Dermatology Flashcards
Atopic Dermatitis - Diagnosis
Itchy skin + 3 or more of the following:
Involvement of skin creases or face History of asthma or hay fever History of dry skin Visible flexural eczema Onset < 2 years
Atopic Diathesis
Atopic Dermatitis
Asthma
Allergic Rhinitis
Atopic Dermatitis - Pathogenesis
Disruption of skin barrier, likely due to filaggrin mutation
Secondary infection with Staph aureus often exacerbates inflammation
Patients often show elevated serum IgE and eosinophilia
Atopic Dermatitis - Clinic Presentations by age group
Infants - dry, red, scaly areas confined to cheeks; flushes with cold
Childhood - erythematous papules, redness, scaling, characteristic involvement of flexural skin
Adult - characteristic involvement of eyelids & hands
Atopic Dermatitis - Associated Features
Dry Skin (Xerosis) Ichthyosis vulgaris (plate-like dry skin) Keratosis Pilaris (bumpy skin) Hyperlinearity of the palms
Irritant Contact Dermatitis - Definition
Non-immunologically mediated reaction resulting from direct cytotoxic effect caused by a chemical irritant
Intertrigo
Rashes of the skin folds caused by trapped sweat and exacerbated by friction
Treated with mild topical corticosteroid, i.e. Hydrocortisone
Secondary infection with yeast is common
Allergic Contact Dermatitis - Definition
Type IV, delayed-type hypersensitivity reaction to contact allergen; immune response involves presentation of the antigen by Langerhans cells in the skin and development of memory T cells which release inflammatory cytokines TNF-a and IL-1
Diagnosed by patch test
Stasis Dermatitis - Associated Features
Other signs of venous insufficiency of the lower extremitie:
Varicose veins
Chronic lower extremity edema
Venous Stasis Ulcers
Stasis Dermatitis - Clinical Presentation
Dryness
Itching
Lichen Simplex Chronicus
Secondary allergic contact dermatitis due to use of topic agents
Secondary irritant contact dermatitis due to accumulation of purulent material from ulcers
Lichen Simplex Chronicus
Thick, scaly plaques that result from chronic rubbing and scratching
Venous Stasis Ulcers
Primarily found on the medial lower leg just before the ankle; red with yellow, fibrinous base & irregularly shaped borders
Nummular Dermatitis
AKA Discoid Eczema; characterized by red, scaly, crusty patches appearing most often on the legs, sometimes on arms and trunk
Treatment: moisturization & topical corticosteroids
Seborrheic Dermatitis
Flaky, white/yellow, oily scale occurring in areas rich in sebaceous glands (scalp, face, ears, chest)
In children, usually presents on the scalp as “cradle cap”
In adults, often presents as symmetric involvement over the face over medial eyebrows, nasolabial folds, and ears; also presents on the scalp as “Dandruff”
Seborrheic Dermatitis - Pathogenesis
Over-production of skin oil and irritation from Malassezia furfur yeast
Dandruff
Seborrheic Dermatitis of the scalp
Differentiated from psoriasis by more diffuse lesions and finer scale
Psoriasis - Comorbidities
Persistent, low grade, systemic inflammation; risk factor for development of insulin resistance, obesity, metabolic syndrome, and cardiovascular disease
5-20% of patients will develop psoriatic arthritis
Psoriasis - Clinical Subtypes
Chronic Plaque Disease Guttate Erythroderma Pustular Psoriasis Palmar/Plantar Psoriasis
Treatment for local Psoriasis
Localized Disease: Calcipotriol (Vitamin D3 analog) Corticosteroids Topical Retinoids Phototherapy
Treatment for systemic Psoriasis
Systemic Disease:
Methotrexate
Cyclosporin
Biologics - anti-T lymphocytes, anti-TNF alpha
Atopic Dermatitis - Common Locations
Characteristic involvement of flexural skin:
Antecubital fossa Popliteal Fossa Neck Wrists Ankles
Psoriasis - Common locations
Characteristic involvement of extensor surfaces
Vitamin D synthesis
7-dehydrocholesterol in epidermal keratinocytes can be converted by UVB to Vitamin D3; Vitamin D3 is then converted to 25-hydroxy Vitamin D by the liver; 25-hydroxy Vitamin D is converted in to the kidney to the active form, 1,25-dihydroxy Vitamin D (Calcitriol)
Melanocytes
Pigment producing cells of the epidermis; protects DNA from UV damage
Located in the basal layer of the epidermis, within hair follicles; found in a 1:10 ratio of melanocytes: keratinocytes
Produce melanin packaged in granules called melanosomes, each melanocyte supplies melanin to 30 nearby keratinocytes
Langerhans cells
Dendritic cells of the epidermis, found in small numbers in all of the epidermal layers
