Week 3: Derm Flashcards
What primary lesion is: flat, less than 1cm, and only epidermis
Macule (a flat papule)
What primary lesion is: flat, greater than 1cm, only epidermis
Patch (a flat plaque)
What lesion is: raised <1cm; proliferation of cells in epidermis or superficial cells
Papule (a raised macule)
WHat lesion is raised (casts shadow with side lighting), >1cm, proliferation of cells in epidermis or superficial dermis
Plaque (a larger papule)
What lesion is a plaque but with proliferation of cells in mid and deep dermis?
Nodule
What lesion is raised, <1cm and fluid filled?
Vesicle (a fluid-filled papule; blister)
What lesion is raised, >1cm and filled with fluid?
Bulla (larger vesicle; blister)
What lesion is raised and filled with pus (leukocytes and fluid)?
Pustule
What lesion is depressed with loss of part/all of epidermis; may occur after vesicle forms/top peels off or secondary to trauma; weep and b/m crusted; usually heals without scarring
(sorry I don’t know what b/m means!)
Erosion
What lesion is depressed with COMPLETE loss of the epidermis and part of dermis; often heals WITH scarring?
Ulcer
What elements do you want to ensure to describe when talking about a lesion?
Palpability, colour, shape, texture, size, location
Describe the structure of epithelium (are cells spaced apart? What is at the base?
Epithelial tissue is scutoid shaped, tightly packed and forms a continuous sheet. It has almost no intercellular spaces. All epithelia is usually separated from underlying tissues by an extracellular fibrous basement membrane. It has a apical/basal surface
T/F: Epithelium is vascular
False - it is avascular
What is transitional epithelium? Where is it found?
A transitional epithelium (also known as urothelium) is made up of several layers of cells that become flattened when stretched. It lines most of your urinary tract and allows your bladder to expand - bladder, urethra & ureters
What type of epithelium is specialized to produce and secrete (release) substances in the glands?
Glandular epithelium (Duh! :))
What kind of epithelium do you find lining the nasal cavity?
The olfactory epithelium, located within your nasal cavity, contains olfactory receptor cells, which have specialized cilia extensions. The cilia trap odor molecules you breathe in as they pass across the epithelial surface. Information about the molecules is then transmitted from the receptors to the olfactory bulb in your brain, where your brain then interprets the smell.
What is simple squamous epithelium and where do you find it?
Single layer of flat cells.
Location: alveoli, lining of heart, blood vessels & lymphatic vessels
Function of simple squamous epithelium?
Allow materials to pass through by diffusion and secretes lubricating substances
Simple cuboidal epithelium - where and what is its function?
Ducts, secretory portions of small glands and kidney tubules. Fx: secretes and absorbs
Simple columnar epithelium - location and function?
Location: ciliated in bronchi, uterine tubes, and uterus; smooth (non-ciliated) in digestive tract, bladder
Pseudostratified Columnar Epithelium - location & fx
Ciliated trachea & much of upper resp tract
Secretes mucus, cilia move mucous
Stratified squamous epithelium - location and fx
Lines esophagus, mouth & vagina
Protects against abrasion
Stratified cuboidal epithelium - location and function?
Sweat, salivary & mammary glands
Protective tissue
General functions of the epithelium?
Protection
Secretion
Absorption
Excretion
Filtration
Diffusion
Sensory reception
3 layers of the skin
Epidermis, dermis, hypodermis
Functions of the skin
Temperature regulation, protection, fluid retention, sensation, secretion.
Describe the epidermis. What causes it to thicken?
How many sublayers does it contain?
-The superficial or outer layer of the skin, very thin (0.12mm) but can thicken and form corns or calluses with constant pressure or friction
-includes rete pegs that extend into the papillary layer
-Contains 5 sub-layers
What are rete pegs?
Rete pegs (also known as rete processes or rete ridges) are the epithelial extensions that project into the underlying connective tissue in both skin and mucous membranes.
List the layers of the epidermis
Stratum corneum (outermost)
Stratum lucidum
Stratum granulosum
Stratum spinosum
Stratum basale (germinativum)
What cell types do you find in the epidermis?
Keratinocytes, melanocytes & merkel cells (keratinocytes are dead/empty by the time they reach the stratum lucidum & corneum)
What occurs in the stratum basale?
