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.
What bacteria usually cause superinfections on atopic dermatitis?
Secondary bacterial infections (superinfections), especially staphylococcal and streptococcal infections (eg, impetigo, cellulitis) are common.
What is Bowen’s disease?
-A type of squamous cell carcinoma
-Referred to as ‘squamous cell carcinoma in situ’ (SCC in situ)
-In situ meaning: surface form (non-invasive)
What layers of the skin are affected by Bowen’s disease? What kind of cellular changes occur here? Common causes?
Dysplastic lesion, usually confined to epidermis (intraepidermal), but may extend in to the dermis
-Causes of cellular dysplasia is multi-factorial, but most common = UV light, radiation, chemicals (arsenic), and HPV
Epidemiology of Bowen’s disease?
Most frequently diagnosed in Caucasian individuals
-Usually >60 and rarely <30
Time/course of Bowen’s disease?
Insidious onset. Lesions = slow-growing and evolve over months to years. If untreated, can extend laterally (over many years) and become invasive.
What do lesions in Bowen’s disease look like? Common locations?
Location: may be found in both sun-exposed and sun-protected areas
Lesion: solitary, barely raised, red or pink patches or plaques (often mistaken for psoriasis or eczema)
-may have focal areas of pigmentation (mimicking superficial basal cell carcinoma or nevi)
-are minimally symptomatic and mimic other benign processes -> Pt may delay care/dx as a result
If the test says “Bullseye” lesion, what condition is it?
Lyme disease
If the tests says “Burrows” what condition is it?
Scabies
Cellulitis caused by what microorganism is usually stinky?
Pseudomonas
if the test says “cauliflower-like” lesion, what condition is it?
Warts (condylomata acuminata if genital)
If the test says “umbilicated papule” what condition is it?
Molluscum Contagiosum
What condition appears “stuck on”
Seborrheic keratosis
If you see multiple seborrheic keratosis lesions pop up on the body, what concerning condition could this indicate?
Internal malignancy
Which locations metastasize most easily?
Those closest to lymph & highly vascularized areas
What risk do we need to be aware of for prescribing Accutane to people with uteruses?
HIGHLY teratogenic. Requires negative preg test to prescribe & the client should also be on birth control
What key word might be used to describe seborrheic dermatitis?
GREASY
What might you do to differentiate a candidiasis skin lesion from other similar rashes?
Has white layer on top & when you attempt to scrape it away, should see little specks of blood
A shingles lesion is contagious until…
It crusts over (yum)
What is a furuncle?
If several hair follicles become infected and abscesses form in each hair follicle, it can happen that these infections cluster together, leading to the appearance of what is known as a carbuncle.
What is candidiasis? Why is the lesion white on top? When does it become erythemic?
- opportunistic infection caused by the yeastlike fungus Candida albicans.
- C. albicans is found throughout the body but likes mostly moist, warm environments. It’s usually harmless, however it can proliferate when the immune system is weakened. Candida typically lives on the skin or mucous membranes.
- Candida overgrowth can damage nearby tissues the most common being damage of the skin or mucous membrane. Destroyed cells and keratin protein accumulate to form a white lesion - pseudomembranous.
- Overgrowth can also occur when there is less microbial competition. Normal microflora inhibits candida growth. However when conditions such as antibiotics usage reduce bacteria, candida can proliferate leading to inceased blood flow to affected tissues causing red painful lesions - erythematous. In most cases you see a mix of both pseudomembranous and erthyematous components.
What makes a person more susceptible to candida skin infection?
immunodeficiency, antibiotics usage, diabetes, pregnancy, cushing’s, infants 6 months and younger,It neoplastic blood disorders.
What populations most commonly get candida?
Candidiasis is more prevalent in old age and infants 6months or younger. It is also common in pregnant women and kids using inhaled steroids. Oral candidiasis or thrush is the most common infection. It is a global infection but more prevalent in poorly nourished population.
What is cellulitis? What organisms usually cause it?
*It is an infection of the dermis and subcutaneous tissues characterized by fever, erythema, inflammation, and pain
*Commonly caused by S.Aureus, CA-MRSA, or group B streptococci
Can occur near surgical wounds or trauma site
Risk factors for cellulitis?
Diabetes, cirrhosis, poor lymphatic circulation, renal failure, poor nutrition, HIV, ETOH, cancer, chemotherapy, pre-existing skin issues and substance abuse are predisposing factors.
*Trauma and surgery are risk factors
Complications of cellulitis?
sepsis & chronic edema
What S&S does cellulitis often start with? How long does it usually take to heal?
*Localized pain and tenderness occur for a few days before presentation
*Time for healing after treatment is initiated is 12 days
*Most cases improve when pt is on oral antibiotic therapy for 5 days.
S&S of cellulitis - what happens as it gets worse?
Expanding redness, warmth, and pain of the skin. Pus can accumulate under the skin and cause blisters (Power-Kean, p.1050). Vesicles, blisters, hemorrhage, necrosis or abscesses can occur. Skin Is slightly raised and border is indistinct
Pain on palpation.
Where is cellulitis most often seen?
*Very common on lower extremities or pinna (ear) or in local anatomic abnormalities that affect circulation.
What is Condylomata Acuminata and what causes it?
Genital warts . HPV Types 6 & 11 most often.
Risk factors for genital warts
Multiple sexual partners & high risk partners
Unprotected sex
Immunocompromised
Smoking
Not vaccinated (The HPV9 vaccine [Gardasil] protects against types 6 and 11)
Is the HPV infection that causes genital warts usually high risk for cancer?
No but co-infection with other types of HPV (which may be higher risk) is very common
How are genital warts spread?
Sexual transmission (but just needs skin to skin contact, not necessary mixing of bodily fluids…)
If you have an infection for the types of HPV genital warts, will the warts always be apparent?
No, can be chronic and latent for months to years.
Once you remove genital warts, are you cured?
No, not curative.
Warts may recur due to subclinical infection, re-infection, or immunosuppression
May resolve on own within a few months, but may also maintain or progress if not treated
Technical term for wart?