Circulate between the skin & lymph node where they present antigens to the immune system
Stratum Corneum
Outermost layer of epidermis
Made up of dead keratinocytes that have lost their nuclei and organelles
Filaggrin - Normal function & Mutation
Breakdown of filaggrin forms Natural Moisturizing Factor (NMF) which binds H20 to keep the skin moist
Patients with filaggrin mutations have reduced levels of NMF in the stratum corneum, leading to icthyosis vulgaris and atopic dermatitis
Stratum Lucidum
Thin layer of anuclear cells without organelles, seen only in the thick skin between the stratum corneum and stratum granulosum; reduces shear forces between these two layers
Stratum granulosum
Cells in this layer start to lose their nuclei as they migrate toward the epidermal surface; these cells contain keratohyalin granules full of profilaggrin (filaggrin precursor)
Stratum Spinosum
Thickest layer of the epidermis; functions to protect against mechanical injury, UV, pathogens, and chemicals
Desmosomes
Specialized adherence proteins that enable cell-cell adhesion between keratinocytes in the epidermis
Pemphigus Vulgaris
Caused by acquired antibodies to desmosomes in the epidermis
Presents as flaccid intraepidermal blisters in the skin and mucous membranes
Stratum Basalis (Germinativum)
Inner most layer of the epidermis (basal cell layer); consists of a single layer of columnar or cuboidal keratinocytes - these are the stem cells of the epidermis
Hemidesmosomes
Specialized adherence proteins that function in the attachment of basal cells of the epidermis to the basal lamina of the dermal epidermal junction
Bullous Pemphigoid
Most common autoimmune bullous disorder; caused by the production of auto-antibodies to hemidesmosomes at the dermal-epidermal junction
Diagnosed by direct immunofluorescence
Treated with oral steroids or Rituximab
Papillary Layer of the Dermis
Top layer of the dermis, directly underlying the epidermis; forms the dermal component of the dermal-epidermal junction; consists of loose connective tissue rich with capillaries that are the blood supply for the epidermis
Meissner’s Corpuscles
“Pine cone”-like structure, consists of Schwann cells and sensory nerve terminals wrapped by fibroblasts and collagen; most often found in the dermal papillae of thick skin
Sensitive for detection of delicate touch
Reticular layer of the Dermis
Lies deep to the papillary layer; contains extensive collagen and elastic fibers lending strength & flexibility
Houses glands, hairs, and major blood vessels that facilitate thermoregulation
Pacinian Corpuscles
“Onion-like” structures; consist of a single sensory nerve terminating within a concentric layer of connective tissue; found in the dermis of thick and thin skin
Detects vibration
Apocrine glands
Produce a milky, viscous, carbohydrate-rich secretion; secretion is initially odorless but subsequent bacterial action leads to characteristic body odor
Located in axillary, pubic, and perianal regions
Eccrine Glands
Traditional sweat glands distributed over most of the body; secrete watery, electrolyte, enzyme-rich secretion that is initially isotonic but becomes hypotonic as Na+ is reabsorbed by the ducts; important for thermoregulation
Not found on lips, under finger/toe nails, on the glans of the penis/clitoris, or on the labia minora
Arrector pili
Smooth muscle structure that causes hair to “stand on end”
Sebaceous glands
Secrete sebum, a complex mixture of lipids; develop along with hair follicles & empty their secretions into the upper 1/3 of the follicle
Sex hormones are required to secrete sebum, which functions to lubricate and moisturize the skin
Types of Pigment (2)
Eumelanin - Black to brown pigment
Pheomelanin - Yellow to red-brown pigment
Distribution of Melanosomes - Light vs. Dark skin
Light skin: Melanosomes are distributed in clusters above the keratinocyte nucleus
Dark skin: Melanosomes are larger and distributed individually throughout the cytoplasm of the keratinocytes
Vitiligo
Acquired depigmentation due to absence of melanocytes in affected areas of skin
Most often affects the mouth, eyes, and fingertips
Macule vs. Patch
Circumscribed change in skin color that is flush with surrounding skin
Macules are < 1 cm
Patches are > 1 cm
Papule vs. Nodule vs. Tumor
Solid or cystic elevation of the skin
Papules are < 1cm
Nodules are between 1 and 2 cm
Tumors are > 2 cm
Plaque
An elevated skin lesion > 1 cm
Scale
Desiccated, thin plates of epidermal cells that form flakes on the skin surface
