARBAE
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MECHANICAL INFLAMATION
HAIR PENETRATE THE SKIN SHAVING MAY MAKE WORSE INFLAMED PAPULES, PUSTULES, SCARS SECONDARY BACTERIAL INFECTION |
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Melanoma in patients with darkly pigmented skin
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10 TIMES MORE COMMON IN WHITE SKIN
NON-SUN EXPOSED AREAS MORE COMMON IN BLACK SKIN (Compared to White skin) PERIUNGUAL, PALMAR AND PLANTAR 70% ARE ACRAL LENTIGINOUS MELANOMAS IN BLACK SKIN |
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BASAL CELL CARCINOMA in patients with darkly pigmented skin
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MUCH LESS COMMON IN BLACK SKIN
SIMILAR DISTRIBUTION TO WHITE SKIN ALMOST ALWAYS PIGMENTED BCC |
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SQUAMOUS CELL CARCINOMA in patients with darkly pigmented skin
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MOST COMMON SKIN CANCER IN BLACK SKIN
HIGHER MORTALITY IN BLACK SKIN 65% INVOLVE NON-SUN-EXPOSED AREAS VARIABLE CLINICAL PRESENTATION CONFUSED WITH PSORIASIS, ECZEMA, TRAUMA ASSOCIATED WITH ULCERS |
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What type of spectrum is erythema multiforme on?
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Erythema Multiforme Minor Erythema Multiforme Major --> “SJS” --> Toxic Epidermal Necrolysis
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ERYTHEMA MULTIFORME
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Acute, self-limited, reactive eruption
Minor & Major forms Clinical spectrum of disease “Targetoid Macules” Infections & Medication reactions Multiple morphologic presentations |
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What is the clinical picture of erythema multiforme?
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Where: lips, palms, ocular, genital
Erythematous “targetoid” macules / patches Papules / plaques Vesicles Bullae Wheals (urticaria) Erosions separation of the epidermis from the dermis |
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What can cause EM?
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ALMOST ANY MEDICATION !
FREQUENT OFFENDERS: Sulfa containing drugs: Bactrim, Dapsone Anti-epileptic drugs: phenytoin, carbemazepine, phenobarbital, lamotrigine Antibiotics: penicillin, cephalosporins Allopurinol |
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EM MINOR
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Little or no mucous membrane involvement
Few (if any) systemic symptoms If recurrent EM, think HSV HSV may be “subclinical” Medications most likely non-infectious related cause |
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EM MAJOR
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Always with mucous membrane involvement
Stomatitis, balanitis, vulvitis, conjuntivitis/keratitis Skin involvement more widespread Systemic symptoms such as fever, malaise, anorexia Labs may show evidence of hepatitis, nephritis, eosinophilia Often due to medications |
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If you have recurrent EM on the dorsal hand or lips what you might think of?
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Herpes simplex. Treat prophylactically with acyclovir
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TOXIC EPIDERMAL NECROLYSIS
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SJS-TEN OVERLAP
FULL-THICKNESS EPIDERMAL NECROSIS GENERALIZED REDNESS VESICLES AND BULLAE (TENSE) EPIDERMIS EASILY REMOVED THICK SLOUGHING ALL ORGANS MAY BE AFFECTED HEPATITIS, NEPHRITIS, PNEUMONITIS DEATH IN 5- 40% |
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TEN Pathophysiology
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Cytotoxic T-cell mediated disease
Cell death is due to apotosis Cascade started by Fas (“death receptor”) interacting with FasL Perforin and granzyme also involved |
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TREATMENT of EM minor and major
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Antiviral prophylaxis
Cessation of suspected causative drug Conservative, supportive care |
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Treatment of SJS/TEN
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Cessation of suspected causative drug
Supportive care Systemic steroids controversial Growing evidence for the use of IVIG Burn unit if widespread sloughing |
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Another name for SWEET’S SYNDROME
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Acute Neutrophilic Febrile Dermatosis
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Sweet's syndrome overview
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Red-pink dermal plaques
Pseudovesicular or “juicy” Face & hands Fever, leukocytosis, arthralgias Associated with upper airway infections Internal malignancy Acute myelogenous leukemia |
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What malignancy is Sweet's syndrome most often associated with?
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AML
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What cell is prominent in the infiltrate of Sweet's syndrome?
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Neutrophils
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NECROBIOSIS LIPOIDICA DIABETICORUM
|
AKA “NLD”
RED-ORANGE ATROPHIC PLAQUES BILATERAL SHINS MAY BE PAINFUL & ULCERATE DIABETES MELLITUS TOPICAL TREATMENT Most pts with diabetes won’t get this but most people with this do have diabetes so if no known diabetes present definitely look for it |
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GRANULOMA ANNULARE
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People say this is ring worm. It is a dermal process.. Not very scary. Give people topical steroids but it’s dermal so it doesn’t do much but can inject steroids but not the most.
Firm, red-violaceous, annular plaques NO SCALE Dorsal hands & feet Asymptomatic Mostly in children & young adults Self-resolving vs. chronic Can be generalized, rarely! Association (weak) with diabetes |
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PORPHYRIA CUTANEA TARDA
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Inherited blistering disease
Deficiency of UROPORPHYRINOGEN DECARBOXYLASE Skin fragility, bullae & erosions Hypertrichosis Photosensitivity Alcohol, drugs, oral contraceptives, Hepatitis C Clinical, serologic, urine (orange-red fluorescence under Wood’s lamp) Phlebotomy |
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What combination of conditions can cause PCT?
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Alcoholism + Hepatitis C
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PYODERMA GANGRENOSUM
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Inflammatory disease, not infectious
Associated: Inflammatory bowel disease Gammopathy Rheumatoid arthritis Lymphomas and Leukemias Begins as small pustule, develops into painful, indurated ulceration Rolled or “undermined” border Often bilateral legs Biopsy is not diagnostic Requires systemic immunosuppression |
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What's the first thing you should think of when you see that a lesion has a rolled or undermined border?
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PYODERMA GANGRENOSUM
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After pyoderma gangernosum heals what do you end up with?
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stellate scars
Note that there is vascular congestion in pyoderma gangrenosum but it is not vasculitis or vasculopathy |
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PRURITIC URTICARIAL PAPULES AND PLAQUES OF PREGNANCY
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PUPPP
Generalized pruritic eruption Begins in striae Abdomen, buttocks, breasts Third trimester First pregnancy Must distinguish from Herpes Gestationis Resolves after delivery Treat with steroid cream, rarely oral prednisone |
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HERPES GESTATIONIS
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Begins in second trimester
Urticaria becomes vesicles/bullae Prematurity, fetal demise Post partum exacerbations Can recur with subsequent pregnancies Immunofluorescence: shows C3 at basement membrane zone |
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ACRODERMATITIS ENTEROPATHICA
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Worsening “rash”
Small for age Normal pregnancy Weaned from breast milk 2 weeks ago Zinc Deficient There is a conjugating protein in breast milk that helps zinc be absorbed in a breast fed baby with this. Why it presents after breast feeding is done. |
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What is the clinical picture of acrodermatitis enteropathica?
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Pustules, Bullae, Scaly Patches
Oroficial and genital locations Face and groin with patchy, red, dry scaling with exudation and crusting Generalized alopecia, nail dystrophy Diarrhea, growth retardation, etc. Hyperpigmentation with desquamation of the dorsal aspects of the hands and forearms |
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How do you dx and tx acrodermatitis enteropathica?
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DIAGNOSIS: low plasma and hair zinc levels
TREATMENT: zinc supplements |
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Cutaneous Manifestations of HIV and AIDS
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Papular eruption of AIDS Thrush
Xerosis (Dry Skin) Eosinophilic folliculitis Drug Eruptions Kaposi’s Sarcoma Seborrheic Dermatitis Bacillary Angiomatosis Tinea Oral Hairy Leukoplakia Molluscum contagiosum Condyloma acuminata Herpes Simplex Herpes Zoster |
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What are pilosebaceous and nail aparatus derived from?
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epidermal derivatives
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What is the only permanently regenerating organ?
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hair follicle
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What is the significance of The Bulge in the pilosebaceous Unit?
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Injuries above the line even with the bulge will regenerate from cells in the bulge (stem cells). If below this it can't.
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What is the pathophys of gray hair?
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Less melanin pigment because of fewer / loss of melanocytes
irreversible |
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What is the point of the oblique angle of hair?
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Layering effect = protection
Facilitates transport and spread for sebum, debris, and apocrine sweat Angle can be varied by arrector pili muscle Under adrenergic control |
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What are the 3 types of hair?
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Terminal
> 1cm Eyelash/eyebrow, beard, “abnormal beard” in women Vellus Most abundant Fine, < 1cm “normal” beard in women Lanugo Mostly gone at birth Sign of anorexia nervosa |
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What determines whether hair is straight, wavy, curly, or kinky?
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the hair shaft shape
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Anatomy/histology variation relative to African American hair
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Curved hair follicle
Commonly a spiral shaped hair shaft Same number of melanocytes increased number & size of melanosomes |
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What are the 3 phases of the hair follicle cycle?
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Anagen- growing phase, hair production; duration is 3-6 years or 1000 days; makes up 85% of hair
Catagen: Involution phase; lower follicle collapses; duration 2-3 weeks; percentage of hair 3% Telogen: resting phase; club hair produced; 3 months or 100 days; percentage of hair 12% |
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How fast does scalp hair grow?
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0.4 mm/ day (1/2 inch/month)
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What is the physio of eyebrow, extremeties, and trunk hair growth?
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Grows for 6 months or less
Resting phase for 3 months |
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When examining the scalp what might you focus on in physical examination?
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Hair loss pattern
-Diffuse vs Patchy -Scarring vs Nonscarring Presence of inflammation, scale, pustules Condition of remaining hairs -Length: broken into dots or stubble -Diameter: tapered into exclamation point -Nonpigmented |
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How is scarring (cicatricial) alopecia classified?
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Primary
-Lupus erythematosus -Lichen planopilaris -Acne keloidalis -Dissecting cellulitis Secondary -Trauma (burns, traction) |
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What are some examples of non-scarring alopecia?
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Alopecia areata
Androgenetic alopecia Trichotillomania Telogen effluvium Anagen effluvium 2o Syphilis Loose Anagen syndrome Hair shaft disorders |
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What are the 4 most common alopecias?
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Alopecia areata
Androgenic alopecia Anagen effluvium Telogen effluvium |
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Alopecia Areata
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Well demarcated, patchy, hair loss
Any hair bearing area Alopecia totalis (entire scalp) Alopecia universalis (entire body) Etiology: unknown Affects children and adults, M=F |
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Pathogenesis of alopecia areata
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autoreactive T-lymphocytes interact with antigens expressed by keratinocytes & possibly melanocytes in the bulb of the hair follicle.
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Course of Alopecia Areata
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variable, spontaneous remission
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What are some predictors of poor prognosis of alopecia areata
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childhood onset, widespread involvement, acute onset, ophiasis pattern, onychodystrophy, atopic dermatitis
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When would you see "exclamation point hairs"?
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Alopecia Areata
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Androgenetic Alopecia
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Most common form of hair loss affecting men and women
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What is the pathogenesis of Androgenic Alopecia?
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Pathogenesis: androgen dependent, genetically mediated form of hair loss
↑ 5-α-reductase ↑ androgen receptors scalp Miniaturization of hair follicle (shortening and narrowing of hair shaft ) & ↓ hair density |
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Ludwig Patterns
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Female Pattern Alopecia
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Treatment of Androgenetic Alopecia
|
Medical
Finasteride (Propecia): 5 -- reductase inhibition blocks peripheral conversion of testosterone to dihydrotesterone Topical minoxidil (Rogaine): vasodilator Surgical Hair transplantation Scalp reduction |
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Anagen Effluvium
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Direct toxic insult to mitotic & metabolic processes in the hair bulb
leads to hair shaft thinning, fragility, breakage, or failure of hair formation. Shedding 2 - 4 weeks after 1st dose |
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What is the etiology and course of Anagen Effluvium?