Verrucae
Do you typically see pruritis, pain or bleeding with anogenital warts?
Not often but can occur
Where will you see lesions with condylomata acuminata? Possible complications?
Located on genitalia, groin, perineum, anal skin, perianal skin, and/or suprapubic skin
Urethral, cervical, or anal involvement possible
If extensive, may interfere with defection or urination, or urethral bleeding
How will genital warts present differently if client is immunocompromised?
Infections more extensive and difficult to treat in immunocompromised (such as HIV, diabetes)
How do we test for anogenital warts?
Diagnosis usually based solely on clinical presentation and physical assessment
Limited to anogenital region and surrounding areas
Biopsy possible for definitive diagnosis, and to rule out malignancy
Assess for signs of other STIs: ulcerations, vesicles, or discharge & test accordingly
*HPV testing not routine for warts
What does dermatophytoses mean? What conditions are included here?
Fungal infection of the skin
Ringworm (the tineas):
tinea unguium (nail)
tinea pedis (foot)
tinea cruris (groin/thigh/buttock) or “jock itch”
tinea corporis (body)
tinea capitis (scalp)
How are dermatophytes typically transmitted? Who is most vulnerable?
-Dermatophytes originate from animals (zoophilic) and from soil (geophilic)
-Transmission occurs with direct contact of infected animals or humans, or indirectly by contact with contaminated fomites (on shower floors).
-Predisposing factors include moist, macerated skin, exposure to animals (e.g., cows, kittens, dogs), affected family members (especially tinea capitis and onychomycosis), topical corticosteroid use, immunosuppressed states (diabetes, chemo), and athletics (wrestlers).
Which fungi cause dermatophytosis? How do they survive on your skin?
Microsporum
Trichophyton
Epidermophyton.
- The organisms metabolize keratin and cause a range of pathologic clinical presentations
How would you describe the lesions in ringworm? (talks about each type of tinea)
-Classically, dermatophyte infections elicit papules and plaques with a rounded edge and white scale (ringworm lesion)
-Dermatophytes infect hair follicles, causing pink to red papules and nodules.
-Pustules are caused by more intense inflammation.
-Tinea Pedis (foot) patterns:
Interdigital—extend onto plantar and dorsal foot
Scaly-thickened skin or moccasin type
Vesicular-may be pustular-allergic response to fungus
-Tinea Cruris (groin/thigh/buttock)
Half-moon red plagues with advancing scale and pink-red papules and pustules in the groin
Scrotum rarely involved
-Tinea Corporis (body) patterns:
Annular plagues (classic)
Deep inflammatory-red nodules and pustules
Majocchi’s granuloma-deep hair follicle infection
-Tinea Capitis (scalp) patterns:
Seborrheic dermatitis-most common
Inflammatory-boggy scalp-may be confused with cellulitis
Black dot-large areas of alopecia
Pustular minimal scaling. Posterior cervical adenopathy present.
What is erythema multiforme? What causes it?
An acute, immune-mediated condition affecting skin + mucous membranes (including genital)
Produced by a cytotoxic immune response directed against keratinocytes expressing foreign viral or drug antigens
- Infections are the cause for ~90% of cases. Commonly in herpes simplex type 1 & 2. Other common cases are Mycoplasma pneumoniae, and upper respiratory tract infections.
Who gets erythema multiforme most often?
Most common in young adults (20-40) but can happen in children
Do we usually need to treat erythema multiforme?
Usually self-limiting and resolves in 1 month without scarring
What are the characteristic lesions of erythema multiforme?
- Characterized by numerous target-shaped skin lesions with many types of lesion morphologies (hence name multiforme): target lesions, erythematous macules and papules, urticarial-like lesions, vesicles, and bullae.
- Target lesions begin as dusky-red, round macules and papules that may burn and itch.
- Early lesions appear suddenly in a symmetric or crop pattern on the palms, soles, backs of the hands and feet & forearms and legs. Bullae and erosions may be present in the oral cavity (NOT to be confused with SJS)
- Dx not made until early lesions evolve into target lesions during a period of 24 to 48 hours.
- Target lesions have an “iris” because of centrifugal spread à circumference of 1-3cm
- The center of the iris can appear dark red, purpuric, or vesicular.
- This central area is surrounded by a pale area of edematous skin, which is in turn surrounded by a sharp discrete ring of erythema.
What is folliculitis? What causes it?
Inflammation of hair follicle. Develops from proliferation of microorganisms or trauma around the opening of the hair follicle. Inflammation is a result of the release of chemoactive factors/enzymes.
- Often S. Aureus
- Can result from tinea infection in beard
- Prolonged skin moisture, skin trauma, occlusive clothing, topical agents, and poor hygiene are contributing factors.
Does folliculitis usually come on slowly or quickly? Can you spread it? How long does it last?
Eruption is abrupt.
Can spread to other parts of body by shaving.
Symptoms last for a few days. should improve once mechanical irritant is removed or topical/oral antibiotics are initiated.
Can have recurrent bacterial infections if patient has nasal carriage of S. aureus- treat with oral abx.
What does folliculitis look like?
Lesions appear as dome shaped pustules with surrounding area of erythematous halos around follicle. Can be tender. Most prominent on scalp, arms leg, axilla, and trunk. Rarely cause systemic symptoms.
Furuncle vs Carbuncle
Furuncle (boil) – an inflammation of hair follicles. They are walled-off, deep and painful, firm or fluctuant mass enclosing a collection of puss. It often evolves from a superficial folliculitis
Carbuncle – an extremely painful, deep, interconnected aggregate of infected, abscessed hair follicles
The main difference is that a furuncle is one boil on the skin, whereas a carbuncle is a cluster or collection of boils.
Bacteria most often involved in development of furuncles/carbuncles?
S. aureus
S &S of furuncle/carbuncle? WHere do they most often occur?