-Basal layer where keratinocytes divide and move up to replace surface cells
-Melanocytes synthesize melanin (pigment)
-Merkel cells associated with sensory nerve endings
Describe the stratum spinosum
Layer of new keratinocytes. Polygonal shaped, has spinous processes projecting between adjacent keratinocytes
Why is the stratum granulosum have a granular appearance?
due to keratohyalin
Describe cells in the stratum lucidum layer of the epidermis
Clear (dead) layer of cells containing eleidinà they become keratin as the cells move up to the corneum layer
Describe stratum corneum
Tough, superficial outer layer covering body (dead keratinocytes)
What is the dermis? What does it contain?
the “true skin”
-irregular connective tissue layer with rich blood, lymphatic, and nerve supply
-contains sensory receptors and sweat glands (apocrine, eccrine, sebaceous)
What are the 2 layers of the dermis?
Papillary layer and reticular layer
What kind of cell types do you find in the dermis?
Macrophages
Mast cells
Histocytes
Describe the hypodermis. What cells does it contain?
-superficial fascia of varying thickness that connects to overlying dermis and underlying muscle
-contains: macrophages, fibroblasts, fat cells, nerves, blood vessels, lymphatics, hair follicle roots
What is the role of the fibroblasts in the hypodermis?
can synthesize and reorganize ECM
Secrete collagen protein
What is the nail plate made of?
hard, dead keratin
What is the nail fold?
Nail fold includes skin surrounding the lateral and proximal aspects of the nail plate. The proximal nail fold overlies the matrix; its keratin layer extends onto the proximal nail plate to form the cuticle
What is the lunula of the nail?
The lunula (white half moon), which is visible through the nail plate, is the distal aspect of the nail matrix
What is the hyponychium of the nail? What is its function?
The nail bed extends from the distal nail matrix to the hyponychium
Hyponychium = short segment of skin lacking nail cover; begin at distal nail bed & terminates at the distal groove; skin rich in WBCs, prevents bacteria & debris from getting under nail
How long does it take a nail to grow?
Growth: it takes about 5.5 months for fingernail to grow from matrix to free edge (toe nails take 12-18 months to be replaced)
What is the nail matrix?
‘The nail matrix is the area where your fingernails and toenails start to grow. The matrix creates new skin cells, which pushes out the old, dead skin cells to make your nails. As a result, injuries to the nail bed or disorders that affect the matrix can affect your nail growth.
The matrix synthesizes 90% of the nail plate
What is the nail bed?
The nail bed extends from the distal nail matrix to the hyponychium (under the nail plate)
Nail bed consists of parallel longitudinal ridges with small blood vessels at their base.
What are Beau’s lines? Causes?
Transverse depressions or ridges of all the nails that appear @ lunula base after stressful event has temporarily interrupted nail formation
Lines progress distally with normal nail growth, eventually disappear @ free edge
Causes: high fever, scarlet fever, hand-foot-and-mouth disease, chemo
Onycholysis - what is it? What are the causes? What medical conditions might we be worried about?
Separation of nail from nail bed starting at distal end and slowly progressing proximally
S&S – nonadherent part of nail is white, yellow or green-tinged
Causes include nail trauma, repeated wet work, vigorous repeated manicuring (digging under nails), false nails allergy and psoriasis
Screen pts with unexplained onycholysis for hyperthyroidism, asymptomatic thyroid disease and iron deficiency
Treatment of onycholysis
Treatment – cut separated portion of the nail. Promotes dryness and discourages infection.
Yeast can grow in space between the nail and nail bed. Treat with topical agents (fungoid tincture that contains miconazole). Consider oral flucanazole for resistant cases – 150 mg daily for 5-7 days
Paronychia - what is it? Where is it? Greatest risk factor? Caused by what micro-organism most commonly?
What is it? Acute or chronic infection of the cuticle.
Where is it? One or more fingers or toes may be involved
Greatest risk factor? Individuals whose hands are frequently exposed to moisture
Most common cause? Staphylococci and streptococci
Difference between acute and chronic paronychia?