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Etiology: radiation, chemotherapy, drugs
Course: Total alopecia is common Total recovery once toxic insult removed |
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Telogen Effluvium
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3-5 months after “ inciting event”
Premature conversion anagen to telogen hairs Common inciting events: childbirth, fever, diet, surgery, drugs Estimated hair loss 150-400 / day Positive hair pull test Spontaneous growth in a few months |
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Causes of Telogen Effluvium
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Nutritional: protein or caloric deprivation, deficiency in: biotin, Zn, Fe, essential fatty acid
Childbirth Thyroid disease Androgen excess Massive blood loss Fever Surgery Severe medical illness Medications |
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Medications Associated with Telogen Effluvium
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Discontinuation of estrogen containing products, e.g. “birth control pills”
Antidepressants (amitriptyline, nortriptyline) Anticoagulants (Coumarin) Beta-blockers Retinoids (etretinate, excess vitamin A) Lithium |
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Learn the anatomy of a nail
|
Learn the anatomy of a nail
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Nail Plate Growth
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Nail plate synthesized by nail matrix
Thickness is directly proportional to size of matrix Growth rate Fingernails: 0.1 mm/day, 6 months to grow out Toe nails: ½ the rate of fingernails, 12-18 months to grow out Higher rates of growth: children, pregnancy, warm weather |
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Onychodystrophy
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Changes in the nail plate shape occurring as a congenital defect or due to any illness or injury that may cause a malformed nail
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Evaluation of Nail Disorders
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History: Trauma
Past medical history Medications Occupation Personal habits Grooming Physical exam Dermoscopy / Dermatoscopy / Epiluminescence microscopy KOH preparation Culture Biopsy |
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Signs of Psoriasis in the nails
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nail pitting, oil spots, distal onycholysis
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Signs of Lichen Planus in the nails
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longitudinal ridging and fissuring
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Signs of Darier's Disease in the nails
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“candy-cane” nails, v-shaped nicking
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What are nail signs of systemic disease?
|
Cardiopulmonary: cyanosis, clubbing (aortic aneurysm, bronchogenic ca)
Pulmonary / Sinopulmonary: yellow nail syndrome (lymphedema, chronic bronchitis, bronchiectasis) Renal disease: Lindsay’s nails (Half & Half nails) Hepatic cirrhosis: Terry’s nails Autoimmune disease: periungual telangectasias HIV: proximal subungual onychomycosis Heavy metal intoxication: Aldrich-Mee’s lines Toxic insult/chemo: Beau’s lines |
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Yellow Nail Syndrome
|
Next test would be chest x-ray since associated with chest issues (lung disease)
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Lindsay’s nails (Half & Half nails)
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Renal disease
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Onychomycosis
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Onychomycosis: describes any fungal nail infection caused by dermatophytes & non-dermatophyte fungus
Dermatophyte (skin fungi): Trichophyton rubrum Epidermophyton floccosum Trichophyton mentagrophytes Non-dermatophyte molds: Scopulariopsis brevicaulis, Aspergillosis, Fusarium Yeast: Candida typically affects finger nails Clinically causing nail plate separation from nail bed (onycholysis), subungual debris, thickened, brittle, yellow colored nails Clinical types: Distal Subungual Onychomycosis Proximal Subungual Onychomycosis White Superficial Onychomycosis |
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Pigmented Streaks in Nails
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Melanoma
Nevus Physiologic variant |
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Hutchinson’s Sign
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Melanoma
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Longitudinal melanonychia
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Physiologic variant
Longitudinal pigmented bands Longitudinal melanonychia Melanonychia striata longitudinalis Well demarcated longitudinal pigmented streaks in darker skinned patients Usually a normal physiologic finding and involves multiple nails Differentiate from melanoma |
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Terry's nails
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hepatic cirrhosis
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Proximal Subungual Onychomycosis
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HIV
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Periungual Telangietasia
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Autoimmune Diseases
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|
Epidemiology of acne
|
40-50 million individuals each year in the US alone
Annual cost in the US of at least $2.5 billion Highest frequency in adolescence Affects 85% of 12-24 year olds, but… 12% of women and 3% of men will continue to have clinical acne until 44 years of age |
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What are the 4 players in acne pathogenesis?
|
Hyperproliferation and abnormal differentiation of follicular keratinocytes
Increased sebum production Infection from Propionibacterium acnes Inflammation |
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What is the pathogenesis of acne?
|
Multifactorial disorder of the pilosebaceous unit
Exclusively a follicular disease Some genetic predisposition |
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How does abnormal desquamation contribute to acne formation?
|
Normally, keratinocytes are shed into follicular lumen & extruded
In acne, keratinocytes are retained & accumulate in the upper portion of the follicule (infundibulum) Increased intercellular cohesiveness & keratinocyte proliferation -> bottleneck -> microcomedo |
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How does inflammation contribute to acne formation?
|
Comedo expands due to keratinocyte accumulation & cohesion
Contents become closely packed, forces increase, comedone wall ruptures Inflammatory reaction to extruded immunogenic keratin & sebum |
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What is Propionibacterium acnes and how does it cause acne?
|
Gram positive, non-motile rod
Found deep within sebaceous follicles Pathogenecity: Induces proinflammatory mediators via TLR2 on monocytes (IL-1, IL-8, TNF-alpha), activates complement & neutrophil chemotaxis Makes lipase – contributes to comedo rupture |
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What are the non-inflamm clinical features of acne?
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Open comedones: “black heads”
Closed comedones: “white heads” |
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What are the inflammatory clinical features of acne?
|
Papules
Pustules Cystic nodules can be scarring |
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How do hormones affect acne?
|
Both testosterone & DHT can bind to receptors in sebaceous glands & hair follicles
DHT has greater affinity for receptor main androgen in sebum production At adrenarche, adrenals produce increased androgens (DHEAS) resulting in increased sebum production Also high in first 6 months of life |
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What are some general rules of treatment?
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Take a good history
Explain that topicals should be applied to entire affected area, daily Daily to twice daily use leads to prevention Scrubbing increases irritation and acne formation #1 cause of treatment failure = lack of compliance Can take 6-8 weeks to see an effect & acne can worsen during the first month of treatment |
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What are some topical treatments of acne?
|
Topical retinoids
Benzoyl peroxide Topical antibiotics Others: Topical dapsone Topical sulfacetamide Topical azeleic acid |
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What are some systemic tx of acne?
|
Oral antibiotics
Isotretinoin Hormonal acne in females Oral contraceptives Spironolactone |
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How do retinoids treat acne?
|
Comedolytic: promote normal desquamation of follicular epithelium reduce comedones and inhibit new lesion development
Anti-inflammatory: inhibit activity of leukocytes, release of proinflammatory cytokines, transcription factors and TLRs in immunomodulation Helps penetration of other active agents eg Epiduo adapalene + BP Use: nightly, pea-sized amount for entire face #1 Side effect = irritation (so start out every other night) |
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How does benzoyl peroxide treat acne?
|
Anti-bacterial & anti-inflammatory > comedolytic
Bactericidal against P. acnes no resistance! Use w/antibiotics limits resistance, even for short use! Bar soaps, washes, gels and lotions are available in concentrations of 2.5%, 5% and 10% Wash best for mild truncal acne Use: daily or BID dosing Side Effects: May produce some itching and dryness Warn patients about bleaching effect (on towels, pillow cases etc) |
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What topical antibiotics do you use to treat acne?
|
clindamycin & erythromycin
Anti-bacterial, anti-inflammatory > anti-comedogenic Variety of formulations Use: BID Well tolerated for mild-moderate inflammatory acne Increasing antibacterial resistance, so DO NOT use alone Use with benzoyl peroxide or tretinoin ex. Benzaclin |
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When do you use systemic treatment for acne?
|
Moderate to severe acne
Inflammatory disease when topicals have failed Treatment of chest, back, shoulders People who scar with new lesions, or those with inflammatory hyperpigmentation Most oral courses are at least 3-6 months |
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How do tetracyclines affect acne treatment?
|
Mechanism of action: antimicrobial & antiinflammatory
Warn about sun sensitivity, GI upset/esophagitis, staining of teeth, gums, shins, scars Tetracycline is cheapest, but must be taken on an empty stomach OK to take doxycycline and minocycline with food Minocycline: a lipophilic derivative of tetracycline, likely greater penetration into sebaceous follicle |
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Who do you treat with isoretinoin for acne?
|
Severe cystic acne, poorly responsive after 6 months of oral and topical regimens, acne that relapses after oral treatment, scars, psychological distress
Acne variants: Gram negative folliculitis, inflammatory rosacea, acne fulminans, hidradenitis suppurativa |
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How does isoretinoin treat acne? (mechanism)
|
Prohibits maturation of basal cells in sebaceous gland atrophy
Up to 90% reduction in sebum No sebum Poor P. acnes growth Normalizes follicular keratinization |
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Dermatosis
|
any pathologic condition involving the skin
|
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Dermatitis
|
any inflammatory skin disorder
|
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Eczematous Dermatitis
|
The most common inflammatory reaction pattern in skin disease. May have a variety of causes, so should never be considered as a specific skin disease or disorder. It is an immunologic (mainly type IV) response of skin to a variety of antigens. It involves the interaction of both T (thymus derived) and B (marrow derived) lymphocytes. As a result, vasoactive factors are liberated which have inflammatory, destructive, and proliferative effects on the skin and result in characteristic clinical signs and pathologic changes.
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|
What are the clinical signs of acute dermatitis?
|
erythema
edema vesicles or bullae (blisters) oozing |
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What are the clinical signs of subacute dermatitis?
|
crust
scale |
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What are the clinical signs of chronic dermatitis?
|
thickening (lichenification)
Hyper- or hypopigmentation |
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|
What are the pathologic correlation for acute dermatitis?
|
dilation of superficial capillaries
bound serum in dermis free serum in epidermis (separation of epidermal cells by serum (spongiosis)---hallmark!) serum reaching the surface of the epidermis |
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|
What are the pathologic correlation for subacute dermatitis?
|
Dried serum and cellular debris on surface of epidermis
excess keratin |
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|
What are the pathologic correlation for chronic dermatitis?
|
Epidermal thickening (acanthosis) with elongation of rete ridges
Stimulation or inhibition of melanocytes, sometimes destruction of melanocytes |
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|
allergic Contact Dermatitis--what causes it?
|
cell damage resulting from a cellular (delayed, Type IV) immune reaction Acquired through exposure.
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|
Natural history of allergic contact dermatitis
|
5-10% of the population is sensitive to some environmental or occupational chemical.
b. 60% of North Americans are sensitive to plants of the Rhus family (poison ivy, oak, or sumac). May account for 30% of occupational skin diseases |
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|
What are the risk factors of allergic contact dermatitis?
|
increased pressure, friction, heat, H2O exposure
atopic history |
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|
3 characteristics of contact allergens
|
low molecular weight
lipid solubility chemical reactivity aka a hapten... need to invade and bind to be activated |
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|
What are the two phases of sensitization?
|
Induction
elicitation re-exposure takes very little time and can be more severe |
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|
Requirements for T cell activation:
|
Attachment and stabilization
Signal 1: antigen/ MHC-TCR Signal 2: costimulation Signal 3: proliferation and differentiation |
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|
What are the characteristics of mild acne?
|
Some comedones
No more than a few papules/pustules No nodules |
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What are the characteristics of moderate acne?
|
Many comedones
Some inflammatory lesions No more than 1 small nodule |
|
|
What are the characteristics of severe acne?
|
Many comedones & inflammatory lesions
A few nodules, cysts |
|
|
What is the mechanism of action of isoretinoin?
|
Prohibits maturation of basal cells in sebaceous gland atrophy
Up to 90% reduction in sebum No sebum Poor P. acnes growth Normalizes follicular keratinization |
|
|
What are the side effects of isoretinoin?
|
Dry skin, lips, eyes, oral and nasal mucosa: 90%
Pregnancy contraindicated d/t birth defects – iPledge system monitoring Hepatotoxic so must avoid alcohol |
|
|
What qualities increase risk of relapse in those who use isoretinoin?
|
age < 16
adult women and mild acne |
|
|
What factors give you clues that acne is under hormonal influence?
|
Flares around time of menses
Involvement of “hormonal areas”: chin, lower cheeks Worry about excess androgens: Irregular menses Hirsutism Resistant to traditional treatments Severe sudden onset Quick relapse after isotretinoin Women with late acne |
|
|
How would you work up a case where you thought someone had acne due to hormonal influence
|
Labs: DHEAS, 17-OH progesterone, free testosterone, LH/FSH
Elevated DHEA-S or 17-hydroxyprogesterone = Congenital adrenal hyperplasia or adrenal tumor Elevated total testosterone = ovarian tumor, PCOS Elevated LH/FSH = PCOS |
|
|
What treatments would you use to treat a woman with acne due to hormones (excess androgens)?
|
Oral contraceptives: block adrenal and ovarian androgens
Spironolactone: androgen receptor blocker and inhibitor of 5α reductase |
|
|
Is acne influenced by diet?
|
Can be linked to dairy because of the IGF-1 and hormones in milk. Both IGF-1 and androgens increase sebum production.