Any hair-bearing site can be affected. Sites of high friction and sweating are most typically affected (like under the belt, the anterior thighs, the buttocks, the groin, the axillae, and the waste
Furuncle –
*deep dermal or subcutaneous, firm, red, swollen, and painful mass.
* 1 – 5 cm in diameter
*No systemic symptoms
Carbuncle –
*deep, tender, firm subcutaneous erythematous papules enlarge to deep-seated nodules that can be stable or fluctuate
*Favoured sites are back of the neck, upper back, and lateral thighs.
*Malaise, chills, and fever may precede or occur during the height of infection.
How do furuncles/carbuncles resolve? How can we help them drain?
Several Days: they can rupture or be reabsorbed
- Apply warm, moist compresses to encourage spontaneous drainage
If not resolving and becoming systemic, can make an incision and drain, and treat with systemic antibiotics
Which herpes simplex type typically causes oral and genital infections?
Oral - type 1
Genital - type 2
Your patient develops genital herpes lesions for the first time. Is it likely this will recur?
80-90 % of people with symptomatic (Type2) infection will have recurrence within one year
most common location of herpes lesions?
lips
How is HSV transmitted? Where does the virus like to hang out?
via resp. droplets, direct contact with an active lesion or Salva or cervical secretions containing virus
HSV enters nerve endings in the skin directly or travels down peripheral nerves to dorsal root ganglia (DRG) where it stays inactive
What occurs in a recurrent infection of HSV?
Occurs after symptomatic or asymptomatic primary infection
Local skin trauma, systemic changes reactivate virus
Virus then travels via peripheral nerves down to initial infection site
S&S of HSV infection (primary & recurrent infections)
Mostly asymptomatic
Early signs = Tenderness, pain, mild paresthesia
Later: lesions, grouped vesicles (more numerous and spaced out than secondary infection)
Localized pain, tender lymphadenopathy, headache, fever, generalized aches
Lesions on mucous membrane accumulate exudate, lesions on skin form crust
Gingivostomatitis + pharyngitis most frequent (Type1)
Vulvovaginitis/painful vaginal + cervical erosions in women w genital infection
May have proctitis, anorectal pain, discharge, constipation or tenesmus in men or women
Recurrent Infection:
Early signs (same as primary)
lesion formation with rapid formation of papules and then vesicles
dome-shaped, tense vesicles rapidly umbilicate
systemic symptoms rare
What is proctitis?
Inflm of the rectum
Time course of HSV lesions?
Primary Infection:
Early signs occur before onset of lesions 3-7 days after contact
Lesions last 2-6 weeks and heal without scaring
Recurrent Infection:
Early signs last 2-24 hrs
Lesions appear within 12 hrs
after 2 - 4 days vesicles rupture and form erosions or crust
crust sheds in ~8 days
recurrent disease
What viruses have most often been detected with Bell’s Palsy?
Herpes simplex type 1 has been detected in up to 78% of cases, and herpes zoster has been
detected in 30% of cases
- Etiology still not fully known
What two conditions are caused by the herpes zoster virus?
Shingles& chicken box
(Shingles is known as Herpes Zoster)
Where does the virus remain latent after chicken pox?
in trigeminal and dorsal root ganglia.
S & S of herpes zoster? Easy trick for how to alleviate local symptoms?
- initial symptoms of pain and paresthesia localized to the affected dermatome (the
cutaneous area innervated by a single spinal nerve, followed by vesicular eruptions that
follow a facial, cervical, or thoracic lumbar dermatome.
Approximately 15 to 20% of individuals experience
postherpetic neuralgia (pain) with reactivation of the virus.
Local symptoms are alleviated with
compresses, calamine lotion, or baking soda.
What is impetigo? What usually causes is?
Common, highly contagious bacterial superficial skin infection
Caused by Streptococcus pyogene and/or Staphylococcus aureus (80%).
May occur after a minor skin injury, ex. Insect bite, or within lesions of atopic or another dermatitis. Often develops on normal skin.
Who most often gets Impetigo?
Highest rate of infection in children in close physical contact with each other
Most common bacterial skin infection of children
More likely in warm, moist, humid climates
Poor hygiene pre-disposes
How long does Impetigo last? How does it progress?
Self-limited but can spread and last weeks-months if untreated
Chronic untreated impetigo can lead to ecthyma (deeper, dermal infected lesions), Bullous formation
T/F The lesions in impetigo are usually painless
True, generally asymptomatic and painless
Where do the lesions in Impetigo usually form? WHat are the two kinds?
Lesions may be localized or widespread
Common on face
Uncommon on trunk
Lesions generally asymptomatic and painless
Two clinical forms:
Bullous Impetigo
- Thin-roofed bullae turn from clear to cloudy. Bullae quickly collapse, leaving an inner-tube shaped rim with a central thin, flat, honey-colored, stuck on crust
- Lesions enlarge and coalesce, minimal surrounding erythema, thick crust accumulates in longer lasting lesions
- Mild adenopathy
Nonbullous Impetigo (Crusted)
- Vesicles/pustules rupture, exposing red, moist base
- Tinea-like scaling border forms as lesions enlarge
- Firmly adherent crust, ranging in color from honey-yellow to white-brown
- Little surrounding erythema, satellite lesions appear beyond the periphery
Epidemiology of lichen planus
Mostly occurs in 30-60 year old range, rare in children and elderly, 10% have family hx of same, can be linked to certain medications and Hep C
Duration of lichen planus
Lesions are self-limiting, average duration 6-18 months
What kind of disorder is lichen planus? What is it caused by?
Benign autoimmune inflammatory disorder of skin and mucous membranes. Cause unknown, but may involve T cells, adhesion molecules, cytokines, perforin and antigen presenting cells
S& S of Lichen planus? What are the 5 P’s of lichen planus?
Pruritic purple/pink papules and plaques on scalp, extremities, nails, and mucous membranes
(five P’s of Lichen Planus: pruritic, planar (flat topped), polygonal, purple, papules)
Tx of lichen planus?