Acute is rapid, painful inflammation of the cuticle. Abscess may develop, requiring incision and drainage. Pus can develop and expressed from the proximal nail fold. Nail plate is not typically affected, but can become discolored with ridges
Chronic develops slowly, tender + swelling around proximal or lateral nail folds
Treatment of paronychia?
Topical application of thymol. Oral antifungals NOT effective because they do not penetrate affected tissues. Prevention is key by keeping hands dry
Ingrown toenails - what is happening? What causes it? How do we treat it?
Results from increased lateral pressure either by poorly fitting shoes, excessive trimmer of lateral nail plate or trauma
S&S: pain and swelling
Dermis is penetrated by the nail/lateral nail fold, and broken skin becomes purulent and edematous as granulation tissue grows with the penetrating nail
Treatment: removal of the penetrating nail with scissors/curetting granulation tissue and using silver nitrate sticks to treat small areas of granulation
Could lead to cellulitis which may require PO antibiotics
What is a digital mucous cyst? Where does it form and on who?
Focal collections of mucin (macromolecules in mucus) that don’t have a cystic lining
Dome-shaped, pink-white, typically occur on the dorsal surface of the distal phalanx in middle-aged and elderly people
Cysts on the proximal nail fold could cause a longitudinal nail groove as it compresses the nail matrix cells
When incised, exudate is clear, viscous, jelly-like
Treatment of digital mucous cyst?
Typically benign, no intervention if pain free and does not compromise any function
If treatment is needed: cryosurgery of the base:
Remove cyst roof w/ scissors, expel gelatinous exudate
Freeze the base
Treated site will be edematous and exudative, and a bulla will usually develop
Healing takes 4-6 weeks, and retreatment is frequently needed
What are considered PRIMARY lesions?
*Lesions that present at the onset of disease
Macules, papules, patch, plaque, wheal, nodule, tumor, vesicles, bulla, pustules, cyst, telangiectasia
What is telangiectasia?
Fine (0.5–1.0 mm), irregular red lines produced by capillary dilation; can be associated with acne rosacea (face), venous hypertension (spider veins in legs), systemic sclerosis, or developmental abnormalities (port-wine birthmarks)
What are considered SECONDARY lesions?
*Changes to skin overtime due to disease progression
Scales, lichenification, keloid, scar, excoriation, fissures, erosion, ulcer, atrophy
What is a fissure
Linear crack or break from the epidermis to the dermis; may be moist or dry e.g athlete’s foot, cracks at the corner of the mouth
What is “erosion” as a secondary lesion?
Loss of part of the epidermis; depressed, moist, glistening; follows rupture of a vesicle or bulla or chemical injury
What is a wheal?
Elevated, irregular-shaped area of cutaneous edema; solid, transient; variable diameter eg Insect bites, urticaria, allergic reaction
Another description: migratory, well-circumscribed, erythematous, pruritic plaques on the skin. may be accompanied by angioedema, which results from mast cell and basophil activation in the deeper dermis and subcutaneous tissues and manifests as edema of the face and lips, extremities, or genitals.
What is a keloid?
Irregular-shaped, elevated, progressively enlarging scar; grows beyond boundaries of wound; caused by excessive collagen formation during healing
What is lichenification?
Rough, thickened epidermis secondary to persistent rubbing, itching, or skin irritation; often involves flexor surface of extremity eg chronic dermatitis, eczema
What are scales?
Secondary lesion
Heaped-up, keratinized cells; flaky skin; irregular shape; thick or thin; dry or oily; variation in size eg. Flaky skin post medication reaction.
Examples of nodules?
include cysts, lipomas, and fibromas
What is a “crust”?
dried exudate on skin surface (composed of blood/serum/pus or combo)–> I.e. scab.
What is a comdedome?
Small, flesh-colored/white/or dark bumps that give skin rough texture. Clogged hair follicle with keratin+oil. Typical of acne.
What are milia?
tiny white bumps that are clogged eccrine sweat glands, keratin filled little cysts just under epidermis. Found in babies; in adults, typically around eyes/nose/groin. Harder texture than comedone.