High glycemic load might associate with acne Associations but not totally causal |
|
|
What are the complications of acne?
|
Scarring
Often with cystic type of acne Pitted scars, wide depressions, keloids on jaw and chest Prominent hyperpigmentation: Especially in pts w/darker skin |
|
|
Neonatal acne (Neonatal cephalic pustulosis)
|
20% of healthy newborns
Facial papules or pustules, cheeks, nose Cause: Malassezia? Maternal hormones? Days after birth, resolves w/in 3 months |
|
|
Infantile acne
|
Persists beyond neonatal or starts after 4 weeks, more comedonal, resolves 1-2yr
Topicals: BP, erythromycin, retinoids Oral tx: erythromycin, isotretinoin |
|
|
Childhood acne
|
Evolves from infantile acne or starts after age 2
M> F Face: papules, pustules, comedones, nodules Weeks to years +family history |
|
|
Acne Fulminans
|
Rare type of severe cystic acne
Mostly teenage boys Abrupt onset nodular & suppurative acne on chest and back > face |
|
|
What are the systemic complaints associated with acne fulminans?
|
fever, leukocytosis, polyarthralgia, polymyalgia, destructive arthritis, myopathy, osteolytic bone lesions (clavicle/sternum)
|
|
|
How would you treat acne fulminans?
|
Aggressively!
Prednisone for first 4-6 weeks Followed by isotretinoin Intralesional steroids can help resolve opened large cysts |
|
|
Acne Conglobata
|
Eruptive, severe nodulocystic acne WITHOUT systemic symptoms
Back, buttocks, chest, face, anterior neck, shoulders Often adolescent men: can persist into adulthood (posterior neck and back) |
|
|
How would you treat acne conglobata?
|
Pretreat with prednisone
Isotretinoin (may require multiple courses) |
|
|
Acne mechanica
|
Secondary to repeated mechanical & frictional obstruction of pilosebaceous outlet
Due to: rubbing from helmets, chin straps, suspenders, collars, backpacks Linear, geometrically distributed |
|
|
Acne Excoriee
|
Acne excoriee des jeunes filles; picker’s acne
Young women Typical comedones & inflammatory papules are systematically & compulsively excoriated Crusted erosions result +/- scarring |
|
|
What can acne excoriee be a sign of?
|
depression, anxiety, OCD
|
|
|
What is the tx of acne excoriee?
|
SSRIs, behavior modification, psychotherapy
|
|
|
What are some of the more common culprits in drug-induced acne?
|
Anabolic steroids
Corticosteroids Phenytoin Corticotropin Lithium Isoniazid Iodides Bromides Epidermal growth factor receptor inhibitors |
|
|
What are some of the less common culprits of drug-induced acne?
|
Azathioprine
Cyclosporine Vitamins B & D Phenobarbital PUVA Propylthiouracil Disulfuram Quinidine |
|
|
Gram-Negative Folliculitis- who gets it and where?
|
Occurs in pts with longstanding inflammatory acne treated with long-term tetracyclines
On antibiotics, superficial 3-6mm pustules flaring from anterior nares or fluctuant deep-seated nodules |
|
|
What are some common culprits in gram negative folliculitis?
|
Klebsiella, E. coli, Enterobacter, Proteus (deep lesions)
|
|
|
What are the treatments of gram-negative folliculitis?
|
Isotretinoin first-line (clears acne component and eliminates colonization of anterior nares of gram negative organisms)
Amoxicillin or trimethoprim/sulfamethoxazole if isotretinoin not tolerated |
|
|
Acne Keloidalis
|
Fibrosis with firm papules developing into keloids on posterior scalp/neck
Sinus tract formation can occur Not associated with acne vulgaris Variant of scarring alopecia Young healthy adult males of black, Hispanic, or Asian background |
|
|
Hidradenitis Suppurativa
|
“Acne inversa”
Recurrent sterile abscess formation Tender red nodules: firm --> fluctuant and painful Nodules rupture --> suppuration --> sinus tracts --> extensive scarring Axillae, inguinal, perineal > buttock and submammary W > M |
|
|
What is the etiology of hidradenitis suppurativa?
|
Friction, smoking, obesity, endocrinopathies, irritants, immunologic dysfunction: --> none proven to be causative
|
|
|
What is the treatment for Hidradenitis Suppurativa?
|
Cure uncommon
Early lesions: IL steroids, topical clindamycin, PO tetracyclines Incision & drainage not useful Systemic: Isotretinoin: limited success, secondary S. aureus infections Infliximab and finasteride Surgical excision = best recurrence rates |
|
|
Rosacea
|
Persisent erythema +/- acneiform papules of central face
Telangiectasias, flushing, erythematous papules, pustules Cheeks/nose > brow/chin > often spares periocular skin |
|
|
Who gets rosacea most commonly?
|
Often light-skinned women aged 30-50
|
|
|
What changes are seen in men with rosacea?
|
Rhinophymatous changes
|
|
|
What is the etiology of rosacea?
|
Multifactorial
Vascular hyperreactivity Hyperirritable skin Telangiectasia and fibrosis are due to chronic vasodilatation, edema and lymphatic drainage compromise H. pylori and Demodex mites: NOT felt to be causative |
|
|
Erythematotelangiectatic
|
Rosacea Subtype
Prolonged flushing (>10 min) Reaction to stimuli (stress, alcohol, spices, exercise, cold or hot weather) Often burning or stinging sensation |
|
|
Papulopustular
|
Rosacea Subtype
Striking red central face with erythematous papules & pinpoint pustules Flushing, but less irritation |
|
|
Glandular/Phymatous Rosacea
|
Rosacea subtype
Mostly men with thick sebaceous skin Edematous papules, pustules , nodulocystic lesions H/o adolescent acne Flushing less common, but persistent edema Rhinophyma most common |
|
|
Ocular Rosacea
|
Rosacea subtype
Ocular involvement in up to 50% cases of rosacea M = W Can cause: Blepharitis, recurrent chalazion, conjunctivitis Keratitis, iritis, episcleritis Gritty, stinging, itchy, burning, or foreign body sensation Can occur before skin findings |
|
|
What is the treatment for erythematotelangiectatic rosacea?
|
Light green foundation
Pulse dye lasers |
|
|
What is the treatment for papulopustular rosacea?
|
Topical: metronidazle, sulfacetamide +/- sulfur, and azelaic acid, benzoyl peroxide
Systemic: tetracycline antibiotics |
|
|
What is the treatment for ocular rosacea?
|
Tetracycline antibiotics
|
|
|
What is the treatment for glandular rosacea?
|
Topicals: above plus benzoyl peroxide/clindamycin
Systemic: tetracycline antibiotics (help with ocular lesions) Isotretinoin for more resistant disease |
|
|
Periorificial Dermatitis
|
Acneiform papules and pustules around eyes, mouth, or both
Usually symmetric with 5 mm clear zone around lips NO itching, but sometimes burning Women between 20-35 Associated with use of fluorinated steroids (creams, ointments, or inhalers) |
|
|
What is the treatment for periorificial dermatitis?
|
Stop steroids
Steroid-sparing topical: Tacrolimus or pimecrolimus Azelaic acid, metronidazole Oral tetracycline antibiotic |
|
|
Common allergic sensitizers
|
Rhus plants, nickel, rubber compounds, paraphenylenediamine (hair dye), benzocaine, formaldehyde, preservatives, fragrances
|
|
|
What are definitions in the afferent pathway of the sensitization process? (refractory period and induction)
|
(1) Refractory period: The highly variable time from first contact until the sensitization process begins.
(2) Incubation period (induction): From the beginning of the immunologic process leading to allergy until the first clinical manifestation. Usually between 10 and 30 days. Not less than 5 days. |
|
|
What are definitions in the efferent pathway of the sensitization process? (elicitation and persistence)
|
(3) Reaction time (elicitation): The time from the contact of the allergen with sensitized skin until the first clinical signs of reaction. Usually not under 4 hours and may be 24 hours or longer.
(4) Persistence of sensitivity: Usually for life. May diminish somewhat over a period of many years. There is no known way to safely desensitize for this type of allergy. |
|
|
What are langerhans cells and how do they mediate allergic contact dermatitis?
|
. Langerhans cells are the specialized type of macrophage in the epidermis that mediate allergic contact dermatitis by processing contact dermatitis haptens and presenting the antigen to T-lymphocytes.
|
|
|
What cells are involved in the induction phase of allergic contact dermatitis?
|
Keratinocyte involvement via stimulation of toll like receptors with the help of molecules like IL-1, GMCSF, TNF, IL-6.
T-cell/LC involvement: stabilization, presentation, costimulation, proliferation Mast cell involvement Neuronal input |
|
|
What cells are involved in the efferent (elicitation) phase of allergic contact dermatitis?
|
Keratinocyte involvement
T-cell/LC involvement Endothelium involvement |
|
|
What cells are involved in the down-regulation/Tolerance phase of allergic contact dermatitis?
|
Through B7 family of proteins
Through cytokines and Th differentiation Through CD-24/CD25 T cells and other Tregs |
|
|
What are the physical findings in allergic contact dermatitis?
|
An initial erythema may progress to an intense inflammatory response with papules and vesicles. As the vesicles rupture, the surface becomes moist and crusted. Large bullae may form if the reaction is severe. The distribution is often suggestive of the diagnosis; palms are rarely affected. Healing occurs over a few days to weeks.
If contact is repeated, the reaction always recurs and recurrence may be more rapid and severe. The eruption is usually pruritic, and secondary bacterial infection may occur. The severity is proportional to the duration of contact with and concentration of the allergen (contactant). The degree of sensitivity of the individual is also important. May generalize - ID reaction. |
|
|
What is a variant of allergic contact dermatitis?
|
systemic contact
|
|
|
What are the lab findings in allergic contact dermatitis?
|
Eczematous dermatitis (?)
Patch testing with suspected allergens can be useful in dx. May not be necessary with clear history. |
|
|
What is the differential dx of allergic contact dermatitis?
|
Primary irritant contact dermatitis
Atopic dermatitis Seborrheic dermatitis Light-sensitivity dermatitis: history of sun exposure with occurrence of lesions in sun-exposed areas Dermatophyte or candida infection Stasis dermatitis: [may be complicated by contact dermatitis] |
|
|
What is the tx of allergic contact dermatitis?
|
Avoidance of contactants/education
Cold compresses Topical or systemic corticosteroids Antihistamines Barrier creams |
|
|
What is primary irritant contact dermatitis?
|
Cell damage develops on first exposure in most people, given sufficient time and adequate concentration of the agent. Acute/Absolute irritants (ie., strong acids and alkalis). Chronic/Relative irritants (ie., solvents, detergents)
|
|
|
What increases susceptibility for primary irritant contact dermatitis?
|
cold, windy weather, decreased humidity, increased temp (which causes increased sweat), friction/injury, atopic hx, age (both very old and very young more susceptible)
|
|
|
What kind of skin is more sensitive to irritants?
|
fair-skinned whites are more sensitive to irritants than darker-skinned individuals
|
|
|
What is the pathophysiology of primary irritant contact dermatitis?
|
Irritants may induce reactions by binding to Toll like receptors (TLR) on the keratinocytes and thereby stimulate the immune system.