Wheal
Circumscribed, flat-topped, firm elevation of skin with a well demarcated and palpable margin
i.e. Hives
Vessicle vs. Bulla
Circumscribed, elevated lesion containing clear serous or hemorrhagic fluid
Vessicles are < 1 cm
Bulla are > 2 cm
Pustule
A vesicle containing purulent exudate
Atrophy vs. Erosion vs. Ulceration
Atrophy - a depression on the surface of the skin with loss of underlying epidermal or dermal substance
Erosion - a depression on the surface of the skin with loss of all or part of the epidermis
Ulceration - a depression on the surface of the skin with loss of the entire epidermis and some of the dermis
Telangiectasias
Visible, persistent dialation of small, superficial capillaries
Eschar
A thick, dry, crusty scab - usually black in color
Lichenification
Dry, leathery thickening of the skin with exaggerated skin markings
Dermal Matrix
A mixture of collagen, elastin, and ground substance
Ground substance is mostly comprised of GAGs; these molecules are highly hydrated, allowing for diffusion of nutrients from the dermis into the epidermis
Ehlers-Danlos Syndrome (EDS)
Congenital disorder of collagen synthesis, leading to the production of abnormal collagen
Causes skin hyperextensibility, joint hypermobility, tissue fragility, and poor wound healing
Solar Elastosis
Accumulation of sunlight exposure leads to degeneration of elastin fibers; fibers become dystrophic and tend to clump
Pseudoxanthoma Elasticum (PXE)
Caused by a mutation in a gene encoding for the MDR efflux pump; this mutation also causes elastic fibers of the dermis to become tangled and calcified
Skin of flexural areas develops a “plucked chicken” look
Elastic fibers of blood vessels are also damaged, leading to hypertension and bleeding disorders
Leukocytoclastic Vasculitis
Caused by precipitation of immune complexes in the walls of post-capillary venules, secondary to drug hypersensitivity, infection, etc.
Leads to inflammation, degranulation of neutrophils causing vessel wall damage, and extravasation of RBCs into the dermis
Manifests as palpable, non-blanchable purpura
Hair follicles - structural elements
Divided into into metrical area (lower 1/3), isthmus (middle 1/3), and infundibulum (upper 1/3)
Also comprised of lower bulge (attachment for arrector pili), middle bulge (sebaceous gland), and upper bulge (apocrine gland)
Terminal vs. Vellus Hairs
Terminal hairs - large, thick, and coarsely pigmented; present on the scalp, beard, and pubic area
Vellus hairs - small, fine, and apigmented; located diffusely on the body
Acne
Acquired disorder of the pilosebaceous unit caused by plugging of the follicle by hyperkeratotic debris leading to the accumulation of oil; normal bacterial commensals multiply within the follicle and convert sebum to pro-inflammatory fatty acids
Anhidronic Ectodermal Dysplasia
Aberrant eccrine gland formation; patients do not sweat, leading to problems with thermoregulation
Chromhidrosis
Disorder of apocrine glands, characterized by the presence of lipofuscin pigment that colors apocrine sweat yellow/green/blue/black in various oxidative states
Cherry angioma
Most common vascular tumor in adults; primary lesion is a bright red, smooth topped papule
Can be treated with electrodessication, liquid nitrogen, or shave biopsy
Infantile hemangioma
A benign endothelial cell neoplasm - the most common soft tissue tumor of infancy
Often a precursor lesion is noted at birth followed by rapid proliferation in the first 1-3 months
Complications: Peri-ocular lesions may interrupt vision, lip lesions prone to ulceration
Many cases resolve spontaneously by age 5; persistent cases treated with beta blockers (propanolol), steroids, or laser
Port Wine Stain
A vascular malformation that is present at birth and persists into adulthood; caused by somatic mutation GNAQ
Complications: Varicose veins, venous stasis, edema, ulceration
Sturge-Weber Syndrome
Associated with port wine stain, ocular and neurologic abnormalities including glaucoma, seizures, and developmental delay
Sebaceous Hyperplasia
Benign tumor of the oil gland often located on the face, trunk, and extremities
Primary lesion is a 1-6mm yellowish-white papule
Treatment is for cosmetic reasons only by electrodessication or cryotherapy
Nevus sebaceous
A papillomatous, yellow-orange, linear plaque on the face or scalp; lesions on the scalp are associated with alopecia
Rapid growth may occur during puberty with enlargement of sebaceous glands and epidermal hyperplasia