Corticosteroids (topical or systemic), Antihistamines, glucocorticoids, systemic or topical retinoids
Who gets molluscum contagiosum most often?
Most common in children under 10 and older adults
Risk factors:
Sexual activity
Contact sports
immunocompromised (previously late marker in HIV)
Warm moist environments like steam rooms, saunas, and pools
Atopic dermatitis – mixed evidence
WHat causes molluscum contagiosum?
Caused by molluscum contagiosum virus infection in the skin
Belongs to poxvirus family
MCV1 and MCV2 as the most common genotypes of virus
Genetics similar to variola and vaccinia viruses, also replicates in cytoplasm of cell
Virus DNA codes for proteins that inhibit host immune response
How is molluscum contagiosum spread? Is it always contagious?
Spread by direct skin-to-skin contact, fomites (such as towels) and sexual contact
Can also spread on a person’s body via autoinoculation
Remains contagious until the bumps are gone
Is molluscum self limiting? How long before the lesions resolve?
Considered chronic, localized infection
2-6 week average incubation period
Lesions often resolve on their own within 2-12 months, minority of cases take up to 3-5 years
Is molluscum a protective infection (ie: can you get reinfected?)
No it’s not protective - you can get reinfected
Are molluscum contagiosum lesions typically painful? Pruritic?
Not painful. May or may not be pruritic
Describe the lesions in molluscum
Presents as small 2-5mm flesh-coloured dome-shaped papules that often have dimple in center (“umbilicated”)
Lesions may be alone or grouped
Firm lesions
May have larger, more extensive lesions if immunocompromised (such as HIV)
May have inflammation, erythema and scaling around lesions
Can occur anywhere on the skin but most often trunk, axillae, face, genital regions
Does not occur on palms or soles
Is Molluscum considered an STI?
Considered STI when spread to genitals of adult
If seen in genitalia of children, likely due to autoinoculation (do not presume STI or sign of child abuse)
What is molluscum dermatitis?
common, eczematous patches or plaques surrounding lesions
How do we diagnose molluscum?
Diagnosis usually based solely on clinical presentation and physical assessment
Distinguishing feature is umbilication (central indent) in papules
Can be mistaken for many other skin conditions – skin biopsy can help differentiate
Those with genital lesions should be tested for STIs
What is Onychomycosis
Tinea of the nails
Who usually gets onychomycosis?
-prevalence increases with age
-affects 15-20% of 40-60 year olds
-trauma (i.e., from tight fitting shoes) and immunosuppression increase risk for infection
How long does onychomycosis last?
-starts in 1-2 nails and spreads
-most patients develop lifelong infection (unless treated)
S&S of onychomycosis?
-yellow/ white nail plate
-elevated due to accumulation of hyperkeratotic debris within the plate
-brittle, thick nails
-may disrupt surrounding skin and predispose to bacterial infection of surrounding area (paronychia)
What is pediculosis?
Lice infection
WHo gets lice?
children affected most frequently
-typically diagnosed by teacher, school nurse, camp nurse
-girls> boys
-rare in African American patients
What is the lifespace of lice? How long can they live off of a host?
-life span of louse is about 1 month, lays 7-10 eggs per day. These take 8 days to hatch and another 8 days to mature
-adult lice can survive 55 hours without host
What are the three kinds of pediculus infecitons? (different locations on body)
Head louse (pediculus capitis)
Body louse (pediculus corporis)
Crab/ pubic louse (phthirus pubis) (most contagious sexually transmitted infection!)
How do you get lice?
Acquired by personal contact or indirectly (sharing brushes, towels, contact with clothes, toys, furniture, carpet, bedding infested by lice)
How do lice survive? What can this cause in our skin?
-Parasites infest hair of scalp, body, pubic region; survive by sucking blood: mouthparts attach to host, pierce skin, secreting a toxic saliva. This mechanical trauma and toxin produce pruritic dermatitis.
Primary lesion is pinpoint red macule, papule, or wheal with hemorrhagic puncture site
Usually can’t see this due to excoriation, wheals, crusts
S&S of pediculosis?
pruritus, crawling sensation
-sometimes have posterior cervical adenopathy
-can occur on eyelashes in children (can cause blepharitis (inflammation of eyelid), purulent discharge
-visible nits/ ova (oval, yellow) on hair shaft- usually about 6.5 mm to 1 cm from surface
-diagnosis confirmed by visualization of live lice- systematically comb hair with fine tooth nit comb
What is pemphigus?
= a vesiculobullous disease
Pemphigus is a group of rare skin disorders that cause blisters and sores on the skin or mucous membranes, such as in the mouth or on the genitals.
Can be life threatening (mostly due to cutaneous infection)
What causes pemphigus disorders?
-rare
-most prevalent between 40-50 years, but can occur in all ages
-genetic component
-environmental (viral infections, medication-induced, dietary intake, radiation, surgery) and endogenous (emotional or hormonal) influences
Time/course of pemphigus?
-oral erosions precede onset of skin blisters by weeks or months
-erosions last for weeks before healing with brown hyperpigmentation
-weeks to years- may go into remission
Patho of pemphigus
BASICALLY IMMUNE RESPONSE DESTRUCTS CELL TO CELL ADHESION –> fluid accumulation –> blister formation
-caused by circulating antibodies targeting the cell surface adhesion molecule “desmoglein” (cell to cell adhesion in epithelium) at the desmosomal cell junction in the suprabasal layer of the epidermis (layer above the basal layer)
-IgG antibodies and complement (C3) bind to the desmoglein adhesion molecules, resulting in destruction of cell-to-cell adhesion (acantholysis) in the basal layer of the epidermis, fluid accumulation, and blister formation
How do we describe the lesions in pemphigus? Are they painful? Pruritic?
-bullae from 1-3cm or larger (localized moving to generalized if untreated)
Rupture easily
Traction on skin increases formation
-painful, superficial erosions (loss of part of epidermis following rupture of vesicle or bulla- appears depressed, moist, glistening)
-minimal itching (more tender, irritated)
WHat is the most common type of pemphigus?
