DERMATOLOGY: BOARDS AND BEYOND Flashcards
It contains STEM cells that are capable of regenerating keratinocytes in the epidermis.
Stratum basalis
Order of the layers of the epidermis.
- Stratum basale
- Stratum spinosum
- Stratum granulosum
- Stratum lucidum
- Stratum corneum
Meant to be the tough outer layer of the skin that protects your body.
Stratum corneum
Processes that cause leaky vessels are going to tend to swell the ?, not the epider
Dermis
Acantholysis means a loss of connections between keratinocytes it’s often a loss of desmosomes that significantly affects the
Stratum spinosum
The classic malignancy, in which to see acanthosis nigricans is
Gastric adenocarcinoma
Erosion is a wider lesion that involves the epidermis and an ? is similar to an erosion, but it’s deeper and involves both the epidermis and the dermis.
Ulcer
- Epidermis: keratinocytes (squamous epithelial cells)
- Dermis: connective tissue, vessels
- Subcutaneous fat (also called hypodermis or subcutis)
Layers of the skin
Stratum Basalis
Stem cells
Stratum Spinosum
Desmosomes form spines
Stratum Granulosum
- Keratohyalin granules
- Form keratin filaments
Stratum Lucidum
- Clear layer of dead skin cells
Stratum Corneum
- Anucleated cells
- Filled with keratin filaments
Dermis
- Connective tissue
- Blood vessels
Hyperkeratosis
- Thickening of stratum corneum
- Excess quantity of keratin
Seen in psoriasis and callus
Parakeratosis
- Hyperkeratosis + retained nuclei in stratum corneum
- Indicates hyperproliferation
- Seen in skin diseases (psoriasis) and malignancies
Hypergranulosis
- Increased thickness of stratum granulosum
- Classic finding in lichen planus
Spongiosis
- Fluid accumulation (edema) of epidermis
- Seen in eczema, many other skin disorders
Acantholysis
- Loss of connections between keratinocyte
- Often loss of desmosomes
- “Rounded” keratinocytes
- Detached, floating freely in epidermis
Key feature of pemphigus vulgaris
Acantholysis
- Diffuse epidermal hyperplasia
- Elongated rete ridges
- Spinous layer thickening
Acanthosis
- Nigricans = darkened
- Hyperpigmented (dark) plaques on skin
- Intertriginous sites (folds)
- Classically neck and axillae
***Hyperkeratosis - Mild acanthosis
- Associated with insulin resistance
- Rarely associated with malignancy
Acanthosis Nigricans
Primary skin Lesions
- Directly caused by disease process
- Macules, papules, vesicles, bulla
Macules and Patches
- Flat lesions (not raised)
- Macule: <1cm
- Patch: >1cm
Secondary skin lesions
- Modification of primary lesion
- Or caused by trauma, external factors
- Scale, crust, erosion, fissure, ulcer
Papules and Plaques
- Raised lesions
- Papule: <1cm
- Plaque: >1cm
Mole/nevus
Papule
Psoriasis
Plaque
Maculopapular Rash
- Collection of small skin lesions
- Some flat (macules)
- Some raised (papules)
- “Morbilliform” – looks like measles
- Common in many disorders
- Drug rash
- Scarlet fever
- Syphilis
- Rubella
Vesicles and Bulla
- Fluid-filled lesions (blisters)
- Vesicle: <1cm
- Bulla (plural = bullae): >1cm
Bulla
Bullous pemphigoid
Vesicle
Chickenpox
- Pus-filled vesicle
- White center
Pustule
- Smooth, elevated papule or plaque
- Surrounded by erythema (redness)
- Itchy
- Caused by dermal edema
- Component of urticaria (allergic reaction)
Wheal
- Secondary lesion
- Peeling/flaking of stratum corneum
Scale
- Secondary lesion
- Dried exudate of skin lesion
Impetigo
Crust
Characteristic histopathologic findings include hyperkeratosis (thickening of the stratum corneum), enlarged dermal papillae, and increased pigmentation of the basal cell layer.
Acanthosis nigricans
Urticaria is characterized by ?: transient, itchy, raised lesions that arise from edema in the dermis. ? are pale to red (often with pale centers and red borders) and blanch with pressure. This boy’s reaction is an immediate type 1 hypersensitivity reaction triggered by egg antigens binding to IgE antibodies on mast cells. Activated mast cells release granules of histamine and other vasoactive mediators that promote vasodilation, dermal edema, and inflammation.