Petechia vs. purpura
Petechia - <2-3mm, Nonblanchable punctate foci of hemorrhage. Causes: Platelet abnormalities (eg, thrombocytopenia, platelet dysfunction), vasculitis, and Infections (meningococcemia, Rocky Mountain spotted fever, other rickettsioses)
Purpura - 3-10mm larger area of hemorrhage that may be palpable. Causes: leukocytoclastic vasculitis, coagulopathy. Large areas of purpura may be called ecchymoses (>1cm) or, colloquially, bruises.
WHat is a burrow?
A thread-like linear or serpiginous (wavy, serpent-like) tunnel in the epidermis typically made by a parasite (such as scabietic mites)
What kind of exudate do you expect to see early in the inflammatory process?
Serous
What is fibrinous exudate?
thick and clotted, in more severe or advanced inflammation. Ex: lungs in pt w/pneumonia
When do you see purulent exudate?
large number of leukocytes as in persistent bacterial infection.
What causes a fever? How can it be beneficial? Harmful?
Induced by endogenous pyrogens (meaning the person infected produces them), specifically cytokines (.e.g IL-1, released from neutrophils and macrophages).
Pathogens can also produce exogenous pyrogens (meaning they come from outside the body, from a pathogen)
Beneficial effect: most microorganisms are highly sensitive to small increases in body temperature
Harmful effect: may enhance the host’s susceptibility to the effects of endotoxins associated with Gram-negative bacterial infections
What are 3 systemic signs of acute inflammation?
Fever
Leukocytosis
Increase levels of circulating plasma proteins
What is a “left shift” with leukocytosis?
more immature WBC’s are present than normal.
How can testing sedimentation rate (ESR) indicate acute inflm?
Increased Fibrinogen (one acute-phase reactant) -> increased adhesion among erythrocytes -> increased sedimentation rate, so testing for increased sedimentation rate can show you that the acute inflammatory response is underway.
Increased levels of circulating plasma proteins in acute inflammation - where do they come from and when do they peak?
Liver increases production of specific plasma proteins, called acute-phase reactants
Acute-phase reactants reach max circulating levels 10-40 hrs after inflammation start
IL-1 & IL-6 work together to make these proteins
Increased Fibrinogen (one acute-phase reactant) -> increased adhesion among erythrocytes -> increased sedimentation rate, so testing for increased sedimentation rate can show you that the acute inflammatory response is underway. (Left Shift)
Differentiate chronic inflammation from acute inflammation: duration, etiology (processes), physical findings QUESTION 8 in
TO BE ANSWERED ONCE IN ILO ANSWERS
What are the 3 phases of wound healing?
1) Inflammation & Coagulation: first 24h
2) Proliferation & New tissue formation: 3-14 d
3) Remodeling & Maturation: weeks to months
What happens during the first phase of wound healing?
1) Inflammation & Coagulation: first 24h
Fibrin acts as scaffold for cells for healing
Platelets: clot, release growth factors that initiate proliferation of undamaged cells
Neutrophils: clear wound of debris, bacteria
Macrophages (come after neutrophils): Clear debris, release wound healing mediators and growth factors (GF), recruit fibroblasts, promote angiogenesis
What happens during the 2nd phase of wound healing?
2) Proliferation & New tissue formation: 3-14 d
Wound sealed, fibrin clot replaced with normal or scar tissue
Macrophage invasion of dissolving clot
Recruitment and proliferation of fibroblasts–>collagen synthesis; epithelialization, contraction, differentiation
Granulation tissue grows into wound from surrounding CT: has invasive cells, new lymph/capillaries
Epithelial cells migrate under clot or scab; contact similar cells from all sides of wound to heal it
Epithelialization of skin can be quickened if wound kept moist—> prevents fibrin clot from becoming scab
What happens during the third phase of wound healing?
Continued cell differentiation, scar formation, remodeling
Fibroblast action mainly: deposition collagen
Tissue regeneration and contraction continue
Scar is avascular
What is the general structure of bacteria? What are the functions of the cell wall?
Bacteria = prokaryotes
Lack nucleus
Lack membrane-bound organelles (eg mitochondria, ER, golgi complex)
CELL WALL - One of the most important structures of a bacterial cell
Functions:
- Protect bacteria from bursting
- Help maintain their shape
- Control molecules going in & out of the cell.
What are the two ways to classify bacteria?
Thickness of cell wall (gram stain)
Shape of bacteria
Explain gram staining
Use GRAM STAINING to determine the THICKNESS of the cell wall to identify and categorize different types of bacteria.