Soaps, detergents, and most solvents require repeated and/or prolonged contact at a threshold concentration to produce the initial inflammation. Interestingly some potent contact allergens may initiate skin reactions by binding to TLR also. |
|
|
What are the physical findings of primary irritant contact dermatitis?
|
A careful history of occupational, home, environmental, hobbies, medications, clothing, cosmetics, and other contactants will usually disclose the irritant or predisposing event. (Water, detergent, alkalis, solvents, and cutting oils are common irritants.)
Early, dry skin with fissures may be followed by the formation of red papules and vesicles with oozing and crusting with relative sparing of the palms. If the process persists, lichenification and further fissuring may occur. An irritant dermatitis often begins under rings and jewelry without allergic sensitivity. The course may be prolonged, with exacerbations and remissions dependent on exposure. Hardening occurs with time. Once irritant discontinued, rash improves over 1-3 weeks. |
|
|
What are the lab findings associated with primary irritant contact dermatitis?
|
Eczematous dermatitis on biopsy. Negative patch tests to suspected antigens.
|
|
|
What is the differential dx for primary irritant contact dermatitis?
|
Allergic contact dermatitis
Atopic dermatitis Psoriasis (1)Distribution of lesions will most likely be on the elbows, knees, and scalp. (2) Contact dermatitis may precipitate or aggravate psoriasis in susceptible person. Dermatophyte or candida infections. Skin scrapings will show fungal forms. |
|
|
What is the tx for primary irritant contact dermatitis?
|
Protection of the affected hands or area with avoidance or reduction of heat, moisture, soaps, perspiration, friction, and pressure.
Compresses to acute eruptions: Burrow's solution (1:20 dilution) cold compresses for 20-30 min q 4-6 hr Topical or systemic corticosteroids (depending on severity)-vasoconstrictors, immunosuppressors, stabilize lysosomes Antihistamines for control of pruritus |
|
|
What is the difference in the mechanism of response for irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: Activation of innate immune system
Via Toll like receptors Allergenic: Delay hypersensitivity reaction Activation of adaptive immunity |
|
|
What is the difference between who is at risk for irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: everyone
Allergenic: genetically predisposed |
|
|
What is the difference in the # of exposures required for irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: Few to many; depends on
Individual's ability to maintain an Effective epidermal barrier Allergenic: One or several to cause sensitization |
|
|
What is the difference in the nature of contactant for irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: organic solvent, soap
Allergenic: low molecular weight hapten (metals, formalin, epoxy) |
|
|
What is the difference in the concentration of contactant required for irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: usually high
Allergenic: may be very low |
|
|
What is the difference in the mode of onset for irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant:usually gradual as epidermal barrier becomes compromised
Allergenic: once sensitized, suually rapid; 12-48 hours after exposure |
|
|
What is the difference in the distribution for irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: borders usually indistinct, stays localized, red and itchy/burning sensation
Allergenic: may correspond exactly to (watch band, elastic waistband), may generalize, blistery and itchy |
|
|
What is the difference in the investigative procedure for irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: trial of avoidance
Allergenic: Trial of avoidance, path testing, or both |
|
|
What is the difference in the management of irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: protection and reduced incidence of exposure
Allergenic: complete avoidance |
|
|
What is the difference in the symptoms of irritant chemical vs allergenic chemical contact dermatitis?
|
Irritant: burning and stinging sensation
Allergenic: often intense pruritus |
|
|
Seborrheic Keratoses
|
Proliferation of keratinocytes
80-90% of >50 population will have some Etiology unknown |
|
|
How do you treat seborrheic keratoses?
|
Treatment may not be necessary
When symptomatic: Liquid nitrogen Electrodessication Curettage |
|
|
Dermatosis Papulosis Nigra
|
Variant of Seborrheic Keratosis
Common with darker skin Strong familial tendency |
|
|
Acrochordon
|
Skin Tag
Common benign skin polyp Usually in intertriginous areas Common in pregnancy and obesity |
|
|
Epidermal Cyst
|
Occluded pilosebaceous follicles
Cyst formed by production of keratin and lack of communication with surface Treat in symptomatic lesions by complete removal of sac May I&D acutely inflamed cysts |
|
|
Gardner’s Syndrome
|
Multiple epidermal cysts
Intestinal polyps with high malignant potential Autosomal dominant inheritance |
|
|
Pyogenic Granuloma
|
Proliferation of capillaries in response to local trauma
More common in children and pregnant women Bleeds easily Treat by shave removal and cautery |
|
|
Pilar Cyst
|
Nodular lesion of scalp
Derived from follicular cells Strong familial tendency Treat symptomatic lesions with excision, particularly proliferating cysts |
|
|
Dermatofibroma
|
Common, firm papule
Overlying erythema or hyperpigmentation Characteristic dimpling with palpation May arise from trauma or insect bite |
|
|
Actinic Keratosis
|
Up to 10% may become squamous cell or basal cell carcinoma
Most common in sun-exposed areas Treat with superficial destruction Liquid nitrogen Chemical destruction Curettage |
|
|
Squamous Cell Carcinoma in-situ
|
Also called Bowen’s Disease
Changes limited to the epidermis Erythema, scaling, thin plaque Locations Trunk—arsenic exposure Penis—erythroplasia of Queryant Mucosal surface--leukoplakia |
|
|
How do you treat Bowen's disease?
|
Treatment
Excision Curettage Chemical |
|
|
Squamous Cell Carcinoma
|
Arise from keratinizing epidermal cells
UV light exposure primary etiology Metastatic potential Greater risk in immunocompromised patients CLL Solid organ transplants Usually solitary, enlarging nodule Frequently painful Most common in >60 yo |
|
|
How to treat squamous cell carcinoma?
|
Confirm diagnosis with biopsy
Excision is standard |
|
|
Keratoacanthoma
|
Low grade squamous cell carcinoma
Sun damaged skin Rapid growth Dome-shaped, volcano appearance with central plug Treat with excision |
|
|
Basal Cell Carcinoma
|
Arise from pluripotential stem cells (basal cells) of epidermis
Stromal dependent Rarely metastisize Local destruction and tissue invasion |
|
|
What is the pathophys of basal cell carcinoma?
|
UV light exposure
Change in DNA structure Errors in DNA replication UVL induces tolerance to tumor growth UVB (290-320 nm) most important |
|
|
What are the genetic factors involved in the etiology of basal cell carcinoma?
|
Fair skin, blue eyes, Celtic origin
rare in dark skinned populations Common with conditions involving defects in genetic repair such as Xeroderma Pigmentosa Basal Cell Nevus Syndrome |
|
|
What are some non-genetic predisposing factors to basal cell carcinoma?
|
X-ray exposure
Ingestion of arsenicals Skin Injury Chronic Inflammation of the skin |
|
|
What are the physical findings in basal cell carcinoma?
|
Nodular: pearly, telangiectatic papule which may have pigment
Superficial: erythematous, scaly, thin plaque Morpheaform (sclerosing): whitish, scar-like appearance Cystic: translucent, gelatinous papule |
|
|
What is the differential dx of basal cell carcinoma?
|
Adnexal tumors
Seborrheic keratoses Melanoma Scars |
|
|
What is the tx for basal cell carcinoma?
|
(First confirm it with biopsy)
Specific tx tailored to type of BCC. Possible treatments: C&D, excision, radiation, cryotherapy Mohs microsurgery: recurrent, aggressive or large tumors, anatomically sensitive areas PREVENTION IS THE BEST TX!!! |
|
|
Nevus Definition
|
”Birthmarks”
Umbrella term for a group of benign, circumscribed overgrowth of cells composed of tissue elements normally present in the skin. |
|
|
melanocytic nevus
|
“mole”
most well known of the nevi composed of an increased proliferation of melanocytes, but multiple other types of nevi exist, such as vascular nevi, epidermal nevi, connective tissue nevi. |
|
|
Types of Nevo-melanocytic nevi
|
Junctional
Compound Intradermal |
|
|
Phases of nevo-melanocytic nevi
|
growth, maturation, resolution
|
|
|
Classification of nevo-melanocytic nevi
|
Acquired
Congenital: implies present at birth or near birth |
|
|
What would you see histologically in a compound nevus?
|
see nests of cells along the rete ridges that are "bridged" (interconnected along their bases)
|
|
|
What would you see histologically in a junctional nevus?
|
"nests" that are junctional (only in epidermis)
|
|
|
What would you see histologically in an intradermal nevus?
|
"nests" that are only within the dermis
|
|
|
What is the typical distribution of the 3 types of nevi: intradermal, compound, and junctional?
|
Intradermal: Head and Neck
Compound: Neck to groin Junctional: groin to feet. |
|
|
Lentigo
|
Not a nevus
Small circular to oval brown macules Elongation of rete Increased pigmentation No melanocytic hyperplasia |
|
|
Halo Nevus
|
White halo around nevus
Common in teenagers on upper back Due to infiltrating lymphocytes Most often idiopathic ↑ frequency in vitiligo and malignant melanoma |
|
|
Spitz nevus
|
(spindle and epithelioid cell nevus)
Benign melanocytic neoplasm vs. neoplasm of uncertain malignant potential Pink to brown papules Common on the head and neck Variants: multiple (grouped or disseminated) Atypical Spitz nevus “Malignant” Spitz nevus |
|
|
Blue Nevus
|
Solitary blue macule or papule
Due to spindle shaped cells in the dermis Tyndall effect |
|
|
Dermal Melanocytos
|
Baby looks blue but not from hypoxia
More common in darkly pigmented babies Due to ribbon-like melanocytes in the dermis Entrapment of melanocytes in the dermis during their migration from the neural crest to the epidermis Usually regresses by 3 to 5 years of age |
|
|
Congenital melanocytic nevus
|
mole that is found at birth.
1% of infants. Larger in diameter than normal nevi and often have excess hair too |
|
|
Vascular Nevi
|
Hemangiomas of infancy
Vascular malformations Nevus araneus Cherry angioma (hemangioma) |
|
|
Epidermal nevi
|
Linear epidermal nevus
Nevus sebaceus Becker’s nevus |
|
|
Hemangiomas of Infancy
|
Most common childhood tumor
Present: 1st days - weeks 5x more common in girls Typical growth pattern/involution Proliferation – up to 12 months Rest – 1 to 2 years Involution – years Head and neck is a common site (80%) Liver |
|
|
What are the worrisome locations of hemangiomas of infancy?
|
Beard area
Eyes |
|
|
How are glucose-1 transporters involved in dx of hemangiomas of infancy?
|
GLUT-1 positive distinguishes from vascular malformations.