Wheals
Staphylococcal scalded skin syndrome (SSSS), a skin disorder caused by strains of Staphylococcus aureus that produce exfoliative toxins. These exfoliative toxins cleave desmosomes (attachments between keratinocytes) in the stratum granulosum, causing ?.
Acantholysis (loss of connections between keratinocytes)
Histologically, acantholytic keratinocytes appear
Rounded and detached
Acantholysis can lead to
Fragile blisters, skin exfoliation, and a positive Nikolsky’s sign where gentle stroking of intact skin causes exfoliation of the top layer.
Nikolsky’s sign is not specific to SSSS and can also be seen in other skin disorders like
Pemphigus vulgaris and toxic epidermal necrolysis
Plaque psoriasis, a chronic inflammatory skin disorder characterized by well-demarcated pink plaques with a silver white scale. These plaques commonly affect the extensor surfaces of the knees and elbows. Psoriasis leads to
Acanthosis: diffuse epidermal hyperplasia (thickening) with thickening of the stratum spinosum and elongated rete ridges.
Other common histological findings in psoriasis include
Parakeratosis (retained nuclei in the stratum corneum) and neutrophils within the stratum corneum (Munro microabscesses).
Psoriasis leads to
Hypogranulosis (thinning of the stratum granulosum).
Pemphigus vulgaris
An autoimmune blistering disorder where antibodies are formed against desmoglein proteins in the skin and mucosa. Desmogleins form an important component of the desmosomes that attach keratinocytes together in the epidermis.
The histologic hallmark of pemphigus vulgaris is
Acantholysis (loss of intercellular attachments between keratinocytes) above the stratum basale (suprabasal). The stratum basale is intact, and the separation of the blister occurs above it in the stratum spinosum.
- Fibrous, extracellular matrix of proteins
- Anchors epithelial cells to connective tissue
Basement Membrane
Pemphigus vulgaris leads to ? on the skin and mucosa that are fragile and usually already ruptured on examination. Oral lesions especially are rarely intact and often precede skin lesions by months when pemphigus vulgaris first develops. The oral lesions are usually irregular, ill-defined erosions and ulcers that are slow to heal. Immunosuppressants are the mainstay of treatment.
Flaccid blisters and bullae (large blisters)
2 LAYERS:
- Basal lamina
* Extracellular matrix secreted by epithelial cells
* Contains laminin proteins
* Type IV collagen (Goodpasture’s/Alport syndrome)
- Reticular lamina (reticular connective tissue)
* Reticular = like a net
* Anchors basal lamina to connective tissue
Basement Membrane
- Sheets of epithelial cells bind together
- Different functions for each side of cell (“polarized”)
Cell Polarity
Side facing cavity/lumen:
* Lumen of blood vessel
* Lumen of GI tract
* Lumen of nephron
* Outside of body
Apical membrane
Side away from cavity/lumen:
Basolateral membrane
- Join plasma membranes of adjacent cells
- Four types:
- Tight junctions
- Adherens junctions
- Gap junctions
- Desmosomes
Epithelial Cell Junctions
- Seals two cell membranes together
- Barrier to paracellular movement between cells
- Found near apical membrane
- Most apical adhesion between cells Built from key proteins:
- Occludin
- Claudin
Tight Junctions (Occluding Junctions or Zonula Occludens)
- Found below tight junctions
- Anchors cells to one another
- Forms belt around cells
Cadherin - Cell membrane glycoprotein
- Attach to actin filaments in cells
Adherens Junctions (Belt Desmosomes or Zonula Adherens)
- Calcium-dependent adhesion (CAD) proteins
- Glycoproteins
- Many subtypes
Cadherin
Lost in some forms of breast cancer
E-cadherin
- Macula = Latin for spot
- “Spots” of cell-cell attachment (not belts)
- Common in the skin
- Attached to intermediate filaments
- Made of keratin and found in cell cytoplasm, Linked by cadherins.