Bacteria are stained with a dye called crystal violet. A thick cell wall retains the violet colour. A thin cell wall does not.
Note: It is the peptidoglycans within the cell walls that retain the dye.
Gram Positive bacteria = THICK cell walls. When dyed, they appear blue or purple.
Gram Negative bacteria = THIN cell walls. When dyed, they appear pink or red.
What are the 3 classifications of bacteria bases on shape?
Cocci = round/spherical shape
Bacilli = rod shape
Spirilla = spiral shape
What are aerobic bacteria? Examples?
Thrives/grows in oxygenated environment
Soil, water, different surfaces
Derive their energy from aerobic respiration (oxidative phosphorylation, Kreb’s cycle) → produces more energy
Examples:
Lactobacillus
Tuberculosis
Anaerobic bacteria - how do they derive their energy and examples
Grows in the absence of oxygen → cannot survive in the presence of O2
Lives in O2 depleted areas (eg digestive tract)
Derive their energy from anaerobic respiration and by lactic acid or alcoholic fermentation → produces less energy
Examples:
E. coli
Clostridium
Define mycoses
Diseases caused by fungi
Can be superficial (on or near the skin or mucous membranes), deep or opportunistic
What are dermatophytes? What immune cells are important in controlling fungi?
Fungi that invade the skin, hair, or nails
The disease they produce are called tineas (ringworms)
Ie. Tinea capitis (scalp), tinea pedis (feet), tinea cruris (groin)
The pathological fungi cause disease by adapting to the host environment. The fungi colonizes the skin and digest keratin.
Phagocytes and T cells are important in controlling fungi
Common pathological bacterial infections in the skin?
Staphylococcal (skin), Cholera (mucuous membranes), Streptococcal pneumonia (extracellular), TB (intracellular)
Common pathological fungal infections of the skin?
Tinea pedis (skin), Candidiasis eg. Thrush (Mucous Membranes), Sporotrichosis (extracellular), Histoplasmosis (intracellular).
What is THE most common cause of fungal infections in humans? (which fungus)
Candida albicans –> causes cutaneous candidiasis
What is the real name for athletes foot, jock itch and ringworm?
Tinea pedis
Tinea cruris (jock itch)
Tinea corporis (ringworm)
Acne Rosacea - what is it?
Common facial eruption characterized by redness, telangiectasia, flushing, blushing (vascular component), papules and pustules
Acne Rosacea - who do we most often seen this is? What is the cause?
Usually > 30 yrs old
Can occur in children
Cause unknown - genetic factors (Celtic & northern European), UV exposure, microorganisms, skin sensitivity, and food triggers (spicy foods or ETOH)
What do you see on the skin in Acne Rosacea
- Papules & pustules over forehead, cheeks, nose & around eyes (rarely elsewhere)
-Erythema and telangiectasias present - In extreme cases, also have oily skin & edema (cheeks and nose)
- CHronic deep inflammation of nose leads to irreversible skin thickening (rhinophyma)
What are the nonskin findings for Acne Rosacea
Ocular symptoms: mild conjunctivitis
- Conjunctival hyperemai, telangiectasias on lid, and others… (long complicated names I won’t remember!)
Just remember ocular symptoms possible :)
What makes Acne Rosacea worse?
exacerbated by ingestion of hot foods & drinks, ETOH (esp redwine), heat, sunlight, & topical meds such as antiwrinkle creams and chemical peels
Timeline for Acne Rosacea
Chronic (years) with episodes of activity followed by quiescence
- may result in permanent swellling of periocular tissues and firm facial edema
Acne Vulgaris - what is happening here? 4 principles causes?
-develops in sebaceous follicles (primarily on face & upper chest/back)
-lesions are noninflammatory or inflammatory (cystic)
4 principal causative factors:
1) Hyperkeratinization of the follicular epithelium
2) Excessive sebum production
3) Follicular proliferation of anaerobic Propionibacterium acnes (P.acnes)
4) Inflammation and rupture of a follicle from accumulated debris and bacteria
Why is acne vulagaris worse in adolescence? What does the bacteria do?