Pemphigus vulgaris
- Most common, mean onset 60 years
- Oral lesions precede onset of skin blistering
- Most face, scalp, axilla
- Blister ruptures easily (thin fragile epidermis)
**Are many more types that I’m not going to go into - see ILO
Who gets pityriasis rosea? What time of the year is it worse?
-young adults (typically 10-35 years)
-possibly has higher prevalence in winter
-unsure if infectious transmission- there has been temporal case clustering- i.e., outbreaks in frat houses or military barracks
Time/course of pityriasis rosea?
-rash appears over 2-3 weeks and self resolves in 1-3 months
What is pityriasis rosea? What causes it?
-self limiting inflammatory disorder
-may be triggered by virus- herpeslike virus (HHV6 or HHV7) is most likely cause
Lesions in pityriasis rosea? Are they itchy?
-itching
-characteristic rash: starts with HERALD PATCH on trunk, then develops numerous pink papules and plaques following langer lines, sloughing of scales leaves collarette pattern
-occasionally preceded by headache, fatigue, sore throat development of lesions
Diagnosis of pityriasis rosea?
-diagnosis follows clinical appearance of lesion
-differentials include secondary syphilis (consider serologic test for syphilis if lesions on palms or soles), psoriasis, medication eruption, nummular eczema, seborrheic dermatitis
-skin biopsy only if atypical or recurrent
What is psoriasis? What causes it?
Chronic, relapsing, proliferative inflammatory disorder involving skin, scalp, and nails. Caused in large part by abnormal T-lymphocyte function.
Inflammatory cascade of immune cells and inflammatory mediators
What can trigger a flare up in psoriasis?
Flares triggered by local factors (skin injury, scratching); systemic factors (Strep and HIV), stress, meds (Lithium, beta blockers, interferons, antimalarials)
WHo most often gets psoriasis?
Can be all ages
Onset: usually presents by 40 years old; onset usually 20-30 years and 50-60 years.
If onset later in life, associated with comorbidities of obesity, HTN, smoking, DM
Marked by remissions and exacerbations; can be mild/moderate/severe
Commonly family history (90% of cases)
Patho of skin changes in psoriasis
Thick dermis and epidermis due to cellular hyperproliferation, altered keratinocyte differentiation, and expanded dermal vasculature
Increased turnover time for shedding epidermis (from 3-4d to 14-20d). More germinative cells, increased transit time through dermis.
Bypass cell maturation and keratinization
Epidermis thickens, forms plaques that are silvery due to loosely cohesive keratin
Capillary dilation and increased vasculature to accommodate increased cell metabolism—> erythema
Appearance of typical psoriasis lesions?
Pink to red papules and plaques with thick white scale.
Types of psoriasis and their lesions? (Not sure we need to know these details!)
Plaque (psoriasis vulgaris): most common, 80-90% of cases
Lesions: well-demarcated, thick, silvery, scaly, erythematous plaque surrounded by normal skin.
Small erythematous papules enlarge and coalesce into larger lesions.
Typically on face, scalp, elbows, knees and sites of trauma.
Inverse (intertriginous) psoriasis: rare, involves red, moist, fissured lesions that develop in skin folds (axillae, groin, intergluteal cleft).
Guttate psoriasis: more common in young adults and children. Small round oval red papules all over trunk/extremities post streptococcal respiratory tract infection. Can resolve in 6-12 months.
Pustular psoriasis: intense inflammation resulting in blisters of noninfectious pus (collections of neutrophils)
Erythrodermic psoriasis: severe form; onset can be acute if drug-induced or steroid withdrawal, or chronic if from poorly controlled psoriasis; pruritus or pain with widespread, scaling lesions that cover large area of body. Can also have fever, weight loss, protein loss, and lymphadenopathy.
What other areas of the body can psoriasis affect?
Joint Disease: 30% develop psoriatic arthritis of hands, feet, knees and ankle joints
Psoriatic nail disease: pits, nail whitening, friable nails, yellow spots, splinter hemorrhage, thickened nail beds, separation of distal end of nail plate from nail bed (onycholysis)
Epidemiology of scabies
Est. worldwide prevalence is 200 million people. Can affect all ages and socioeconomic status groups but is common in resource-limited regions
Transmitted by close personal contact with lesions or affected clothing or bedding
Common in tropical settings (The Pacific and Latin America)
Crusted scabies more common in epidemic situations such as among institutionalized (long term care, prisons) or immunocompromised patients
What is scabies?
Caused by parasitic infestation of the epidermis with Sarcoptes scabiei var. hominis
Mite feces causes and allergic response which causes itching
S&S of scabies? WHere do you most often see the lesions? What do they look like?
Key word = BURROWS
Intensely pruritic, inability to stop scratching, worse at night
Typically other family members will also be experiencing the symptoms
Lesions: linear, curved, or S-shaped burrow, slightly elevated vesicle or papule, 1-2mm wide
May develop into scattered inflamed pustules, linear vesicles, papules or even larger nodules
Due to itching, lesions may be excoriated, hemorrhagic, or crusted
Found in intertriginous areas (skin folds) including finger webs, wrists, sides of hands and feet, lateral fingers and toes, genitalia including glans penis, buttocks, scrotum
In infants, the palms, soles, and scalp may be more commonly affected
Pruritis may persist after treatment completed for weeks to months
How is scabies diagnosed?
Identification of mites, eggs, feces with microscopy
Scabies preparation: mineral oil over burrow then scraped with #15 blade and applied to glass slide
Potassium hydroxide and heat make it easier to identify mites, but destroys mite feces
What is crusted (Norwegian) scabies?
Subtype “crusted (Norwegian) scabies”
Common among patients with dementia, Down syndrome, immunosuppression
Thick crusting and eczematous dermatitis on hands and feet
Epidemiology of seborrheic dermatitis
Occurs in all ages
In 5% of adults
Affects men more than women
More severe in patients with neurologic disorders (Parkinson’s, stroke, head trauma) and pts infected with HIV
What is known about the cause of seborrheic dermatitis?