Desmosomes (Spot Desmosome or Macula Adherens)
Keratins
- Tough, fibrous structural proteins
- Found in hair, skin
- Also horns, claws, hooves
- Keratin monomers assemble intermediate filaments
- Similar to desmosomes
- Contain intermediate filaments of keratin
- Linked by integrins
- Attach epithelial cells to basement membrane (Laminin (basal lamina), collagen)
Hemidesmosomes
- Channel connections (electrolytes)
- Connexins: protein molecules
- Form structure called connexon
- Allow small molecules to pass
- Too small for proteins, nucleic acids
Gap Junctions
Autoantibodies to desmosomes
Pemphigus vulgaris
Autoantibodies to hemidesmosomes
Bullous pemphigoid
Air sacs of lungs and the lining of the heart, blood vessels, and lymphatic vessels
Simple squamous epithelium
Allows materials to pass through by diffusion and filtration, and secreates lubricating substance
Simple squamous epithelium
Secreates and absorbs
Simple cuboidal epithelium
In ducts and secretory portions of small glands and in kidney tubules
Simple cuboidal epithelium
Ciliated tissues are in bronchi, uterine tubes, and uterus; smooth (nonciliated tissues) are in the digestive tract, bladder
Simple columnar epithelium
Absorbs; it also secreates mucuos and enzymes.
Simple columnar epithelium
Cilliated tissue lines the trachea and much of the upper respiratory tract
Pseudostratified columnar epithelium
Lines the esophagus, mouth and vagina
Stratified squamous epithelium
Secretes mucus; ciliated tissue moves mucus
Pseudostratified columnar epithelium
Protects against abrasion
Stratified squamous epithelium
Protective tissue
Stratified cuboidal epithelium
The male urethra and the ducts of some glands
Stratified columnar epithelium
Sweat glands, salivary glands and the mammary glands
Stratified cuboidal epithelium
Secrets and protects
Stratified columnar epithelium
Lines the bladder, urethra and the ureters
Transitional epithelium
Allows the urinary organs to expand and stretch
Transitional epithelium
Is an inflammatory bowel disease associated with increased permeability of the intestinal wall. Tight junctions between intestinal epithelial cells form a barrier that regulates the paracellular (between cell) uptake of water, electrolytes, and nutrients, like glucose. Tight junctions vary in their selective permeability based on environmental stimuli and location within the intestine.
Crohn’s disease
The intestinal inflammation in Crohn’s disease is associated with ?, which increases intestinal permeability.
Tight junction dysfunction and changes in the expression of tight junction proteins
Changes in the expression of the tight junction proteins ? are thought to be an important part of the barrier dysfunction seen in inflammatory bowel disease. Inflammatory cytokines can affect the expression of ? to make the intestinal wall more permeable. In addition, some evidence suggests that dysregulated tight junction proteins and the subsequently impaired epithelial barrier may even precede and promote the intestinal inflammation seen in inflammatory bowel disease.
Claudin and occludin
These are important in the heart, where they allow depolarization to spread from one myocyte to another.
Gap junctions
Pemphigus vulgaris, an autoimmune blistering disorder where antibodies are formed against ?, a major component of desmosomes.
Desmoglein
Desmosomes form attachments between keratinocytes, and their destruction leads to
Acantholysis (loss of attachments between keratinocytes).
Acantholysis and blister formation occur predominantly in the stratum spinosum, while the underlying stratum basale remains intact.
Pemphigus vulgaris
Bullous pemphigoid, an autoimmune blistering disorder in which antibodies target ? important components of hemidesmosomes. Hemidesmosomes attach keratinocytes to the basement membrane between the dermis and epidermis. Destruction of these hemidesmosomes leads to blisters at the dermo-epidermal junction (where the epidermis and dermis meet).
Bullous pemphigoid antigens (BPAG1 and BPAG2),
Bullous pemphigoid usually affects people over the age of 70. Blisters in bullous pemphigoid are
Itchy, tense, and do not rupture easily. Commonly-affected areas include the trunk, upper arms, and thighs. Rubbing the skin usually does not cause exfoliation of the top layer of skin (a negative Nikolsky’s sign).
A genetic disorder in which defective type IV collagen leads to progressive kidney disease, hearing loss, and eye abnormalities.
Alport syndrome
Eighty-five percent of patients with Alport syndrome inherit an
X-linked mutation in the alpha-5 chain of Type IV collagen.
Is an important component of the basement membrane in renal glomeruli, the inner ear, and the eye.
Type IV collagen is
The only symptom at birth may be microscopic hematuria, but progressive kidney disease eventually leads to gross hematuria, proteinuria, and, ultimately, end-stage renal disease by middle age. Sensorineural hearing loss can start in late childhood and progress to deafness by age 40. Vision is often normal, but eye abnormalities can include lenticonus (an abnormal conical shape to the lens), corneal opacities, and macular thinning.