Increased androgen production during puberty causes increased size and productivity of sebaceous glands, which promotes P. acnes
P. acnes produces extracellular enzymes that convert triglycerides into free fatty acids (FFAs)
FFAs activate T-cells and th17 cells which cause inflammation and edema that results in pus formation and breakdown of the follicle wall
Epidemiology of Acne Vulgaris
-Occurs primarily between ages 12-25
-tends to occur in families (if both parents have acne, 75% change that a child will develop it)
-incidence same for all genders, although severe disease more often in males
-associated with diets high in simple carbohydrates and dairy products
Time course of acne vulgaris? What makes it worse?
-flare-ups may be seen during periods of stress, before menstrual periods, with certain medications (corticosteroids, lithium, anticonvulsants, antituberculosis medications, iodides)
-redness and pigmentation after resolution may take many months to fade
-usually lasts 5 to 10 years after onset in adolescence
-adult women can have chronic low-grade acne that can be challenging to manage
S&S of acne vulgaris. Differentiate noninflammatory and inflammatory forms of the condition
Development of lesions in sebaceous follicles (primarily on face and upper chest/back)
Noninflammatory: comedones are open (blackheads) or closed (whiteheads) with accumulated material that causes distension of the follicle and thinning of follicular canal walls
Inflammatory: in closed comedones when the follicular wall ruptures and expels sebum into the surrounding dermis and initiates inflammation
-pustules form when the inflammation is close to the surface
-red papules & cystic nodules develop when inflammation is deeper, causing mild to severe scarring
what kind of reaction occurs in Allergic Dermatitis/ Allergic Contact Dermatitis (ACD)
Type IV, T-cell–mediated, delayed-type hypersensitivity reaction to an environmental allergen that has 2 phases:
Describe the two phases of development of allergic contact dermatitis (sensitization phase & allergic response)
Sensitization to an antigen: allergens (through complex pathway) causes T cells to differentiates into memory/effector T cells.
- asymptomatic, may be brief (6 to 10 days for strong sensitizers such as poison ivy) or prolonged (years for weak sensitizers such as sunscreens, fragrances, and glucocorticoids). During differentiation, sensitized T cells become able to express cutaneous homing antigens (eg, cutaneous lymphocyte antigens) that enable them to migrate from cutaneous capillaries to the epidermis.
Allergic response after reexposure: When antigen-presenting cells present the antigen to the sensitized T cells, the T cells can expand and trigger an inflammatory reaction at that location (elicitation phase of ACD), resulting in the characteristic symptoms and signs of ACD.
How quickly does allergic contact dermatitis occur?
- sensitization phase may be brief (6 to 10 days for strong sensitizers such as poison ivy) or prolonged (years for weak sensitizers such as sunscreens, fragrances, and glucocorticoids).
- Typically takes ≥ 1 day after exposure to become noticeable and takes 2 to 3 days to become further aggravated (crescendo reaction)
Allergic Contact dermatitis S&S?
- more pruritic than painful
- Skin changes range from erythema, scaling, and edema, through vesiculation to severe swelling with bullae
- pattern usually suggests a specific exposure, such as linear streaking on an arm or leg (eg, due to brushing against poison ivy) or circumferential erythema (under a wristwatch or waistband).
The site of contact is where the allergen contacted the skin, very often the hands, because they touch so many substances. Although the palms and the palmar sides of the fingers are most exposed, ACD often starts in the web spaces between fingers because the thick stratum corneum prevents or delays allergen penetration on the palms and palmar sides of the fingers (also on the soles).
- With airborne exposure (eg, perfume aerosols), areas not covered by clothing are predominantly affected. Although ACD is typically limited to the site of contact, it may later spread because of scratching.
What is Irritant Contact Dermatitis?
ICD is a nonspecific inflammatory reaction to toxic substances contacting the skin. Numerous substances can irritate the skin, including
Chemicals (eg, acids, alkalis, solvents, metal salts)
Soaps (eg, abrasives, detergents)
Plants (eg, poinsettias, peppers)
Chronic moisture (eg, from body fluids, urine, and saliva)
Properties of the irritant (eg, extreme pH, solubility in the lipid film on skin), environment (eg, low humidity, high temperature, high friction), and patient (eg, very young or old) influence the likelihood of developing ICD.