Unknown.
Proposed theories include genetic predisposition, phospholipases from Malassezia yeasts, immunosuppression and epidermal hyperproliferation
What is seborrheic dermatitis in infants known as? How long does it last?
Cradle cap - usually resolves by 1 year old
S&S of seborrheic dermatitis
Chronic inflammation of the skin
pink to yellow papules and plaques with greasy scale involve scalp, central face, ears and presternal areas.
Common adult locations eyebrows, base of eyelashes, nasolabial folds and paranasal skin, and external ear canals. May effect flexural skin – postauricular (behind ear), inguinal and inframammary folds (underneath breasts) as well as anogenital area
Common peds locations – scalp (cradle cap), diaper area and axillary skin
What is urticaria?
Hives
S&S of urticaria
Circumscribed area of raised erythema and edema of the superficial dermis. Angioedemia (welts or swelling deeper within the skin or mucous membranes, most seen in eyes and mouth) associated with both chronic and acute urticaria.
What kind of reaction is urticaria?
Most associated with type I hypersensitivity reactions to medications (penicillin, Aspirin), certain foods (strawberries, shellfish, food dyes), environmental exposure (pollen, animal dander, insect bites), systemic diseases (intestinal parasites, lupus erythematosus), or physical agents (heat or cold)
PAtho of urticaria
Histamine release –> blood vessels in skin contract –> fluid leakage appears as wheals, welts, hives
Time/course of urticaria?
Can occur almost instantly depending on the exposure. Most lesions resolve spontaneously within 24 hours, but new lesions may appear. All possible causes of the reaction should be removed.
Quick overview of chronic urticaria…
S&S: Circumscribed area of raised erythema and edema of the superficial dermis
Epidemiology? Either idiopathic or autoimmune in origin
Pathophysiology? Involves inappropriate activation of mast cells
Time course? Recurrent wheals for more than 6 weeks
Treatment? Avoiding triggers, non-drowsy antihistamines, treating underlying causes if autoimmune. (Page 2034 of patho book)
What is verruca vulgaris
= the common wart!
Epidemiology of warts - who gets it most often? What underlying conditions predispose?
Occur most commonly in children and young adults
More common among certain occupations, I.e. handlers of meat, poultry, and fish.
Predisposing conditions for extensive or recalcitrant involvement include
atopic dermatitis
conditions associated w/decreased cell-mediated immunity (e.g. AIDS, organ transplants)
What causes common warts (verruca vulgaris)?
HPV Types 2, 4, 7
How do common warts spread?
Infection occurs by direct skin contact, w/maceration or sites of trauma predisposing patients to inoculation
Reservoir for HPV = individuals with clinical or subclinical infection
Transmission via inanimate objects has been proposed but has not been proven
Time/course of common warts?
Incubation time approx 2-6 months
Course is highly variable; spontaneous resolution w/time and development of cell-mediated immune response is the rule
In children approx 2/3’s of all warts spontaneously regress w/in 2 yrs
Warts in immunocompromised pt can be widespread, intractable, and chronic
Where on the body do warts develop? WHat happens around the nail?
Can develop anywhere on skin around the nail and frequently appear on the cuticle, and sometimes the area beneath the nail. Warts involving the cuticle can affect nail growth and cause nail deformity.
WHat is Vitiligo?
Acquired disorder characterized by a loss of functional melanocytes resulting in depigmentation of skin
What is the cause of vitiligo?
Unknown etiology, commonly attributed by triggering events including physical injury, illness, sunburn, emotional stress or pregnancy, but no definite cause
May be associated with autoimmune diseases such as thyroiditis, pernicious anemia, Addison’s disease, systemic lupus erythematous, rheumatoid arthritis or diabetes, or genetic syndromes such as Vogt-Koyanagi-Harada syndrome
Theories for melanocyte destruction include genetic, autoimmune, neural, biochemical, oxidative stress, viral infection and melanocyte detachment mechanisms
Epidemiology of vitiligo
Most frequent cause of skin depigmentation
Prevalence rates 0.1 - 2 % in adults and children
Affects males and females equally, no racial, ethnic or socio-economic differences
May appear at any age from early childhood to late adulthood but 1/2 of patients experience onset before age 20
Peak incidences between 20-30 year old’s, 70-80% of adults develop vitiligo prior to age thirty, and 1/3 of those with vitiligo are children
Does vitiligo spread?
Variable course, may be localized or rapidly spread to generalized depigmentation
S&S of vitiligo. What is the difference between segmental and nonsegmental?
White macules coalesce into patches, pigmentation may remain around hair follicles
2 types: segmental and nonsegmental
Segmental vitiligo do not cross the midline
Nonsegmental vitiligo may be distributed or localized to the acral sites (distal extremities, face, gluteal area)
Diagnosis of vitiligo?
Physical exam, skin biopsy usually unnecessary
Lab tests for lupus, RA, thyroid disease, CBC may be helpful to exclude causes
Differential diagnosis: lupus erythematosus, pityriasis alba, piebaldism
What is keratoacanthoma
A slow growing cancer of the skin that looks like a dome
Benign, squamous cell differentiation arising from hair follicles
Rapidly growing, “volcano craters” nodule with a distinctive clinical appearance = low grade squamous cell carcinoma
The epidermis is expanded with atypical keratinocytes
The keratin core is composed of eosinophilic, glassy appearing, atypical, prematurely keratinized cells
Who gets keratoacanthoma?
50-70 years. Rare <40yrs of age
White people with fair complexions are more often affected
Highest among smokers and males
Chemical exposure and human papillomavirus have been implicated as causes in animal models, although in humans is controversial.
How does keratoacanthoma progress? Does it go away on its own? 3 phases?
Left undisturbed, keratoacanthomas may resolve spontaneously or progress into invasive squamous cell carcinoma
Historically described as a regressing or absorptive lesion – however now are being treated like squamous cell carcinoma
3 Growth phases:
1) Proliferative phase, a solitary papule appears suddenly, then rapidly grows to its max size over 2-4wks.