Can be treated with surgical excision
Acrochordon
Aka “Skin Tag”
Soft, flesh-colored papules with a narrow base
Complications: Recurrent trauma, torsion
Treatment: Snip excision, cryotherapy, electrodessication
Lipoma
Benign tumor of adipose tissue - the most common form of soft tissue tumor
Usually soft to the touch, movable, and painless
Dermatofibroma
Primary lesion is a firm, round nodule
May be depressed or dome-shaped, rarely larger than 1cm; color is tan or brown and dimples when squeezed
Generally solitary distribution over the legs
Keloid
A raised scar that extends beyond the borders of the original wound; results from an overgrowth of granulation tissue at the site of a healed skin injury
Generally present as firm, rubbery lesions or shiny nodules; can vary in color from pink to red to dark brown
Seborrheic Keratosis
Benign tumors of the hair follicle typically found on the head, neck, and trunk
Primary lesion is a brown papule with a “stuck on” appearance; may be smooth or slightly raised, often studded with small pits
Treatment: Cryotherapy
Clinical subtypes of Seborrheic Keratosis
Dermatosis Papulosa Nigra
Stucco Keratosis
Inflamed Seborrheic Keratosis
Sign of Leser-Trelat
Nevocellular Nevi
“Moles”
Age of onset from infancy to childhood; distributed over any skin surface including mucous membranes; increased on sun-exposed skin
May be intradermal, junctional, or compound
Congenital Nevi
Caused by melanocytes that migrate from the neural crest and remain inappropriately within the dermis and do not progress into the epidermis
Giant congenital nevi are associated with a slight increased risk for melanoma
Familial Atypical Mole and Melanoma (FAMM) Syndrome
Diagnosis requires:
The occurrence of malignant melanoma in 1 or more first or second degree relatives
Presence of many (>50) nevi, some of which are clinically atypical
Risk of melanoma approaches 100%
Neurofibromatosis
Autosomal dominant mutation of the neurofibromin (NF-1) gene, a tumor suppressor; exhibits variable expression & pleiotropy
Signs include: Cafe au lait spots Neurofibromas Axillary freckling Lisch nodules
Basal Cell Carcinoma (BCC)
Most commonly diagnosed malignancy in the US
Rarely fatal but can become invasive, causing complications that involve the eye or brain
Originates from keratinocytes
Moh’s surgery
Tissue-sparing tumor removal technique, indicated for tumors that are located in cosmetically sensitive areas, large in size, or recurrent
Clinical subtypes of BCC
Superficial
Nodular (75%)
Infiltrative
Sclerosing/Morpheaform
Risk factors for Basal Cell carcinoma
Fair skin
UV exposure
Risk factors for Squamous Cell Carcinoma
UV damage Thermal injury Radiation HPV Chronic injury / inflammation Immunosuppression
Squamous Cell carcinoma
Hyperkeratotic papule of variable size and thickness, typically found on chronically sun damaged skin
Metastasis occurs in .5-5% but is more common in SCC of the lip (10-30%)
Clinical subtypes of SCC
SCC In Situ - Full thickness atypia of the epidermis; does not involve the dermis
Keratoacanthoma - rapidly growing, volcano-like nodule with central crater
Invasive SCC
Melanoma Risk Factors
Fair skin Sun exposure Age Immunosuppression MM in first degree relative Large congenital nevus FAMM
Clinical subtypes of Melanoma
Superficial spreading
Nodular
Lentigo Maligna Melanoma
Acral Lentiginous
Actinic Keratosis
AKA Intraepidermal neoplasia
The most common pre-cancerous lesion: 65% of all SCCs and 36% of all BCCs arise in lesions that were previously diagnosed as AKs
Treatment:
Cryotherapy
Topical agents - chemotherapies, immunotherapies, NSAIDs
Phototherapy
Major mutation in BCC + Specific Therapy
The majority of BCCs have a loss of function in the PTCH1 gene, which normally acts to block smoothened (SMO), an oncogene involved in tumor signaling
Vismodegib is an inhibitor of smoothened, approved for targeted treatment of advanced BCC
Common mutation in Melanoma + Targeted Therapy
50% of melanomas have a mutation in the BRAF gene
Treatment: Vemurafenib, a BRAF inhibitor
Clark’s Levels
I. Epidermis
II. Papillary Dermis
III. Mid Dermis
IV. Reticular Dermis
Breslow Depth
Tumor invasion measured in millimeters
Tumor biopsy is indicated for patients with tumor invasion > 1 mm
Solar spectrum & Sunburn
UVB is the shortest wavelength (highest energy) and is responsible for more severe sunburns; UVA is somewhat lower energy and is associated with use in tanning beds to cause tanning without burning
Why do sunburns peel?