Alport syndrome
Inflammation of hair follicles and sebaceous glands
* Exocrine glands in skin in dermis
* Secrete oily substance called sebum
* Often contain hair follicles (“Pilosebaceous unit”)
* Complex, multifactorial etiology
Acne
Acne:
Sebaceous glands enlarge at puberty
* ↑ androgens → ↑ sebum
* Adolescent acne: men > women
- Men with androgen insensitivity: no acne
- Women with excess androgens (PCOS): acne
- Comedo: debris blocking sebaceous duct (bumps on face)
- Comedone: plural of comedo
- Microcomedo: microscopic comedo (not visible)
- Lipid-rich environment for bacterial growth
- Bacteria use triglycerides in sebum as fuel
ACNE: Comedones allow bacterial growth
- Propionibacterium acnes (cutibacterium acnes)
- Anaerobic bacterium
- Normal skin flora
- Inflammation from bacterial proliferation
ACNE: Sebum: growth medium for bacteria
Increased sebum and keratin
* Keratinocytes line hair shafts → keratin
* Blocks ducts
* Bacterial growth behind blockage
Acne
Face, neck, chest, upper back
Acne: Affects most hormone-responsive glands
- Open comedos: blackheads
- Closed comedos (by skin): whiteheads
- Inflammatory lesions (papules/pustules)
- Scarring and hyperpigmentation may occur
Acne: Multiple lesion types
- Benzoyl peroxide (topical)
- Breakdown keratin, unblocks pores (comedolytic)
- Bactericidal to P. acnes
- Antibiotics
- Decrease P. acnes colonization of skin
- Clindamycin and erythromycin
- Retinoids (vitamin A derivatives)
Acne: Treatment
- 13-cis-retinoic acid
- Metabolites bind to nuclear receptors
- Retinoic acid receptors (RAR)
- Retinoid X receptors (RXR)
- Decreases keratin production in follicles
- Less follicular occlusion
- Highly teratogenic
- OCP and/or pregnancy test prior to Rx
Isotretinoin
Accutane
- Red plaques with scale (flaky skin)
- Occurs on face and scalp (areas with lots of sebaceous glands)
- Poorly understood pathogenesis
- No inflammation of sebaceous glands
- Associated with fungal infection by Malassezia
Seborrheic dermatitis
Topical antifungals and corticosteroids
Treatment of seborrheic dermatitis
- Benign neoplasm of melanocytes
- Tan/brown pigmented lesions
- Uniform color
- Often round or oval shape
- Usually <6mm
Melanocytic Nevus (Moles)
- Present at birth
- Often have hairs growing from lesion
Melanocytic Nevus
Moles (congenital)
- Appear in childhood
- Increase in number during adolescence
- Peak count in 30s
- Regress with age
Melanocytic Nevus
Moles (acquired)
- Rarely develop dysplasia → melanoma
- Atypical features may warrant biopsy/removal
- Not removed prophylactically for prevention
Melanocytic Nevus
Moles
- Junctional nevi
- Growth along dermal-epidermal junction
- Often found in children
- Compound nevi
- Growth extends into dermis
- Intradermal nevi
- Loss of junctional lesion
- Found only in dermis
- Common in adults
Acquired Nevi
- Chronic inflammatory skin disorder
- Well-demarcated plaques
- Pink or salmon colored
- Silver-white scale
- Most commonly on extensor surfaces (Knees and elbows)
Psoriasis
- Inflammation from trapped hairs
- Associated with shaving
- Entrapment of recently cut, very short hairs
- Firm papules/pustules in area of beard growth
- Common in black men (up to 80%)
- 3% white men
Pseudofolliculitis barbae (Razor bumps, shave bumps)
- Pathogenesis poorly understood
- Combination of genetic and environmental factors
- Believed to be autoimmune
- Strong association with HLA-C
Psoriasis
Acanthosis (thickening of epidermis)
Parakeratotic scaling
* Retained nuclei in stratum corneum
* Indicates hyperproliferation
Stratum spinosum
* Increased in size
Stratum granulosum
* Thinned or absent
Munro microabscesses
* Neutrophils in stratum corneum (munro absceses)
Psoriasis
Psoriasis: Dermis blood vessels close to surface
Scale breaks →
Bleeding (Auspitz sign)
Psoriasis: most common type
Plaque psoriasis
- Guttate psoriasis
- Pustular psoriasis
- Erythrodermic psoriasis
- Inverse psoriasis
Psoriasis (Multiple other less common subtypes)
Commonly involves nails
* Nail pitting
* Onycholysis (separation of nail from nailbed)