2) Mature phase, the lesion is stable in size and appearance for wks – months; may appear crateriform if the core has been partially removed
3)Resolving phase, the base becomes indurated, the central core is expelled, and the base resorbs, leaving a pitted scar. Resolution may take several months.
Describe the lesion in keratoacathoma. Where do they occur on the body?
Solitary flesh-coloured to dull red, volcano like, crater shaped, 0.5cm-2cm. Rarely will attain a size from 1cm to 10cm and are locally destructive. Central keratotic plug or depression conceals a deep keratinous cavity – gives volcano shape
Sun-exposed extremities, forearm, neck, legs, face, dorsal hand
Does not appear on palms or soles
Nodule is firm, tender to palpation/pressure, grows rapidly
Subungual (under toenail or fingernail) can occur, painful and locally destructive
DIagnosis of keratoacanthoma
Presume diagnosis of squamous cell carcinoma pending biopsy result and clinical follow-up
An excisional biopsy or shave biopsy shld be preformed
Excise deep enough to evaluate the dermis for possible invasion
Radiation therapy is considered for tumors in area, where excisional surgery might result in deformity
What is the most common cancer in humans?
Basal cell carcinoma
Who most often gets basal cell carcinoma?
History of intense intermittent ultraviolet exposure
More common with increasing age
More common for those with white or fair skin, less common for Hispanic, Asian skin, very rare in African American individuals
Do tumors in basal cell carcinoma grow quickly? Do they met easily?
Initial tumours are small and hard to detect
Lesions grow slowly over months to years
Metastasis is rare because tumors do not invade blood or lymph vessels
What does basal cell carcinoma look like?
Mostly occurs on sun exposed areas of the body
Pink, violaceous, pearly-white; may have speckled brown, black, blue
Papules or nodules
Smooth surface, telangiectasias
Enlarges slowly, flattens centrally, or may develop raised rolled border
Often bleed, erode, become crusted, ulcerate at the centre
Diagnosis of basal cell carcinoma
Based on clinical assessment, history of sun exposure, progression of lesion
Biopsy
7 subtypes of BCC? (probably excessive!)
Nodular (most common, head and neck)
Pigmented (similar to nodular but with speckled melanin)
Morpheaform and Sclerosing (most recurring, subtle, aggressive, difficult to visualize and excise entire lesion)
Superficial (least aggressive, trunk and extremities, flat lesion)
Micronodular (microscopically extends beyond visible border thus difficult to fully excise and will likely recur)
Advanced BCC (large, untreated, have invaded deeper tissues and may impair function or visibly deform surrounding structures)
2nd most common cancer in the world?
Squamous cell carcinoma (SCC)
What less dangerous type of skin condition may progress into SCC?
Actinic keratosis
RIsk factors for SCC
Less common but with a higher mortality rate in dark-skinned people, often diagnosed at an advanced stage
Increased risk with cumulative sun exposure over time.
Occupational exposures: coal, tar, pitch, creosote, arsenic, radium
Immunosuppression, chronic infections
Men>women
Increasing age.
Scar tissue. SCC here = 30% chance of mets. A Marjolin ulcer is a deep aggressive SCC that develops over a thermal injury scar.
Chronic ulcers and chronic inflammatory diseases ie. lupus, hidradenitis suppurativa, lichen planus/sclerosis, osteomyelitis
Some strains of HPV
Genetic disorders that affect the skin.
Actinic keratosis (AK) may become SCC.
What causes SCC? General patho
Originates in dermis
Can extend into epidermis
UVR absorbed by the DNA of cutaneous keratinocyte cells, cause mutation of the progenitor cells.
Affects pathways = decreasing cell apoptosis, increasing cell growth/proliferation.
Does SCC metatstasize?
More likely than BCC to metastasize, through lymphatic system or parotid glands. If untreated, can mets to bone, salivary glands, muscle or even distantly to brain, liver or lungs
<2mm tumour depth = rarely metastasizes
> 5 mm tumour depth = 20% rate of mets
How does SCC progress? Where are the lesions particularly concerning and why?
Can take months or years to invade surrounding tissue.
Presentation is constant or can recur after excision.
Can form slowly from a present AK or can form/progress suddenly and aggressively.
Of particular concern are lesions on the lip, ear and scalp – can mets to regional lymph nodes.
What do clients with SCC usually present for? What are the most common first signs/symptoms?
Patients’ first presentation to a healthcare provider is commonly with an enlarging non-healing lesion that sometimes bleeds.
The next common presentation is pruritis.
Describe the typical SCC lesion
Pink -> dull red
Firm
Dome-shaped nodule
Yellow-white scale/crusting over central cavity
Can become red, more raised, with necrotic tissue in centre. May smell foul.
Multiple lesions may appear
May be painful or pruritic
Commonly found on lower lip
Other name for SCC in situ?
Bowen’s Disease
Full thickness SCC. Slow to advance. Appears as pink, scaly patch with clear borders. Usually only in the epidermis but may extend to dermis.
What is melanoma?
Melanoma = malignant tumour of the skin originating from melanocytes (cells that produce the pigment melanin).
4 types of melanoma?
Superficial spreading melanoma (SSM) – the most common;
Lentigo malignant melanoma (LMM) → frequently found in older adults and confused with age spots;
Primary nodular melanoma (PNM) → aggressive tumour;
Acral lentiginous melanoma (ALM) → rare and aggressive and occurs on non-hair-bearing surfaces (i.e., palms of the hands and soles of the feet) and mucous membranes in people with darker skin.
What do 30% of melanomas develop from?
30% of melanomas develop within a pre-existing nevus… whereas the remaining 70% develop “de novo”
Indications for nevi biopsy:
Colour change, size change, irregular notched margin, itching, bleeding or oozing, nodularity, scab formations, ulcerations.
Pathogenesis of melanomas?