Peeling is evidence of p53 activation of apoptosis in DNA damaged keratinocytes; these cells slough off as they die and are replaced by new cells from the basal layer
Defenses against reactive oxygen in the epidermis
Peroxidases and Catalases - detoxify H2O2 to H2O and O2
Superoxide dysmutase - detoxify superoxide anion to H2O2
Glutathione reductase
Thioredoxin reductase - reduces disulfide bonds
Mechanism of melanosome biosynthesis
Melanosome precursor vesicles from the smooth ER fuse with tyrosinase-containing vesicles from the Golgi that important for production of melanin; fully mature melanosomes transit down the dendrites of the melanocyte and are extruded into surrounding keratinocytes
How does UV damage stimulate melanin content in the skin?
UV radiation stimulates a number of cell signaling pathways, including p53; activation of p53 leads to production of signaling intermediates that are secreted from the damaged keratinocyte and activate receptors on the melanocyte that signal the cell to up-regulate melanogenesis; melanosomes are transported down the axons of the melanocytes and deposited into the keratinocyte
Types of DNA damage produced by UVR
Thymine Dimers - induced by UVB
Pyrimidine-6-4-pyrimidone - induced by UVB
Hydroxyguanosine - induced by UVA
Defense Mechanisms of the skin
Physical barrier
Desquamation
Localized immune response - Langerhans Cells, Immunoglobulins
Anti-microbial peptides - alpha defensins
pH
Warts - Virus & Types
Caused by HPV
Veruca Vulgaris
Veruca Plantar - commonly seen on the plantar surface of the foot
Verruca Plana - commonly spread by shaving
Herpetic Whitlow / Herpes Progenitalis
HSV-1 presenting on the finger tips (Herpetic Whitlow) or genitals (Herpes Progenitalis)
Presents as grouped blisters on a red base; often preceeded by “tingling” prodrome, often recurrent
Streptococcal Non-bullous Impetigo (Impetigo Contagiosa)
Common superficial infection of the face in children
Primary lesion is a plaque with “honey colored” crust
Most common complication (5%) is acute post-streptococcal glomerulonephritis
Staphylococcal Non-Bullous Impetigo
Most commonly affects the face of adults, frequently secondary to injury or dermatitis due to self-inoculation with Staph flora from the naris
Primary lesion is a plaque with “honey crust” over the surface;
Cellulitis
Staphylococcal or Streptococcal
Ill-defined area of erythema on the body (not face)
Lymphatic streaking and lymphadenopathy are common; may lead to sepsis
Eryiseplas
Facial cellulitis variant, may be Staphylococcal or Streptococcal
Bright red, bilateral erythema and swelling of the face with well-demarcated “cliff drop” border
Syphilis
Caused by treponema pallidum spirochete
Primary - painless chancre at site of infection
Secondary - presentation varies greatly but classic presentation is non-pruritic, papulosquamous lesions on the palms and soles; lymphadenopathy in 90%
Diagnosed by biopsy or serology, never culture
Dermatophyte
Fungi that eat keratin on the surface of skin, hair, and nails; cause superinfection only
Epidermophyton - “Socks and Jocks”
Trichophyton
Microsporum
Tinea Capitis
Grey patch variant - Grey patch with associated hair loss; often associated with occipital lymphadenopathy
Black dot variant
May present as a Kerion - inflammated, scaly lesion
Tinea - faciei, barbae, corporis, cruris, pedis, manum
Classic presentation is annular plaque with raised border and central clearing
Tinea faciei - presents on the face of children
Tinea barbae - presents on the bearded face in men
Tinea corporis - presents on the body; “ring worm”
Tinea cruris - presents on the groin area
Tinea pedis - presents on the feet, usually bilaterally; may present as hyperkeratotic variant
Tinea manum - presents on the hand, often unilaterally
Majocchi’s Granuloma
Deeper fungal infection of the hair follicle, occurs secondary to superficial dermatophyte infection
Candidiasis - 3 presentations
Candida fungus uses glucose as a food source; often causes deeper infection
Thrush - fungal plaque infection of oral mucosa
Perleche - chronic infection at the edges of the mouth
Diaper dermatitis - beefy red rash with satellite pustules