It is the protein that facilitates the transport of glucose across the plasma membranes of mammalian cells. |
|
|
PHACES Syndrome
|
Posterior fossa malformation (Dandy-Walker variant)
Hemangioma of the cervicofacial region Arterial anomalies Cardiac anomalies and Coarctation of aorta Eye anomalies Sternal and/or supraumbilical raphe |
|
|
PELVIS Syndrome
|
Perineal hemangioma
External genitalia malformations Lipomyelomeningocele Vesico-renal abnormalities Imperforate anus Skin tag |
|
|
Vascular Malformations- what are they? How are they classified?
|
Anomalies of blood and lymphatic vessels due to abnormal development
Classified by vessel type and flow characteristics |
|
|
Sturge-Weber Syndrome
|
Sporadic
Capillary malformation V1 -Upper eyelid involvement Seizures Glaucoma Developmental delay |
|
|
Nevus Araneus
|
Spider angioma
Failure of the sphincteric muscle surrounding a cutaneous arteriole Dot is the dilated arteriole “Spider legs" are small veins Childhood-resolve spontaneously High estrogen states OCP Pregnancy Liver disease |
|
|
Cherry Angioma
|
AKA
-de Morgan spots -Cherry hemangioma Benign proliferation of capillaries Number and size increase with advancing age Eruptive may signal internal malignancy (this is rare) |
|
|
Epidermal Nevus
|
Hamartomas that are characterized by hyperplasia of the epidermis and adnexal structures
Linear epidermal nevi follow Blaschko’s lines |
|
|
Blaschko’s Lines
|
Trace migration of embryonic cells
Stripes are type of genetic mosaicism |
|
|
Nevus Sebaceus
|
Yellowish plaques
++ sebaceous glands Scalp and face Present at birth At puberty, become raised and verrucous In adulthood, can develop tumors |
|
|
What is the most common benign tumor that a nevus sebaceus could become?
|
syringocystadenoma papilliferum
|
|
|
What is the most common malignant tumor that a nevus sebaceus could become?
|
basal cell carcinoma
|
|
|
Becker’s Nevus
|
Male
First appears as an irregular pigmentation usually by age 20 Torso or upper arm Gradually enlarges irregularly, becomes thickened and hairy Benign |
|
|
Which skin cancer is responsible for 80% of deaths related to skin cancer?
|
Melanoma
|
|
|
What is the epi of melanoma?
|
Men > women (overall)
Males: 1 in 37 Women: 1 in 56 Increased incidence in Hispanics and African Americans compared to whites |
|
|
What is the most common cancer in women age 25-29 and second most common cancer in women age 30-34?
|
Melanoma
|
|
|
What are the ABCDEs of Melanoma detection?
|
Asymmetrical shape
Border irregularity Color variation Diameter > or = 6 mm (pencil eraser width) Evolution: change in the lesion over time |
|
|
What do the different colors in melanoma indicate?
|
Might see black in a variety of shades of also browns, pink, red, white, blue.
Red= inflammation, vascular dilation White= focal regression Blue= deep melanin pigment |
|
|
Besides the ABCDE qualities for dxing melanoma what are other suspicious factors?
|
Definite increase in size
Mottling of color, color change Ulceration Development of pain, tenderness or itch Heightened awareness of the lesion The “ugly duckling” lesion- just doesn’t fit in or look similar to patient’s other nevi Inflammation within or around the nevus “Little red riding hood” Bleeding or crust in absence of trauma |
|
|
Methods of Early Stage Melanoma Detection
|
Skin exam
Dermoscopy & clinical inspection Total body photography Computerized evaluation of pigmented lesion dermoscopic images |
|
|
Superficial spreading melanoma
|
~70%
Radial growth phase prior to invasion |
|
|
Nodular melanoma
|
~10-15%
Rapid growth from the outset Most common in 6th decade |
|
|
Lentigo maligna melanoma
|
~ 10%, elderly “the postage stamp”
Long horizontal growth phase Sun exposed skin of the elderly |
|
|
Acral lentiginous melanoma
|
~2-8% in Caucasians
~29-72% of melanoma in dark skinned individuals |
|
|
Amelanotic melanoma (not pigmented)
|
~ 2%
|
|
|
How does superficial spreading melanoma grow?
|
SSM- or superficial spreading melanoma has horizontal (or epidermal) growth initially. Later, a vertical (invasive) capacity is acquired. Thus, the urgency of diagnosis early to prevent that vertical growth phase, since DEPTH (Breslow, in mm) of the lesion correlates best with capacity for invasion and ultimate prognosis.
|
|
|
What is the melanoma distribution in women?
|
Leg: 56%
Arm: 17% Head and Neck: 14% Trunk: 13% |
|
|
What is the melanoma distribution in men?
|
Trunk: 35%
Leg: 25% Head and Neck: 23% Arm: 17% |
|
|
“Forgotten” Melanoma Locations
|
Periungual (or subungal) - around the nail or under the nail
Mucosal ~5% Genital 4.7% of melanomas in Caucasian/12%Hispanic/2%African American, Oral 1.9%, Anus and rectum .3%, urethra .2%, esophagus 0.1% Ocular ~5 % “Melanoma of unknown primary” – metastatic melanoma presents internally, but no original source from the skin is known. |
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|
More Common Anatomic Locations for melanoma in Blacks and Hispanics
|
Lightly pigmented skin of sole
-Mucous membranes -Subungual |
|
|
Is it worth it to screen the general population for melanoma?
|
There are no randomized control studies on it so it is not the recommendation but it is recommended to make the public aware of prevention/recognition and screen high risk individuals.
|
|
|
What are predisposing factors to melanoma?
|
Fair Complexion: poor tanning ability, light hair, light eyes, easily freckles, burns easily
UV radiation: sunburns in childhood/ sun exposure in childhood, intermittent sunburns in unacclimatized fair skin, cumulative sun exposure Types of nevi: large congenital nevi (>20cm)--lifetime risk is 5-20%, Atypical nevi, number of benign melanocytic nevi > 50 that are > 5mm Hx of melanoma- risk 3-5% of another melanoma Immunosuppression- increased risk 3x if solid organ transplant or inherited immunodeficiency DNA repair defects like Xeroderma Pigmentosum |
|
|
What are some genes implicated in melanoma?
|
CDKN2A (INK4a/ARF)
(Tumor Suppressor Gene) Correlation of mutations and families with atypical nevi/dysplastic nevus syndromes Germ line mutations in about 20-40% melanoma prone families Encodes 2 protein products that regulate cell cycle division P16(INK4) proteins inhibit cell cycle kinase CDK4– p16: RB pathway p14ARF acts on p53 pathway Both are negative regulators of cell cycle progression Associated with 25-60% if familial melanomas |
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|
RISK FACTORS FOR P16 MUTATION
|
1) personal history of 3 or more blood relatives with melanoma
2) Pancreatic cancer and melanoma in the same family (probability of mutation 45%), 3) an individual with multiple primary melanomas and a family history of melanoma (35% chance of p16 mutation), 4) an individual with multiple primary melanomas >3 (20-40% risk of p16 mutation), A first degree relative of a p16 mutation carrier (50% chance of p16 mutation). 5) Patient with numerous nevi > 5mm, many irregular nevi 6) strong family hx of melanoma and pancreatic cancer |
|
|
What is the next step if you suspect melanoma?
|
Complete surgical excision rather than incisional or partial biopsy
of the ENTIRE lesion (recommended: small-- 2mm margin) for histopathologic exam |
|
|
Breslow Depth
|
Measure in mm of depth of melanoma invasion; taken from granular layer to deepest area of melanoma cells
Predictive of prognosis Important for further staging work-up recommendations |
|
|
What combo of things will cure 9 out of 10 melanoma patients?
|
appropriate surgical tx of low-risk melanoma (<1mm Brewlow depth) with 1cm margins
|
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Treatment of Melanoma
|
Surgical excision is the primary treatment
Wide local excision; size of excision depends on the Breslow depth of invasion < 1mm depth: 1cm margin 1-4 mm tumor: 2-3 mm margin Sentinel lymph node biopsy for melanomas 1mm and consider > .75mm or greater and no palpable nodes or ulceration Chemotherapy not great Immunotherapy IFN alpha – patients at high risk for recurrence Melanoma Vaccines Melanoma Immunotherapy trials |
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|
What is lupus?
|
a multisystem disease that often has prominent skin involvement
characterized by autoantibodies to components of cell nucleus (antinuclear antibodies) caused by deposition of immune complexes in various tissues -> leads to complement activation and tissue damage |
|
|
What are the derm sx of SLE?
|
malar rash, discoid rash, photosensitivity
|
|
|
What are the 3 main types of cutaneous lupus?
|
Acute (90% have systemic disease)
Subacute (50% have systemic disease) Chronic (10% have systemic disease) The type of cutaneous lupus helps you determine how hard if at all to look for internal organ damage |
|
|
Acute cutaneous lupus
|
it is the most common rash in the setting of systemic lupus erythematosus
flare of skin disease may reflect activity of disease in other organ systems may be associated with presence of anti-dsDNA antibodies often photosensitive Erythematous but can also have a decent amount of scaling... think about psoriasis too |
|
|
Subacute cutaneous lupus
|
subset of cutaneous lupus characterized by
marked photosensitivity presence of anti-Ro and anti-La antibodies may be primarily skin problem, but can have systemic involvement (50%) some cases drug induced HCTZ NSAIDS terbinafine diltiazem |
|
|
What forms of lupus in a pregnant woman poses a risk to her fetus?
|
Subacute cutaneous lupus
neonatal lupus is a risk for children born to mothers with SCLE, anti-Ro abs (abs cross the placenta) transient skin rash on face, around eyes, trunk risk of complete heart block may require pacemaker may have associated hepatobiliary disease, thrombocytopenia |
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|
How might a baby present if it has neonatal lupus?
|
transient skin rash on face, around eyes, trunk
hepatobiliary disease, thrombocytopenia risk of 3rd degree total heart black and may need a pacemaker |
|
|
Chronic cutaneous lupus
|
old terminology: “discoid lupus”
discoid lesions can be seen in setting of systemic lupus (~10%) purely cutaneous disease: CCLE low risk of progression to SLE: 5-10% should rule out at initial diagnosis this type of cutaneous lupus can cause significant scarring, particularly since it often favors the face and scalp. |
|
|
Treatment of cutaneous lupus
|
sun protection
High SPF sunscreen with physical blockers topical and intralesional corticosteroids antimalarials (hydroxychloroquine) Usual choice for SCLE Risk of retinal toxicity systemic immunosuppressants retinoids thalidomide |
|
|
Dermatomyositis
|
one of the idiopathic inflammatory myopathies
affects both children and adults average age onset 7.6 yrs children 52 yrs adults female preponderance in adults children more likely to get calcinosis cutis |
|
|
What are the dx criteria for dermatomyositis?
|
symmetrical proximal muscle weakness
abnormal muscle biopsy elevation of skeletal muscle enzymes (CPK) abnormal electromyogram characteristic skin lesions |
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|
Is dermatomyositis associated with malignancy?
|
It is NOT associated with malignancy in kids.
It IS associated with malignancy in adults ranging from 10-50%. |
|
|
What are the cutaneous signs of dermatomyositis?
|
skin lesions similar in children and adults; children more frequently develop calcinosis and vasculitic skin lesions
heliotrope rash Gottron’s papules: Gottron’s papules: small violaceous flat papules on the extensor hands (usually over the joints) Gottron’s sign: Gottron’s sign: symmetric, scaly,erythematous rash over the extensor surfaces of the hands (usually over the joints) severity of skin and muscle involvement do not necessarily correlate |
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|
Heliotrope rash
|
Dermatomyositis associated
May look like a malar rash but have patient close their eyes... heliotrope rash includes the eyelids whereas a malar rash DOES NOT |
|
|
Skin findings with malignancy
|
cutaneous vasculitis
“malignant erythema” ulcerations skin disease refractory to treatment |
|
|
Dermatomyositis: diagnosis
|
skin biopsy may be helpful
evaluate for muscle involvement muscle enzymes MRI muscle biopsy EMGs ANA may be negative; may have antisynthetase antibodies (inc. Jo-1) associated with pulmonary disease |
|
|
Dermatomyositis: treatment
|
skin and muscle disease may respond differently to treatment
systemic corticosteroids initial therapy for muscle disease steroid-sparing agents (methotrexate, azathioprine) may be added skin disease may respond to topical corticosteroids, antimalarials |
|
|
Scleroderma
|
characterized by sclerosis (thickening of the skin and other tissues)
|
|
|
What are 3 types of scleroderma?
|
morphea: scleroderma localized to the skin
CREST syndrome: limited scleroderma systemic sclerosis: diffuse scleroderma involving skin and multiple other organ systems, especially the lungs and GI tract |
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|
Morphea
|
inflammatory disease localized to skin and subcutaneous tissues
No associated systemic disease No sclerodactyly or Raynaud’s No lab abnormalities Not fatal characteristic clinical lesions inflammatory patches that expand may initially be lilac or hyperpigmented over time, patch becomes sclerotic and may lose pigment to become ivory white may involve fat with loss of subcutaneous tissue involvement over joints, bone may affect function |
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|
If you suspect someone of having morphea what is it vitally important that you check for and treat if present?
|
cut of the saber in the head. It will continue to grow and cause issues if it is not addressed.