Acute vs. Chronic ICD (Irritant contact dermatitis)
Acute ICD: Potent irritants, such as caustic chemicals, can damage the skin immediately, typically manifesting with acute burning or stinging pain.
Chronic or cumulative ICD: Less potent irritants require longer (chronic) or repeated (cumulative) periods of skin contact to cause ICD; these forms typically manifest with pruritus.
What is occupational ICD?
Occupational ICD is ICD caused by one or more of the many possible work-related skin irritants. It can be acute, chronic, or cumulative.
Atopic disorders increase risk of ICD because of impaired skin barrier function and lower threshold for skin irritation.
What is phototoxic dermatitis?
Phototoxic dermatitis is a variant in which a topical (eg, perfumes, coal tar) or ingested (eg, psoralens) agent becomes a skin toxin only after exposure to ultraviolet light, most typically long-wave ultraviolet light (UVA). Phototoxic dermatitis, therefore, occurs only in UV-exposed skin, typically with a sharp demarcation.
Time course of ICD
- Can be immediate depending on the irritant and potency, or chronic and need repeated exposure before causing a reaction.
- Resolution may take up to 3 weeks after discontinuation of exposure. Reactivity is usually lifelong, so identified allergens must be avoided lifelong. Patients with phototoxic dermatitis can have flare-ups for years when exposed to sun (persistent light reaction); however, this is very rare. ICD typically decreases in intensity [decrescendo reaction] after 1 or 2 days.
ICD S&S? Painful or pruritic?
- more painful than pruritic (pruritis more common if chronic/cumulative)
- Signs range from erythema, scaling, and edema to erosions, crusting, and blistering.
What is the common name for Atopic Dermatitis?
Eczema
What causes eczema?
“Results from a viscious cycle of dermatitis associated with elevated T-cell activation, hyperstimulatory Langerhans cells, defective cell-mediated immunity & overproduction of immunoglobulin by B cells.
- Stratum corneum barrier dysfx and ceramide (epidermal lipid) deficiencies
- Genetic factors: familial predisposition
- Environmental factors: triggered by excessive bathing, harsh soaps, Staph aureus colonization, sweating, rough fabrics & wool
Why are those with eczema more susceptible to skin infection?
Epidermal barrier dysfunction: cutaneous inflm is T-cell mediated delayed-type hypersensitivity reaction –> hypersensitivity downregulates antimicrobial peptides –> more susceptible to skin infection!
Epidemiology of atopic dermatitis
- Primarily affects children in urban or developed countries
- Most people with the disorder develop it before age 5, many of them before age 1; however, atopic dermatitis may even begin during late adulthood.
- Childhood atopic dermatitis frequently resolves or lessens significantly by adulthood.
- Many patients or their family members who have atopic dermatitis also have allergic asthma and/or immediate-type hypersensitivities that manifest, for example, as allergic seasonal or perennial rhinoconjunctivitis. The triad of atopic dermatitis, allergic rhinoconjunctivitis, and asthma is called atopy or atopic diathesis.
Time course of atopic dermatitis: how does it change throughout the lifespan?
Atopic dermatitis in children often abates by age 5 years, although exacerbations are common throughout adolescence and into adulthood.
- Girls and patients with severe disease, early age of onset, family history, and associated allergic rhinitis or asthma are more likely to have prolonged disease. Even in these patients, atopic dermatitis frequently resolves or lessens significantly by adulthood.
Describe the lesions that occur in the acute and chronic phases of atopic dermatitis. Is it itchy?
Acute phase - lesions are intensely pruritic, red, thickened, scaly patches or plaques that may become eroded due to scratching.
Chronic phase - scratching and rubbing create skin lesions that appear dry and lichenified.
Intense pruritus is a key feature. Itch often precedes lesions and worsens with dry air, sweating, local irritation, wool garments, and emotional stress.
Where do atopic dermatitis lesions usually develop?
Distribution of lesions is age specific. In infants, lesions characteristically occur on the face, scalp, neck, eyelids, and extensor surfaces of the extremities. In older children and adults, lesions occur on flexural surfaces such as the neck and the antecubital and popliteal fossae.
Erythroderma (Erythema that covers more than 70% of the body surface area) is rare but can result when atopic dermatitis is severe.