About 1/3 of patients develop psoriatic arthritis
* Seronegative spondyloarthritis
* More common in patients with nail findings
Psoriasis
- Common skin disorder (3% population)
- Affects adults > 30
- Celtics and Northern Europeans: greatest risk
- Affects light-skinned individuals
Rosacea
- Inflammatory skin condition
- Complex, poorly understood pathology
- Chronic redness of nose and cheeks
- Papules and pustules
- May look similar to acne but no comedones
Rosacea
Facial flushing
* Often triggered by environmental stimuli
* Cold, heat, sun, hot drinks, spicy foods, alcohol
Phymatous rosacea
* Skin hypertrophy
* Thickened skin
* Most commonly on nose (rhinophyma)
Rosacea
- Common benign tumors
- Proliferation of immature keratinocytes
- Occurs in older patients (>50)
- Arise spontaneously
- Commonly on trunk
Seborrheic keratosis
- Flat
- Well-demarcated
- Round or oval
- Dark, velvety surface
- “Stuck on”
Seborrheic keratosis
- Dark cells similar to basal skin cells
- Keratin-filled cysts (“horn cysts”)
Seborrheic keratosis
- “Explosive onset” of multiple itchy SK lesions
- Probably caused by cytokines
- Associated with malignancies (gastric adenocarcinoma most common)
Leser-Trelat Sign
- Warts
- Cellular proliferation caused by HPV
- Many types
- Verruca vulgaris (skin - most common)
- Verruca plana (skin - flat wart)
- Condyloma acuminatum (venereal warts)
Verrucae
- Most common manifestation of HPV infection
- Transmitted by contact with virus
- Common on hands
- Epidermal hyperplasia
- Koilocytosis (cytoplasmic clearing (“halos”) around nucleus)
Verruca Vulgaris (cutaneous Warts)
Pre-malignant lesions
Actinic keratoses
Blocking pilosebaceous follicles in that area and causing comedones to form. This occlusion can happen with tight gear like headbands and helmets (“acne mechanica”) or with oily cosmetics and hair products (“pomade acne”).
Acne
Sign of Leser-Trélat, the explosive onset of seborrheic keratoses associated with internal malignancy, most commonly gastrointestinal adenocarcinomas. Seborrheic keratoses are typically round or oval lesions that are well-circumscribed and hyperpigmented with a “stuck on” appearance. Their proliferation with internal malignancy is likely due to ?. The velvety, hyperpigmented (dark) plaque on his neck is acanthosis nigricans, which is also commonly associated with the Leser-Trélat sign.
Cytokines produced by the neoplasm.
Acquired immune deficiency syndrome (AIDS) can be associated with cutaneous findings such as fungal, bacterial, and viral infections of the skin, as well as skin malignancies such as Kaposi sarcoma. AIDS can also be associated with ? which consists of red, scaly skin on the face and scalp.
Seborrheic dermatitis
Can cause a diffuse, maculopapular, erythematous (red) rash that may involve the back as well as the palms and soles.
Secondary syphilis
Which is caused by human papillomavirus (HPV) infection of epidermal cells. Histologic findings include epidermal hyperplasia (thickening of the epidermal skin layer) and a thickened stratum granulosum with koilocytes – epithelial cells with perinuclear cytoplasmic clearing, causing “halos” around the nucleus.
Verruca vulgaris, or common warts
? (collections of neutrophils in the stratum corneum) and a thinned stratum granulosum are findings in psoriasis.
Munro microabscesses
Isotretinoin (13-cis-retinoic acid) is a retinoid, meaning a compound similar to vitamin A. It is converted to metabolites that activate retinoic acid receptors (RAR) and retinoid X receptors (RXR) located in the
Nucleus (“nuclear receptors”)
When a retinoid binds to its nuclear receptor, the retinoid-receptor complex becomes active and binds to a segment of DNA to promote
Gene transcription
Is used to treat severe acne and works by reducing the size of sebaceous glands and decreasing sebum production, inhibiting the sebum-dependent bacteria Cutibacterium acnes (formerly Propionibacterium acnes). It also reduces follicular hyperkeratinization (excess keratin deposition), leading to fewer comedones.