(looks like Worf) |
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|
What is the clinical course of morphea? treatment options?
|
disease usually progresses for several years, then regresses (“burns out”)
treatment options often ineffective corticosteroids Phototherapy (PUVA) vitamin derivatives (Vits A and D) immunosuppressive agents |
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|
CREST syndrome
|
subset of patients with limited scleroderma
Calcinosis cutis (nodules in skin, painful) Raynaud’s phenomenon Esophageal involvement (makes you miserable)--may have dysphagia as a sx Sclerodactaly- looks like the skin on someone's fingers is 2 sizes two small and affects mobility Telangiectasias- more organized than average telangiectasias and so will probably notice more easily than in better prognosis than diffuse systemic sclerosis anticentromere antibodies often present |
|
|
Raynaud’s phenomenon
|
very common in the general population... less commonly it can be associated with autoimmune diseases so look for other sx if you suspect greater pathology.
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|
|
Systemic sclerosis
|
is the most severe form of scleroderma
has either limited or diffuse cutaneous involvement in addition to involvement of multiple internal organs. diffuse cutaneous involvement can involve the entire body and carries a generally worse prognosis often fatal; 10 year survival = 20% |
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|
what are the cutaneous findings in systemic sclerosis?
|
diffuse hyperpigmentation
telangiectasias sclerodactaly digital ulcers other cutaneous ulcers Raynaud’s phenomenon |
|
|
what are the internal organ findings in systemic sclerosis?
|
arthralgia
esophageal and bowel involvement lung disease renal disease sicca symptoms-- dry mouth and eyes |
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|
When might digital ulcers occur?
|
systemic sclerosis... could happen in CREST syndrome but way more common in systemic sclerosis
|
|
|
How would you dx systemic sclerosis?
|
diagnosis clinical
skin biopsy can confirm cutaneous component ANA usually positive antinucleolar antibody pattern most specific antibodies to Scl 70 (topoisomerase I): often associated with pulmonary fibrosis |
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|
Systemic sclerosis tx
|
treatment remains challenging; skin disease often poorly responsive to treatment, multiple immunomodulators used (methotrexate, cyclophosphamide, steroids, thalidomide, UV light, etc.)
calcium channel blockers for Raynaud’s IV alprostadil (PGE1) for refractory Raynaud’s prostacyclin infusion for pulmonary HTN use of ACE inhibitors has made lung disease rather than renal crisis main cause of death |
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|
What are the two types of bacteria most often responsible for skin infections in immunocompetent patients?
|
staph and strep
|
|
|
Normal skin flora
|
functions largely to prevent
skin infections common organisms: Staphylococcus epidermidis Corynebacterium spp.: intertriginous areas Propionibacterium spp.: sebaceous glands (acne) Gram-negative bacteria in axillae, groin Yeasts (Pityrosporum spp.) on skin rich with sebaceous glands (central chest, upper back) |
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|
Impetigo: most common in who? causes? variants?
|
most common cutaneous infection in children
pathogens: S. aureus, group A (ß-hemolytic) strep, or both prior to 1980s: Group A strep most common past several decades: staphylococci predominant two clinical variant: nonbullous (crusted) and bullous |
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What are some predisposing conditions to impetigo? How is it spread?
|
heat, humidity, crowding, poor hygiene predispose
occurs year-round spread by direct contact, autoinoculation nasal colonization may serve as source of infection (S. aureus) |
|
|
What are some clinical features of impetigo?
|
often located around nose and mouth
moist, honey colored crusts on erythematous base characteristic fever, systemic symptoms rare may itch may be preceded by skin trauma often complicates atopic dermatitis (called “secondary impetiginization”) |
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|
Bullous impetigo
|
may arise without obvious trauma
large, flaccid bullae may develop blisters rupture leaving shiny, shallow erosions adenopathy, systemic symptoms rare cleavage result of epidermolytic toxin produced by staphylococci (exfoliatin) doesn't usually affect mucous membranes |
|
|
Impetigo: treatment
|
antibiotic coverage should cover for both staph and strep
mild cases: topical mupirocin 2% cream/oint widespread or complicated cases: penicillinase-resistant penicillins first generation cephalosporins culture/sensitivities recommended due to rise of resistant organisms |
|
|
How would you treat recurrent impetigo cases?
|
recurrent cases: treat nares (mupirocin) and body (chlorhexidine (Hibiclens) or bleach baths (1/2 cup bleach in bathtub full of water, soak for 15 minutes from neck down))
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|
|
Impetigo: complications
|
if untreated, may progress to ecthyma (a deeper infection)
staphylococcal scalded skin syndrome may complicate cases from toxin-producing staph most cases are uncomplicated Glomerulonephritis (but not rheumatic fever) can complicate streptococcal (Group A strep) impetigo antibiotic treatment does not prevent development of nephritis |
|
|
Staphylococcal scalded skin syndrome: what is it? causes?
|
part of spectrum of diseases that result from toxin produced by bacteria rather than from infection per se
usually affects children < 6 yo; rarely immunosuppressed adults, esp with renal failure most cases caused by S. aureus, phage group II strains produce exotoxins (exfoliatin) (ET-A, ET-B) that circulate systemically, split the skin at superficial granular layer |
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|
Staphylococcal scalded skin syndrome: clinical picture
|
clinical picture
usually affects children < 6 yo site of infection may/may not be apparent prodrome of malaise, fever, irritability skin becomes tender, soon thereafter develops symmetrical sunburn-like erythema around facial orifices, neck, flexures skin superficially blisters, then sloughs leaving behind moist skin, scales heals without scarring 10-14d |
|
|
How is the dx of staph scalded skin syndrome made?
|
diagnosis primarily clinical
cultures from affected skin, blisters negative. may culture staph from nares, conjunctiva, small foci of infection (pustules, etc) |
|
|
What is the prognosis of Staphylococcal scalded skin syndrome?
|
good in healthy children (mortality 3%),
bad in adults (over 50% all adults, up to 100% in adults with underlying diseases) |
|
|
How is TEN different from SSSS?
|
TEN:
usually drug reaction full thickness skin sloughing leads to widespread denudation mucosae involved high mortality treated in burn units +/- IVIg |
|
|
Folliculitis, furuncles, carbuncles: what is the difference?
|
superficial: folliculitis
entire follicle and surrounding tissue: furuncle multiple coalescing furuncles, deep tissues: carbuncle |
|
|
Folliculitis, furuncles, carbuncles: causes
|
bacterial infections of hair follicle
S. aureus usual pathogen: predilection for infecting hair follicles gram-negative organisms occasionally cause folliculitis “hot tub folliculitis: Pseudomonas aeruginosa some yeasts cause folliculitis: Candida, Pityrosporum |
|
|
folliculitis, furuncles, carbuncles: predisposing factors
|
trauma, maceration, occlusion, diabetes, immunosuppression may predispose
|
|
|
Hot tub folliculitis
|
Can be acquired in swimming pools as well as hot tubs
Caused by Pseudomonas aeruginosa Treat with ciprofloxacin instead of cephalexin |
|
|
What is another name for a boil?
|
furuncle
|
|
|
Folliculitis, furuncles, carbuncles: treatment
|
topical mupirocin for superficial folliculitis
abscesses may rupture or require incision and drainage antibiotic therapy may be needed widespread lesions, critical areas immunosuppressed children valvular heart disease or prosthesis lesions not responding to local therapy, those with cellulitis antibiotic coverage penicillinase-resistant penicillins (dicloxicillin) 1st generation cephalosporin fluoroquinolone for hot-tub folliculitis seek and treat for nasal / perineal colonization if recurrent community-acquired MRSA more often cause of very painful, virulent furuncles: do cultures |
|
|
CDC has identified 5 characteristics that facilitate the transmission of MRSA
|
5 C's
1) Crowding 2) Frequent skin-to-skin Contact 3) Compromised skin (cuts, abrasions) 4) Contaminated surfaces and other items (fomites) 5) Lack of Cleanliness |
|
|
MRSA - Prevention
|
Regularly wash hands or use an alcohol-based cleanser
Cover breaks in skin with a clean bandage until healed Avoid sharing personal items such as towels or razors Clean frequently-touched surfaces |
|
|
MRSA - Treatment
|
Simple furuncles: incision & drainage alone
Culture results should guide abx therapy Most community-acquired strains are sensitive to sulfonamides (TMP/SMX) and tetracyclines Clindamycin is an option but some strains are prone to inducible clindamycin resistance Topical meds: mupirocin (Bactroban) or silver-containing compounds. Chlorhexidine (Hibiclens) scrubs are useful for skin colonization, use as body wash Bleach baths are cheap and effective (1/2 cup bleach in bathtub full of water, soak from neck down) Nasal carriage needs to be addressed (treat with mupirocin) |
|
|
Cellulitis
|
infection of deep dermis and subcutaneous tissues usually by S. pyogenes and/or S. aureus
infects skin either from inside or outside immunocompetent pts: break in skin barrier allows bacterial entry immunosuppressed pts: bloodborne route damage to lymphatic system may predispose to recurrent infections |
|
|
How do you dx cellulitis?
|
clinical: “rubor, calor, dolor and tumor”
red, warm, painful and swollen ill-defined can blister associated fever, chills, malaise common diagnosis clinical; blood cultures usually negative |
|
|
Erysipelas- what is it? what causes it?
|
more superficial cellulitis with significant lymphatic involvement
usually caused by S. pyogenes Hemophilus influenza can cause similar facial infection in non-immunized children; requires IV antibiotics |
|
|
Erysipelas: clinical course? treatment?
|
rapidly progressive, well-demarcated painful erythema, usually on face, with peau d’orange texture
treatment with penicillin x 10-14 d |
|
|
What is the treatment for cellulitis?
|
oral antibiotics (penicillinase-resistant pen, 1st gen. cephalosporins) x 10-14d.
if systemically ill, consider IV abx |
|
|
What are the some potential complications of strep cellulitis?
|
glomerulonephritis, lymphadentis, lymphatic scarring, endocarditis
|
|
|
streptococcal perianal disease
|
recurrent bright perianal erythema in children
|
|
|
Necrotizing fasciitis: what is it?
|
“flesh eating bacteria” syndrome
life-threatening, rapidly progressive necrotic infection of subcutaneous tissue, fascia skin trauma may or may not precede |
|
|
Necrotizing fasciitis: causes?
|
Most cases are polymicrobial
mixed organisms including strep, S. aureus, E. coli, Bacteroides spp, Clostridium spp 10% due to group A streptococcus alone |
|
|
Necrotizing fasciitis: predisposing illnesses?
|
underlying illnesses predispose including alcoholism, diabetes mellitus, vascular disease, cardiac disease
|
|
|
Necrotizing fasciitis: clinical features?
|
resembles cellulitis early on: pain may be unusually severe!
progresses rapidly with necrosis developing within 24-36 hrs: blue-grey skin, blisters, thin watery discharge systemic illness can be profound usually involves extremities |
|
|
Fournier’s gangrene
|
involvement of perineum and genitalia
|
|
|
Necrotizing fasciitis: dx?
|
MRI, surgical exploration
|
|
|
Necrotizing fasciitis: tx?
|
extensive surgical debridement, broad spectrum IV antibiotic therapy, hyperbaric oxygen therapy controversial
|
|
|
Necrotizing fasciitis: complications?
|
complications common, include death, deformity, toxic shock syndrome
mortality 20-40% |
|
|
Which HPV viruses (oncogenic) are the most important?
|
16 and 18
|
|
|
What are the most common HPV viruses (non-oncogenic)?
|
6 and 11
|
|
|
warts: caused by what? where?
|
Human papilloma virus infection (HPV)
Skin and mucous membranes Spontaneous regression common |
|
|
How would you describe a wart's structure?
|
Papillomatous hyperkeratotic surface
mosaic surface pattern |
|
|
Seborrheic keratosis- what? what causes it?
|
Common benign skin growth
Vary in shape and color Look like melanomas or moles Commonly mistaken for wart Not viral Grow faster than cancer. flat, occupying skin lines... keratin accumulates on teh surface, gets thicker, keratin starts to crack on the surface and forms a mole. |
|
|
What does the undersurface of a wart look like?