Pathogenesis of melanoma is complex…
Familial melanomas → associated with CDK4 & CDKN2A genes.
Both are highly penetrant susceptibility genes and result in melanoma.
Melanomas have a high mutation rate stimulated by UV radiation
Relationship between melanoma & nevi is important - Most nevi never become suspicious, however, suspicious pigmented nevi need to be evaluated & removed.
Risk factors for melanomas?
Personal or family hx (or both)
UV radiation exposure (including sunbed use before age 30)
Fair hair
Fair skin with repeated sunburns
Freckles
Immunosuppression
Being a younger female
Being an older male
Geographical location (high UV exposure)
Past pesticide exposure
3+ clinically atypical (dysplastic) nevi/moles
Melanoma is the most common cancer in what demographic?
white women 25-29 years old.
Does melanoma met easily? Can it be cured?
Note: Melanoma metastasizes quickly, so it has a lower 5-yr survival rate than nonmelanoma skin cancers. BUT it is still curable if caught & treated early.
EARLY DETECTION IS CRITICAL TO DECREASE MORTALITY
WHo has more favourable melanoma diagnosis? (ie who is most likely to survive)
Female patients
Younger patients
Thinner melanoma (better prognosis than thicker melanoma)
Melanoma on extremity (vs on the head, trunk, neck)
What does melanoma look like?
Melanomas usually have dark brown or black pigmentation;
They start as small mole-like growths that increase in size, change colour, become ulcerated, and bleed easily from slight injury.
When it develops on a pre-existing nevus, there is usually a focal area of colour change.
Note: Focal colour change is more specific for melanoma than the colour itself (that is, no colour is diagnostic)
What are the ABCDEs of skin cancer?
A – Asymmetry (one half doesn’t look like the other half)
B – Border irregularity
C – Colour variations (varying hughes & colours)
D – Diameter larger than 6mm
E – Elevation or Evolving (raised appearance or rapid enlargement)
What is alopecia androgenica
Not a disease, but a genetically predisposed response to androgens
Males: premature hair loss of hair on central scalp
Females: hereditary, central diffuse hair thinning
Patho of alopecia androgenica in men
= “Male pattern baldness”
Androgen-sensitive follicles are transformed into vellus-like follicles (short, thinned, light coloured hair)
Androgen-sensitive hair follicles are on the top of the scalp, and androgen-insensitive follicles are on the sides and back of the scalp
Over time, these vellus-like hair falls off, and the scalp becomes smooth and shiny
Patho of alopecia androgenica in women
Common hereditary alopecia is poorly understood
Affected scalp hairs have a shortened anagen cycle and progressive miniaturization of hair follicles
Early and late onset of hair loss can happen with or without high androgen levels (androgen – primarily male sex hormones produced in the testes, which contributes to skeletal growth, pubic and axillary hair growth pg.772)
Heavy menses can cause iron deficiency, and increase hair shedding
Recent discontinuation of an estrogenic oral contraceptive may lead to hair loss
Contraceptives containing androgenic progestins may cause or prolong androgenetic alopecia.
What percentage of men have alopecia androgenica?
80%
What percentage of women have alopecia androgenica?
Unknown, but related to genetic and hormonal changes
Prevalence increase with advancing age
May affect 6-25% of premenopausal women
For women with alopecia androgenica, what kind of investigations might you want to do?
thyroid disease (TSH),
iron deficiency (serum iron determination, total iron-binding capacity, ferritin level)
connective tissue disease (checking anti-nuclear antibody level)
should consider further testing if: irregular menses, hirsutism (excessive hair growth on face, chest, & back), virilization (development of male characteristics), acne, galactorrhea, or infertility.
How does balding usually progress in men?
Incease growth of secondary sexual hair (on the chest, axillae, and pubic and beard areas.
First signs of balding: increased frontotemporal (type I) and midfrontal recession (type II – M shaped recession)
The proceeds to hair loss in a round area on the vertex (the crown), then to the top of the scalp (Types III-VII).
Type I – Triangular frontotemporal recession – normally in young men
By what age is male pattern baldness usually fully expressed?
Begin any time after puberty and fully expressed by the 40’s
WHen does alopecia androgenica usually express in women?
Hereditary hair loss begins at an early age: 20’s -30’s, and fully expressed in 40’s
Postmenopausal hair loss: begins in 50’s, 60’s, or 70’s
How does hair loss progress in women with alopecia androgenica?
Women rarely become completely bald like men
Hair loss is gradual, not abrupt
Most experience gradual hair loss on the top of the scalp, with retention of normal hairline, and no frontotemporal recession.
Increased spacing between hairs
Hair on the central scalp are thin and short, while hairs on the frontal hairline are normal
Type I – Triangular frontotemporal recession – usually in women after puberty
What is alopecia areata? What causes it? Patho process?
Non-scarring hair loss
Thought to be immunological- T cell mediated
Triggering cause is unknown- genetic susceptibility plays a role
Hair follicle danger signals attract T cells to the hair follicles resulting in immunological damage.
Stress is frequently cited as the cause but there is little evidence that it plays a role
Epidemiology of alopecia areata?
Most common in children and young adults
May be associated with thyroid disease, pernicious anemia, Addisons disease, vitilgo, lupus, Ulcerative colitis, diabeties, and down syndrome.
Does the hair regrow in alopecia areata?
Regrowth begins in 1-3 months and may be followed by loss in other areas.
Prognosis for total permanent regrowth in cases with limited involvement is good but is poorer for patients with more involvement.
Is hair loss gradual or rapid with alopecia areata? Does it affect all body hair? WHat other organ may be affected?
Hair loss may be diffuse, patchy , or band like at the margins of the scalp
Sudden occurrence of one or several areas of hair loss of 1-4 cm.
Eyelashes, eyebrows, beard, and other parts of the body are rarely involved.
Sharply defined hair loss usually round or oval
Skin is typically very smooth or have short stubs of hair.
Diffuse fine nail pitting occurs in up to 30% of cases
Structural and functional abrnomalities of the thyroid may occur
