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101 Cards in this Set
- Front
- Back
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What is a macule? |
eg. Freckle). Small <2cm. Flat. Altered colour. |
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What is a patch? |
eg. Measles rash). Large >2cm. Flat. Colour change |
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What is a papule? |
(eg. eczema, small mole). Slightly elevated solid mass. indurated (i.e. hard). <1cm small. |
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What is a nodule? |
eg. nevi, enlarged LNs). Medium sized. Similar to papule, but 1-5 cm. |
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What is a tumour? |
(eg. Neoplasm of skin). Nodule >5 cm large. |
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What is a keloid? |
(eg. Overgrown scar). Excessive scar connective tissue. keloid usually grows beyond the borders of the original wound whereas in a hypertrophic scar the tissue stays within the wound border. |
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What is lichenification? |
(eg. Callus on feet, etc). Thickening of skin with accented skin markings. |
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What are scales? |
(eg. Seborrheic dermatitis). Keratin layers that cover the skin in flakes. sheets can be scraped off easily. Small flakes. |
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What are squames? |
(eg. Ichthyosis ). Large flakes. Fish-like scales. |
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What is a wheal? |
(eg. Allergic hives). Transient elevated lesions from local edema. |
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Hives is which type of Hypersensitivity? |
Type I |
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Involving which vasoactive amine? |
Histamine |
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Released from which cells? |
Mast cells |
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What is a vesicle? |
eg. small blisters, cold sores). Fluid-filled elevated of epidermis. Small <1cm. Clear fluid. |
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What is a bulla? |
(eg. Large blisters, burns). Large vesicles >1cm. Clear fluid |
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What is a pustule? |
(eg. Impetigo, Acne). Pus-filled vesicle. |
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What is folliculitis? |
(eg. Staph aureus). Pus-filled hair follicle. Bacteria produce purulent exudate that fills the follicle. |
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What is a furnucle? |
eg. Staph aureus). Deep, necrotizing folliculitis. |
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What is excoriation? |
(eg. Any chronic pruritic skin disease). Superficial skin defect caused by scratching. |
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What is a crust? |
eg. Scab, healing wounds). Skin defect covered with dried plasma or blood. |
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What is a burrow? |
eg. Scabies). ‘S’-shaped papule. 3-5 mm long. intensely itchy. |
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What is a fissure? |
(eg. Athlete’s Foot).Sharp-edged defect (split-like) of epidermis that extends into deep layers of skin. Crack. |
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What is an ulcer? |
eg. Canker sore, DM ulcer). Crater-like necrotic defect of epidermis or mucous membrane. Scooped-out depression. |
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What is contusion? |
(eg. Bruise). Bleeding beneath skin from tissue injury. Traumatic. |
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What is petechia? |
(eg. Bleeding tendency, low Vit C). Small, flat, red-purple spots. < 3mm. |
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What is telangiectasia? |
(eg. Alcoholic’s cheeks/nose, Scleroderma). cluster of superficial dilated blood vessels. Spider veins. |
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What are five causes of skin lesions? |
(1)trauma (mechanical, thermal or chemical), (2)immune diseases (autoimmune or allergy), (3)infectious pathogens, (4)metabolic disease/systemic diseases, (5)neoplasms. |
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What is a primary skin lesion? |
first lesion w distinct structure |
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How does a primary skin lesion become a secondary lesion? |
if primary lesion changes it becomes a secondary lesion. eg. pruritic vesicle (1º) if scratched -- crust (2º) |
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What are nine s/sx of skin disease? |
(1)Pruritis (itching), (2)Urticaria (hives) , (3)Rash, (4)Blisters (vesicle or bulla), (5)Xeroderma (dry skin), (6)Unusual spots, moles, nodules, cysts, (7)Edema or swelling, (8)Change in appearance of nails – nutritional deficiency, (9)Change in skin pigmentation, turgor, texture |
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How does aging affect the skin during puberty, adolescence & adulthood, and old age? |
Puberty – hair, acne, apocrine sweat glands, freckles, moles Adolescence and adulthood – hormone induced changes in pigmentation, incr'd hair growth. Old age – structural and functional changes |
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What is atopic dermatitis? |
Chronic inflammatory skin disease. Affects 10% of children. Sufferers usually go on to develop asthma & allergic rhinitis (“atopic triad”) |
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What is the etiology of atopic dermatitis? |
multifactorial -- genetic (family Hx),environmental, psychological, immunological, pharmacological, food allergens |
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What is the pathogenesis of atopic dermatitis? |
inflammation mediated by IgE or T cells responding to IgE
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What are five clinical manifestations of atopic dermatitis? |
(1)infancy: red, oozing, crusting rash (acute dermatitis), (2)childhood: dry, thickened skin w/ brown-gray colour, (3)usually on flexor surfaces of elbows & knees, neck, side of face, eyelids, backs of hands & feet, (4)dryness (xerosis) and pruritis, (4)excoriation, infection, scarring, (5)2º infection (esp. S. aureus) |
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What is the diagnosis, treatment, and prognosis of atopic dermatitis? |