|
like a smooth bulge... it projects into the dermis. It doesn't have "roots". It pushes the dermis down... can go really far down too
|
|
|
What are the 4 features of common warts?
|
wart on the hand
1. Hyperkeratotic surface 2. Papillomatosis 3. Mosaic surface pattern 4. Punctate micro hemorrhages |
|
|
Plantar Warts
|
1. Appear as a callus or corn
2. Normal surface lines interrupted 3. Punctate micro hemorrhages 4. Painful lesions must be treated 5. Patients call any wart a plantar wart |
|
|
Pearly Penile Papules
|
Anatomic variant of normal - angiofibroma - not treated
|
|
|
corn
|
scar, too much pressure on an area
|
|
|
how many women have genital HPV infection by age 50.
|
80%, 20 million are active infections
|
|
|
mosaic wart
|
cluster of warts on the plantar surface of the foot, difficult to treat, lots of seeds everywhere.
|
|
|
What viruses does gardasil protect against?
|
HPV 6, 11, 16, and 18
|
|
|
molluscum contagiosum
|
look like pink, pearly papules. caused by a DNA poxvirus. Defining characteristic is the dell in them. Often around the eyes in kids. If start to look ugly they may spontaneously regress. You do not treat these because it could cause scarring.
|
|
|
flat warts
|
very hard to treat... have to use topical cancer drugs... very resistant to treatment.
|
|
|
Erythema Infectiosum
|
Parvovirus B 19 infection
Epidemics in 5-14 year olds Blood group P antigen of bone marrow cells Fetal infection can cause death Polyarthropathy syndrome Women - itching, arthralgias, arthritis Mimics rheumatoid arthritis in acute state Lasts weeks or months |
|
|
Characteristic of Herpes Viruses
|
Most infections are acquired from asymptomatic individuals
Most infections are asymptomatic Latency is established in various tissues |
|
|
HSV-1
|
Mostly orolabial (cold sores, fever blisters)
primary genital herpes |
|
|
HSV-2
|
Most genital herpes; oral infection rare
>95% of recurrent genital herpes |
|
|
What is the evolution of lesions in herpes?
|
vesicles to umbilicated pustules to crusts to black crusts
|
|
|
What is the clinical course of HSV infection (Gingivostomatitis or Genital)?
|
Incubation - 6 days
Vesicles - wide area Fever Lymphadenopathy Resolve in 2 weeks |
|
|
What can cause reactivation of HSV?
|
sunlight, skin trauma, cold or heat, stress, infeciton, menstruation
anti-HSV antibodies do not vary significantly during recurrences |
|
|
What is the clinical course of recurrent HSV infection?
|
prodrome-itching pain
vesicles-grouped resolvesi n 5-10 days no fever or lymphadenopathy |
|
|
what causes pustules on the shaft of the penis?
|
herpes, maybe warts, molluscum contageiosum... if becomes pustule then about to degenerate.
|
|
|
Erythema infectiosum
|
looks like slapped cheek then you get a net like pattern on the body... primarily the arms. occurs in clusters. Clears without treatment.
|
|
|
What is the incubation period of herpes?
|
6 days
|
|
|
What is the incubation period of syphilis?
|
21 days but varies
|
|
|
Where might you see HSV-1?
|
oral of cuteanous
|
|
|
What is a virus that erythema multiforme can be associated with?
|
Herpes!
|
|
|
Herpes simplex + atopic dermatitis =
|
eczema herpeticum
|
|
|
Herpes simplex is particularly bad in patients who are...
|
immunocompromised... can be from: things usch as hogkins lymphoma, atopic dermatitis, HIV, and prenisone
|
|
|
Primary HSV - 2
|
Scattered vesicles
2. Macerated under foreskin and vagina to form ulcers |
|
|
What are various causes of genital ulcers?
|
• Herpes simplex
Syphilis Chancroid Scabies Candidiasis Trauma |
|
|
worst case of herpes ever that never recurs... what is the cause?
|
sunburn
|
|
|
What is the most prevalent STD?
|
herpes then HPv, then chlamydia, then Hep B then HIV
|
|
|
Risk of Acquiring HSV -2
|
Women - more likely to be infected
Men - more effective transmitters |
|
|
Subclinical HSV shedding:
|
Culture positive, no lesion
>90% of persons with genital HSV-2 shed Present 1%-10% days Uncommon in HSV-1 genital infection Frequency highest in first year after acquisition Responsible for most transmission |
|
|
Genital herpes
|
serologically HSV-2 +
|
|
|
Diagnosis
HSV-1 or HSV-2 |
Culture the virus
Blood test - serology Polymerase chain reacton |
|
|
Treatment HSV-1 or HSV-2
|
Acyclovir, famciclovir, valacyclovir
Primary infection Recurrent infection Suppressive therapy Frequent recurrence Decrease asymptomatic dissemination Decrease transmission |
|
|
What is the difference between chicken pox and zoster?
|
zoster is the recurrent infection, chicken pox is the primary infection
|
|
|
What predisposes a person to zoster?
|
Impaired function of CD4+ cytotoxic T cells predisposes to infection
such as due to: HIV infection Leukemia Hodgkin’s disease Non-Hodgkin’s lymphoma |
|
|
Syphilis -The great pox
|
Syphilis
large sores Small pox small sores (previously called “the pox”) |
|
|
What causes syphilis?
|
Treponema pallidum - Spiral bacterium (spirochete)
|
|
|
Primary Syphilis:
incubation clinical signs |
21 days - incubation
Chancre - clean, painless, hard, scars Chancroid chancre - dirty, painful, soft Lymphadenopathy Untreated - 75% resolve |
|
|
Secondary syphilis:
timeline clinical signs |
Begins 6 weeks after chancre
Influenza - like syndrome Hepatomegaly Generalized adenopathy Mucocutaneous lesions (polymorphism) |
|
|
Gonorrhea:
cause clinical sx |
Gram negative diplococci
Arthritis-dermatitis syndrome Fever + joint and tendon pain and swelling Few hemorrhagic pustules |
|
|
Lymphogranuloma Venereum
cause: incubation: clinical sx: |
C. trachomatis
Incubation 5 - 21 days Vesicle erodes, ulcerates, heals rapidly Headache, fever arthralgia Lymphadenopathy, buboes “Groove sign” Labial edema elephantiasis of the labia |
|
|
Chancroid
cause: clinical sx: |
H. ducreyi - gram-negative rod
Painful, soft ulcer, dirty chancre Ulcers are highly infectious Suppurative regional adenopathy Nodes may break down |
|
|
Granuloma inguinale (Donovanosis)
cause: incubation period: clinical sx: |
C. granulomatis G negative rod
Painless red beefy lesions Pseudo-elephantiasis of the labia Long incubation period Lymph nodes rarely involved Australia, India |
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Digene HPV Test
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Performed on material from Pap test
Detects the 13 high–risk HPV types Does not determine which type Primary screen for woman over 30 Triage of women of any age with risk factors |
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In what race is shingles most common?
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caucasian.
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Natural history of scabies
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one of most common infestatiosn seen by physicians
can become epidemic in wartime-- and other situations with overcrowding and lower personal hygiene |
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Pathophysiology of scabies
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mite Sarcoptes scabiei causes it
caused by close prolonged physical contact, venereal female burrows into epidermis at junction of stratum corneum and granulosum and lays 10-25 eggs before she dies in about 4 weeks. larvae emerge from eggs in 3-5 days may not devo sx on first exposure but may on subsequent re-exposure. Suggested that mites cause a Th1 delayed type hypersensitivity rxn. |
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Physical findings in scabies
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scabietic burrow: 5-10 mm curved ridges or thread-like lesions usually excoriated, resulting in crusted papules
lesion areas: genital areas, flexor wrists, elbows, finger and toe webs, buttocks, breasts, waistline. Head and scalp spared in adults. Lesions are very pruritic especially at night!! eczematous changes are primary expression Secondary infection frequently leads to impetiginization, ecthyma, cellulitis Variations: nodular scabies, scabies infants (more on head and neck), crusted scabies, clean scabies with only 1-2 mites found |
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What are the potential secondary complications of scabies?
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excoriation, secondary bacterial infection, post streptococcal glomerulonephritis, acarophobia (parasitophobia)
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Lab findings in scabies
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mites, ova, feces can be demonstrated in scrapings of fresh papule or burrow
biopsy shows scale crust (which can contain all of that fun), epidermal spongiosis, and dermal infiltrate of lymphocytes, histocytes, eosinophils ELISA testing |
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Differential dx of scabies
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other eczematous dermatoses, especially atopic dermatitis
other arthropod bites, e.g. fleas pyoderma |
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Treatment of scabies
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gamma benzene hexchloride lotion
crotamiton cream or lotion, antipruiritic; recommended tx for infants, young kids, pregnant woman Other things: permethrin lotion, precipitated sulfur ointment, benzyl benzoate, malathoin, terpenoid Oral ivermectin (not FDA approved yet) all close physical / sexual contacts and family members should be tx'ed at the same time. wash, dry clean and store in plastic all clothes and bedding for one week. treat the head in kids too. |
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Crusted scabies
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infestation with huge numbers of mites (thousands to millions) possibly representing an abnormal host immune response.
Manifests by hyperkeratotic, crusted eczematous or papulo-squamous appearing dermatitis in widespread distribution involving face, palms, sores, and nails. Seen more often in senile, mentally retarded, Down's syndrome, immunosuppressed. |
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Pediculosis: overview on the organisms
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Two species of anoplura are human ectoparasites--Phthirus pubis and pediculus humanus variants capitis and corporis. These organisms are obligate, blood sucking, host-specific parasites. Lice are true insects and can be important vectors of human disease.
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natural hx of pediculosis capitis
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occurs most commonly in children and can be epidemic in schools, day care centers, playgrounds
uncommon in black population Transmitted by close contact, shared hats, hair care articles |
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Pathophysiology of pediculosis capitis
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Caused by infestation with Pediculus humanus variant capitis
Lice favor scalp hair, especially of the occipital scalp, but may infest the beard, pubic hair. Lice leave hairs to bite and obtain a blood meal from surrounding skin, releasing a mild toxin which causes purpuric spots and irritation. Sensitization to louse products creates more inflammatory lesions, thus initial symptoms typically occur only after prior exposure. Secondary infection frequently occurs. Nits are egg cases which are laid near the scalp surface. Eggs hatch in average of 7 days. Adult female lives approximately 1 month. Adult can live off host without a blood meal only 2-3 days; nits can live off host for 3 weeks. |
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Physical findings in Pediculosis Capitis
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Pruritus is the most common symptom.
Lice are seen especially on temporal, occipital scalp. Nits are small, oval, whitish-to-translucent, oblong objects firmly cemented to hair shaft. Erythematous papular bites are seen in peripheral scalp and onto neck. These are often excoriated, with oozing and crust formation. Regional adenopathy is common-secondary to pyoderma. |
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Treatment of pediculosis capitis
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Lindane lotion or shampoo (shampoo lathered in, left on 5-10 minutes, then washed out, repeated in 9 days)
Malathion lotion (Ovide) Also repeat treatment in 9 days Pyrethrin (A-200, RID) with piperonyl butoxide-containing shampoo. Permethrin (Nix) Remove nits with a fine-toothed comb. Treat all close contacts and family members. Clean cloths and house Bactrim DS-taken bid for 3 days, repeat in 1 wk Treatment resistance to all therapy becoming a problem. Clear 1,2,3 (oil of anise) PawPaw Tree Lice Remover Shampoo Suffocation – e.g., 5% benzyl alcohol lotion (Ulesfia) Coming soon: Spinosad – a neurotoxin derived from a soil fungus |
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natural hx of pediculosis corporis
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A disease of vagrants or persons with poor hygiene who rarely change or launder clothing
Transmitted by infected clothing or bedding A major vector in epidemic typhus, trench fever, relapsing fever |
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pathophysiology of pediculosis corprois
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Caused by infestation with Pediculus humanus variant corporis
Lice live in seams of clothing and are only found on the skin when feeding. Nits are attached to cloth fibers on clothing. Sensitization to lice and their products contributes to signs and symptoms of infestation. Secondary bacterial infection frequently occurs. Nits may remain viable as long as 1 month. Lice die in 2-10 days without a blood meal. |
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Physical findings in pediculosis corporis
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Louse bites start as red macules with a central punctum which rapidly become papular and are quickly excoriated.