Scabies
Caused by Sarcoptes scabiei mites
Classic presentation is pruritic, erythematous papules and burrows distributed symmetrically over the interdigital web spaces, flexural wrist, waistband, axilla, and groin
Diagnosed by skin scraping or biopsy
Lice - 3 varieties
Pediculus humanus var. capitis - head lice
Pediculus humanus var. corporis - body lice; presents as truncal, erythematous papules and macules; louse found on clothing only
Phthirus pubis - Crab louse; presents with pruritis of genital area; crabs are easily found attached to the base of hair follicles
Clubbing
Enlargement of the soft tissue of the distal digit with excessive curving of the nail plate
Associated with :
GI disease - Crohn’s, Ulcerative Colitis
Malignancy - Thyroid cancer, Hodgkin Disease
Pulmonary or Cardiac disease causing hypoxia
Kaposi’s Sarcoma (3 types)
Slowly progressive endothelial malignancy triggered by HHV-8; 3 types:
- Classic - primarily in elderly men of Eastern European descent; presents in the lower leg
- Lymphadenopathic - aggressive form primarily affecting young men in equatorial Africa
- AIDS-associated
Alopecia Areata - Systemic associations
3 presentations:
- Non-scarring alopecia occurring as round patches of hair loss
- Alopecia totalis - total scalp hair loss
- Alopecia univeralis - total body hair loss
Often associated with auto-immune disease including thyroid disease, vitiligo, and irritable bowel syndrome
Vitiligo - Systemic associations
Commonly associated with thyroid disease (Hashimoto’s, Graves), and other endocrine disorders
Erythema Nodosum - Systemic associations
Deep inflammation of the subcutaneous fat (panniculitis); presents as painful, erythematous subcutaneous nodules usually symmetrically over the pretibial lower extremity
Considered a delayed type hypersensitivity reaction to antigenic stimuli, most commonly infection; often associated with streptococcal infections, especially URI
Pyoderma Gangrenosum - Systemic associations
Lesion usually begins as a pustule on an erythematous base and evolves into an ulcer with a necrotic border; often begins at sites of minor trauma
Associated with:
Inflammatory Bowel Disease
Arthritis
Hematological Disorder
Lichen planus - Systemic associations
Purple, polygonal, pruritic papules with Wickam’s striae (overlying pattern of white lines on the surface)
Associated with Hepatitis C
Oral LP associated with contact allergy to dental metals
Acanthosis Nigricans - Systemic associations
Velvety hyperpigmentation of intertriginous surfaces, especially neck and axilla; caused by factors stimulating epidermal keratinocyte proliferation
Associated with obesity, Diabetes, and other endocrinopathies
Also associated with malignancy - adenocarcinoma of stomach; often with rapid onset of the skin condition as well as rapid weight loss
Urticaria - Systemic associations
Immediate type I (IgE-mediated) hypersensitivity reactions; may be acute or chronic
Acute - <6 weeks; often associated with infection, drugs, and food
Chronic - development of auto-antibodies to self Fc receptors
Drug eruptions
Typically eczematous drug eruptions; delayed type hypersensitivity reaction, usually with onset within 7-14 days of starting a new medication
Treated with topical steroids and systemic anti-histamines
Stevens-Johnson Syndrome
Drug eruption caused by immune complex-mediated hypersensitivity; characterized by a rash that begins on the face and upper trunk and evolves to skin necrosis and flaccid bullae involving mucous membranes; detachment of epidermis often results
SJS involve < 10% of body surface
Toxic Epidermal Necrolysis involves > 30% body surface
Type A nerves
Heavily myelinated, fast conducting nerve fibers
Convey localized pain
Type C nerves
Unmyelinated, slow-conducting nerve fibers
Convey sensation of diffuse, dull, non-localizing itching and temperature
Hair Cycle
Hairs are randomly engaged in 1 of 3 cycles
Anagen - Growth Phase
Telogen - Rest Phase
Catagen - Involution Phase
Male Pattern Baldness - Causes & Treatment
Caused by conversion of testosterone to DHT
Treated by Propecia: selective inhibitor of 5-a-reductase, which prevents this conversion