Dx: clinical diagnosis Tx: good hygiene, moisturizers, avoid irritants, symptomatic tx (topical cortisone, antihistamines), antibiotics Prognosis: No cure but often resolves spontaneously |
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What is contact dermatitis? |
Inflammation resulting from skin contact w/ substance to which person is allergic or sensitive |
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What is the etiology of contact dermatitis? |
Exposure to chemical, physical, mechanical, or biologic agent such as metal (Ni), detergents, skin cream, latex, topical Rx drugs, poison ivy/oak. |
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What is the pathogenesis of contact dermatitis? |
acute or chronic inflammatory condition of skin. cell mediated (type IV) hypersensitivity |
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What are three clinical manifestations contact dermatitis? |
(1)transient erythema, severe itching, edema, (2)vesicles, oozing, crusting, scaling, (3)more pronounced response in younger persons |
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What is the diagnosis, treatment, and prognosis of contact dermatitis? |
Dx: clinical examination, patch testing for allergen Tx: remove / avoid agent, treat skin (hydrocortisone, emollients) Prognosis: once agent is removed, lesions will clear in ~3 wks |
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What is acne rosacea? |
Chronic form of facial acne affecting middle-aged /older people; large vascular component; no comedones |
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What is the etiology of acne rosacea? |
Unknown; may be linked to GI problems |
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What are risk factors for acne rosacea? |
fair skin; triggers: sun, heat, humidity, summer |
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What are five clinical manifestations of acne rosacea? |
(1)erythema of cheeks, nose, chin, (2)flushing, (3)inflammatory papules/nasal bumps, (4)burning or stinging, (5)May lead to permanent telangiectasis |
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What is the diagnosis, treatment, and prognosis of acne rosacea? |
Dx: clinical Tx: topical or systemic anti-inflammatories Prognosis: episodic with triggers |
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What is the etiology of acne vulgaris? |
hereditary factors, hormonal factors,Propionibacterium acnes
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What is the pathogenesis of acne vulgaris? |
Sex hormones stimulate the development of sebaceous glands -- increased sebum production. Sex hormones promote hyperkeratosis at orifice of hair follicles -- blocked discharge of sebum. Stagnant sebum colonizes P. acnes -- comodones (white heads and blackheads). Bacterial lipases break down sebum -- inflammation. |
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What is the treatment of acne vulgaris? |
OCP, Retinoic acid (dcr'd keratinization), benzoylperoxide (abx) or systemic abx |
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What percentage of the population is effected by seborrheic dermatitis? |
Effects 10-20% of US population |
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What is the etiology of seborrheic dermatitis? |
Thought to be abnormal immune response to Malassezia yeast |
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What are two clinical manifestations of seborrheic dermatitis? |
(1)reddening, scaling and itching of the skin esp. scalp, nasolabial folds, eyebrows and upper chest -- DANDRUFF, (2)Cradle cap in infants |
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What is the treatment of seborrheic dermatitis? |
Topical steroids or sulfur based soaps (Selsun blue) |
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What is perioral dermatitis? |
Chronic papulopustular facial dermatitis. Women and children. |
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What is the etiology of perioral dermatitis? |
Unknown |
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What is the clinical manifestation of perioral dermatitis? |
Skin lesions occur as grouped reddish papules, papulovesicles, and papulopustules on an red base with a perioral distribution. |
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What is the treatment of perioral dermatitis? |
Ant-inflammatory & Abx treatment |
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What is a skin infection? |
Many are contagious, possible septicemia if untreated or immunodeficient |
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What are six risk factors for skin infections? |
(1)immunosuppression (young/old, chronic dz, HIV, transplant, malnourished), (2)decreased vascularization (DM, obese, atherosclerosis), (3)dehydrated skin, (4)burns or pressure ulcers, (5)poor hygiene, (6)crowded living conditions |
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Describe bacterial skin infections? |
Enter via abrasions or puncture wounds. Clinical infection occurs 3-7 days after inoculation. Septicemia can result if no treatment or immunocompromised. HANDWASHING to prevent spread of infection. |
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What is impetigo? |
Superficial infection of skin by Staph aureus or Strep. Common in infants, children and elderly. Often 2º to eczema or herpes zoster. |
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What are three risk factors for impetigo? |
(1)close contact, (2)poor hygiene, (3)malnutrition |
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What are three clinical manifestations of impetigo? |
(1)focal erythema --> macules --> pruritic vesicles --> pustules --> golden crust, (2)Adenitis (inflammation of gland), cellulitis (inflammation of tissue) and itching, (3)Spread by scratching (autoinnoculation) |
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What is the diagnosis and treatment of impetigo? |
Dx: clinical or skin swab culture Tx: soak skin, oral Abx, rarely IV Abx to prevent post-Strep glomerulonephritis |
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What is ecthyma? |
Ecthyma is an ulcerative pyoderma ( skin infection with pus) of the skin caused by group A beta-hemolytic streptococci (strep pyogenes). Because ecthyma extends into the dermis, it is often referred to as a deeper form of impetigo. |