Lesions are most common about shoulders, interscapular areas, trunk, buttocks. With long-standing infestation, can see a crusted, eczematous widespread dermatitis, thickened, dry, scaling, hyperkeratotic, hyperpigmented skin. Nits and lice are found in seams of clothing. |
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Treatment of pediculosis corporis
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Clothing must be washed or dusted with DDT or lindane, or sterilized, washed, and ironed, or stored in plastic for 30 days.
Pyrethrums-sprayed onto clothing another option. |
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natural hx of pediculosis pubic
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An infestation usually transmitted by close physical or sexual contact
May be transmitted by clothing, towels, bedding Other STD often evident. |
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pathophysiology of pediculosis pubic
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Caused by infestation with Phthirus pubis - smallest louse
Lice generally live in pubic hair, but also may infest eyebrows, eyelashes, chest, beard, axilla or legs. Primary changes are due to pruritus and scratching. Secondary infection is uncommon. Lice can live 2-3 days off the host. |
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physical findings in pediculosis pubic
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Itching in the pubic area is the primary symptom.
Excoriations, erythematous papules, or maculae cerulea (steel gray macules) are seen. Lice may be seen as small brownish organisms on pubic hair or surrounding skin. Nits are present near base of hair shaft. Other hairy skin may be infected (e.g., eyelashes) |
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Treatment of pediculosis pubic
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Kwell or pyrethrin/piperonyl butoxide-containing shampoo
all sexual contacts should be tx'ed |
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Tinea capitis
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head or scalp) is common in children
-Pink scaly patch(s), ring-like shape, with some central clearing -Large, inflamed, crusted nodule, boggy and weeping, called a kerion |
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Tinea barbae
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(beard area) is often an infection with a zoophilic species
-Usually vigorous inflammatory reaction -Inflamed scaly patch, follicles may be involved, pustules are common -Secondarily infected with bacteria -Can lead to scarring |
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Tinea cruris
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(groin area or crural folds)
-Pink to violaceous scaly patches, linear along the crural folds -"Jock Itch" |
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Tinea pedis
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(feet, toes and toe web spaces), many clinical variants
-Pink changes to the skin of the feet, with burning and pruritus -Vesicles or pustules along the periphery of the plantar surface, "moccasin distribution" -Thick pink patches or plaques with heavy scale in annular or arcuate pattern |
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Tinea unguium or onychomycosis
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-One or all nails may be involved
-Rare in children, very common in the elderly |
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Tinea manum
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(hands and fingers)
-Pink scaly patches with central clearing and leading edge of scale - Nails are usually not involved |
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Tinea corporis
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-Patches can be large, coalescing, become diffuse
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Tinea incognito
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Dermatophyte infection, in any location, which has lost its clinically diagnostic features
-Usually due to inappropriate treatment with topical corticosteroids -Resulting in a delayed diagnosis, expansion and spreading of the fungus |
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Looks like ringworm... how do you confirm?
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scrape it... test KOH... if positive then you know.
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tinea versicolor
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specific genus and species
looks a little lighter in dark skinned people... looks darker or salmon or pink in light skinned people common in V of the back where there are lots of oil glands which it loves... also under the breast. usually don't see it below the belt or in the groin area worse in summer time when sweat more but can be in winter too. |
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tinea versicolor under the microscope
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KOH positive;
spaghetti and meatballs=spores and hyphae |
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tinea versicolor: why hypopigmentation? tx?
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Carboxylic acid inhibits melanin which causes hypopigmentation in some people.
Treat with topical and oral therapy. Ketokonazole. Can also use selenium shampoos and zinc soaps. |
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organism that causes tinea versicolor
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malassezia furfur
thrives on lipids: central chest and back. Inherit susceptibility |
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What happens when you think you have fungus in your crotch and you put hydrocortisone cream on it?
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It feeds it and creeps up all over your back. Don't do it.
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MAIN look of tinea
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annular, advancing border, trailing scale, central clearing. Don't mess this up.
could have serpiniginous border and some pustules but would scrape to confirm |
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tinea on hands and feet looks...
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kind of different.. may just see some white in creases/ splotches and would really really need to do a KOH on it.
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tinea facei complications
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secondary infection... often mistaken for other things and is not treated... gets down in the hair follicles causing the infection.
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what aspect is most important on KOH prep of tinea?
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the hyphae!! sometimes criss-crossing even wooooo hyphae
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kerion
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large, inflamed, crusted nodule, boggy and weeping
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Differential dx for lesion that might be tinea
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tinea
psoriasis eczema pityriasis rosea maybe even lupus! |
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who gets tinea capitis?
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pretty much kids. adults immune systems take careo f it... may have other processes but usually not tinea.
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How do you test a kerion?
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pluck out a hair and KOH it. that will show you the fungus.
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tinea unguium: to tx or not to tx
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pretty much don't treat because the meds for it 'cause liver and something else toxicity and then it reoccurs... just really not worth it.
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What causes a kerion?
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the exaggerated immune response to the fungus
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tinea imbricata
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concentric rings, annular pattern... if you get it, you can be the chief of the village in some tribes.
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what makes people susceptible to fungal infections?
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contact with someone or something and your immune system isn't ready for it allowing proliferation.
not a hygiene issue. |
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difference between yeast and tinea
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a bit more bright red, less of a central clearing, white macerated stuff in middle and satellite lesions around the outside.
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where does candida show up?
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often in the skin folds, can be in mouth, vulva, penis etc
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candida's KOH
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spores and PSEUDOhyphae... very important distinction.
KOH positive |
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Yeast you see _____
Fungus you see _____ |
Yeast more spores
Fungus more hyphae |
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Candida albicans
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NORMAL INHABITANT
IMMUNOLOGICALLY SENSITIVE MUCOUS MEMBRANES, SKIN FOLDS BRIGHT RED PATCHES “SATELLITE LESIONS” KOH |
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Who should / shouldn't get thrush?
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Babies can get thrush and if it leaves it's not so bad.
Adults shouldn't get thrush unless immunocompromised. |
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A gardener is cutting roses and scrapes his arm, spreads moss around. what would he get?
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sporotrichoid spread--would have nodule or scrape and swollen lymphatics
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SPOROTRICHOSIS
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Sporothrix schenckii
SOIL ORGANISM BEGINS as PAPULE or NODULE ULCERATION LYMPHADENOPATHY “SPOROTRICHOID SPREAD” CULTURES RAPIDLY |
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CHROMOBLASTOMYCOSIS
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Phialophora, Cladosprorium, Fonsecaea
WARTY PLAQUES VEGETATING ULCERS DRAINING SINUSES FEET & LEGS CULTURE will suspect this and cancer and really have to do a biopsy... maybe even consider warts. |
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MYCETOMA
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MADUROMYCOSIS
“MADURA FOOT” Allescheria & others SOIL ORGANISM PAPULES ULCERS NODULES VERY DIFFICULT TO TREAT |
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Synonyms for atopic dermatitis
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eczema, neurodermatitis, infantile eczema, childhood eczema, constitutional eczema, endogenous eczema
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How do genetics play a role in atopic dermatitis?
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genetics play a huge role... if it runs in your family then you are predisposed to a certain type of skin reaction.
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People who are predisposed to atopic dermatitis have these cutaneous differences making for a more defective barrier
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Increased keratinization: Ichthyosis vulgaris, increased palmar linearity and Keratosis pilaris
Defective water binding: Asteatosis (dry skin dermatitis, eczema craquelé) Lower irritation threshold: primary irritant contact dermatitis Loss of function mutation in the filaggrin gene leads to the above changes Lower itch threshold(probably NOT histamine driven): excoriations (scratches) Sweat retention: miliaria (prickly heat) Loss of antimicrobial peptides (AMPs) |
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What neurovascular changes are seen with atopic dermatitis?
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Increased peripheral vasoconstrictor tone: white dermographism, delayed blanch to cholinergic agents
Cyclic nucleotide abnormalities such as excessive adenylate cyclase and phosphodiesterase activity and reduced intracellular cyclic AMP. The result may be inappropriate or poorly modulated release of chemical mediators of inflammation. |
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What are some general physical findings in atopic dermatitis?
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A chronic fluctuating disease which may occur at any age
The predominant symptom is itching, which leads to scratching, which produces most of dermatitis. Superimposed bacterial colonization and infection is common and may be a factor in flares. The skin is usually dry and scaly. Ichthyosis vulgaris and keratosis pilaris are common associated disorders. Facial pallor, cool extremities, and white dermographism reflect the neurovascular dysfunction. Extra folds of the lower eyelids (Dennie's Lines) and hyperpigmentation of the lower lids (atopic shiner) are markers of the atopic diathesis. Pityriasis alba |
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What are some age specific physical findings in atopic dermatitis?
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Infancy: acute, generalized eczematous dermatitis
Children and adolescents: subacute and chronic, predominantly flexural eczematous dermatitis Young adults: irritant hand and foot dermatitis. "Housewife's eczema," "dyshidrosis," "pompholyx." A major cause of work-related disability due to skin disease. Middle age: localized areas of persistent eczematous dermatitis. "Lichen simplex chronicus," "nummular dermatitis or eczema," "prurigo nodularis." Senescence: dry skin eczematous dermatitis. "Asteatosis," "winter itch," eczema craquelé." |
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What factors aggravate atopic dermatits?
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1. Antigens such as foods (especially in infants and young children) and inhalants (dust, pollens, animal danders) which stimulate formation of IgE antibody. It is easy to overemphasize these possible factors.
2. Anything that causes sweating (hot baths, hot water, exercise, and strong emotional reactions) 3. Excessive drying of the skin (by excessive bathing or low humidity) 4. Clothing - especially wool 5. Infection - primarily staph aureus 6. Pityrosporon yeast 7. Hormones 8. Stress |
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Lab findings in atopic dermatitis
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1. 70% have a delayed blanch phenomenon with acetylcholine injection (not done routinely).
2. Biopsy is not specific and shows acanthosis, epidermal edema (spongiosis), and infiltration with lymphocytes, macrophages, plasma cells, and eosinophils. In other words, eczematous dermatitis. 3. Moderate peripheral blood eosinophilia 4. Rare patch test + 5. Food Allergy testing (in children) |
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What are the complications of atopic dermatitis?
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1. Exfoliative dermatitis (total body redness and scaling)
2. Premature cataract formation. May occur in up to 10% of the more severe cases. 3. Increased susceptibility to viral, bacterial, and fungal infections a. Patients with active dermatitis or a history of atopic dermatitis should not be vaccinated for smallpox. b. Primary infection with herpes simplex virus or vaccinia virus may be severe and be associated with high fever and systemic symptoms (Kaposi's varicelliform eruption). This reaction may be fatal. c. Colonization and infection with Staphylococcus aureus is common. d. Chronic superficial fungus infections (especially of the feet and body caused by Trichophyton rubrum) are more common in atopics. e. Common virus is increased (e.g., warts/molluscum) |
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What is the differential dx of atopic dermatitis?
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1. Allergic contact dermatitis
2. Primary irritant dermatitis 3. Seborrheic dermatitis/psoriasis 4. Scabies 5. Tinea |
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How is atopic dermatitis treated?
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Control trigger stimuli
antihistamines- oral or topical compressions to acute, wet, or crusted lesions for short periods only Topical corticosteroids Antibiotics to control superinfections: usually erythromycin or dicloxacillin macrolide immunosuppressants: oral cyclosporin and topical tacrolimus and pimecrolimus Interferon-gamma decreases TH2 Thymopentin- increases TH1 UV light Herbal theraby: chinese herbal tea, evening primrose oil mast cell stabilizer phosphodiesterase inhibitors leukotriene antagonist probiotics omalizumab (binds free IgE) TNA-alpha inhibitors Vitamin D therapy |