Oral isotretinoin
Histologic findings in psoriasis include
Epidermal hyperplasia (thickening of the epidermis) with parakeratosis (keratinocytes that do not mature normally and retain nuclei in the stratum corneum).
Clinically, parakeratosis causes the ? on psoriatic plaques and pits in the nails: clusters of parakeratotic cells in the nail plate slough off and leave depressions in the remaining nail.
Typical scale
Psoriasis causes a thinned or absent stratum granulosum
Psoriasis causes a thickened stratum spinosum.
- Infection (most commonly Strep)
- Crohn’s disease (may precede flare)
- Sarcoidosis
- Coccidioidomycosi
Triggers of erythema nodosum
- Type IV hypersensitivity reaction
- Panniculitis
- Inflammation of subcutaneous fat
- Often idiopathic
Erythema Nodosum
- Painful, red nodules
- Most commonly on shins
Erythema Nodosum
“Septal panniculitis”
* Inflammation of septa of fat between dermis and fascia
* Contrast with “lobular”: inflammation of fat lobules
Erythema Nodosum: Pathology Findings
- Rare, chronic inflammatory skin disorder
- “Lichen” = tree moss
- “Planus” = flat
- Occurs in adults
- Unknown pathogenesis
- Resolves spontaneously over years
Lichen Planus
Associated with hepatitis C
Lichen planus
Pruritic
Purple
Polygonal
Planar
Papules
Plaques
Lichen planus: * 6Ps
- Itchy (often intense)
- Purple flat lesions
- Multiple, symmetric usually on arms/legs/wrists
- Wrists, ankles are common sites
Lichen planus
- Mucosal involvement (Mouth, tongue, Glans penis)
Lichen Planus
Wickham striae: white dots/lines
* Caused by hypergranulosis (classic feature of ?)
* Best seen on oral lesions
Lichen Planus
- Lymphocytes at dermal-epidermal junction
- Hyperkeratosis
- Hypergranulosis
- “Sawtooth” pattern of rete ridges
Lichen Planus
- Acute, self-limited skin rash
- Eruption of skin lesions
- Self-limited
- Resolves 2-3 months
- Usually no treatment required
- Cause unknown (possibly viral)
Pityriasis Rosea
Begins with “herald patch”
* Single red/salmon-colored lesion
* Round or oval
* Well demarcated
* Chest, neck, or back
Pityriasis Rosea
Days later: Multiple lesions on trunk
* Multiple similar, smaller lesions
* Groups of lesions
* Follow skin lines on back
* “Christmas tree distribution”
Pityriasis Rosea
Superficial, Epidermis
Burns: 1st
Superficial partial thickness, Epidermis, some dermis
Deep partial thickness
Epidermis, most dermis
Burns: 2nd
Full thickness, Epidermis and dermis
Burns: 3rd
4th degree, Underlying tissue
Burns: 4th
- Epidermis only
- Painful, red, blanch with pressure
- Looks like sunburn
- No blisters
- Heal within 7 days
- Minimal treatment required
Superficial Burn (1st Degree Burn)
- 2nd degree
- Epidermis and some dermis
- Often form blisters
- Painful, red
- Blanch with pressure
- Heal within 7 to 21 days
Superficial Partial Thickness
- 2nd degree
- Epidermis, most dermis
- Erythematous, yellow or white
- Almost always blister
- Easily unroofed (tissue moves)
**Painful to pressure only
** Do not blanch - Usually > 21 days to heal
- Heal with scarring
Deep Partial Thickness
- 3rd or 4th degree
- Entire epidermis and dermis
- Can involve underlying tissue (4th degree)
- Fat, fascia or muscle
- Scarring with wound contracture
Full Thickness (painless)
- Delayed inflammatory response of skin
- Caused by ultraviolet radiation (UVR)
- Two forms UV radiation
- UVB radiation: wavelength 280 to 320 nm
- UVA radiation: wavelength 320 to 400 nm
- Both may cause sunburn
Sunburn
- Damage to epidermis and dermis
- UV radiation → DNA damage → apoptosis
- “Sunburn cells”: keratinocytes undergoing apoptosis
- Vasodilation
- Release inflammatory mediators
- Self-limited
Sunburn
Range most effective at causing sunburn
UVB (280 a 320 nm)
This type of burn is usually red, moist, painful, blistered, and blanches with pressure. It usually heals within 7 to 21 days. Children under age 5 and adults over age 55 are more susceptible to deeper burns because they have thinner skin.
Second-degree, superficial partial-thickness burn