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What is cellulitis? |
Rapidly spreading acute inflammation of tissue due to deeper suppurative infection of dermis and subcutaneous tissues spaces |
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What are five risk factors for cellulitis? |
(1)Elderly, (2)DM, (3)malnourished, (4)presence of wounds or ulcers, (5)venous insufficiency |
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What is the etiology of cellulitis? |
usually from Strep pyogenes or Staph; often 2º to other inflammation or trauma. |
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What are five clinical manifestations of cellulitis? |
(1)redness, (2)inflammation, (3)tenderness, (4)swelling, (5)poss sepsis with red streaks(lymphatic involvement) |
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What is the treatment of cellulitis? |
Tx: IV antibiotics, necrotic tissue debridement Untreated: gangrene, sepsis |
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What is erysipelas? |
A bacterial skin infection involving the upper dermis that characteristically extends into the superficial cutaneous lymphatics. Legs are area affected 80% of the time, the remainder affect the face. |
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What are three clinical manifestations of erysipelas? |
(1)Prodromal symptoms = malaise, chills, and high fever, often begin 48 hrs before the onset of the skin lesions, (2)Erysipelas begins as a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque, well-demarcated, (3)This is in opposition to the slightly deeper involvement seen in cellulitis, in which lesions present with limited edema and less well-defined borders |
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What is hidradenitis suppertiva? |
Also known as acne inversa. Long-term skin disease that causes abscesses and scarring on the skin – usually around the groin, buttocks, breasts and armpits. |
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What are clinical manifestations of hidradenitis suppertiva? |
painful, pea-sized lumps in the area of sweatglands
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What is the prognosis of hidradenitis suppertiva? |
mild to chronic disabling disorder, frequently causing keloids, contractures, and immobility. |
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What is herpes zoster (HSV-3/VZV)? |
Viral infection. Shingles: reactivation of(childhood) chickenpox virus |
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What is a risk factor for herpes zoster? |
immunocompromised state or stress |
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What is the pathogenesis of herpes zoster? |
Virus resides in ganglia of cerebrum or posterior spinal nerve roots. Can destroy the host neuron and spread down sensory nerve to skin. |
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What are two clinical manifestations of herpes zoster? |
(1)Prodromal symptoms (dermatomal pain and tingling – fever, chills, malaise), (2)Unilateral vesicular eruption along dermatome of associated resident ganglia (usually trunk or 5th CN (trigeminal)) |
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What is the prognosis of herpes zoster? |
Good unless spread to brain or eyes (rare). Post herpetic neuralgia - persistent pain in area of recurrence -- occurs in 10-20% of shingles patients (not in children). Healed in 2-4 weeks. |
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What is the diagnosis and treatment of herpes zoster? |
Dx: clinical (differentiate from herpes simplex) Tx: No cure; treat itching and pain, anti-virals may be used in first 48hrs |
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What are warts (verrucae)? |
Common benign viral infection of skin and mucous membranes. Caused by HPV (>50 types). Transmission via direct contact. |
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How are warts different from corns and calluses? |
corns – conic-shaped horny epithelial mass over bony prominence calluses – thickening of stratum corneum dt friction /pressure |
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What is the treatment of warts? |
abrading, salicylic acid, cryotherapy, electric current & surgery, duct tape |
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What is the etiology of molluscum contagiosum? |
a pox virus called molluscs contagious virus
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What are five clinical manifestations of molluscum contagiosum? |
(1)Small (under 6mm) raised round flesh coloured papules with umbilication (small indentation), (2)May be itchy, (3)Can be easily removed by scratching or rubbing, (4)Usually appear on the face, neck, armpits, arms and tops of the hands in children, (5)STI in adults |
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What is the prognosis of molluscum contagiosum? |
Self-limited with heal in several months |
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What is dermatomycoses? |
Fungal infections of hair, skin or nails. Live on skin surface (dead keratin layer). Possible entry point for other infections. Tx: clean, dry skin and antifungal cream or powder (will spread without treatment). |
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What are three specific fungal skin infections? |
(1)Tinea Corporis, (2)Tinea Pedis, (3)Tinea Versicolor |
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What is tinea corporis? |
Ringworm. Tinea pertains to fungal infections of skin, hair, or nails, no association with worms. Ring-shaped pigmented patches w/ vesicles or scales. Can be itchy. Transmission via contact (direct or via fomite). |
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What is tinea pedis? |
Athlete's foot. Erythema, skin peeling, pruritis between toes & sole. Severe infection may result in inflammation and pain on walking. May develop strong foot odour. Tx: clean, dry socks, well ventilated footwear, antifungal cream or powder |
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What is tinea versicolor? |
Pale tan/depigmented patches on upper trunk/arms. Single tx of selenium sulphide (Selsun shampoo), diluted tea tree oil. Depigmented patches may last 1 year. |
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How are parasitic infections transmitted? |
Contact with insects or animals |
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What is scabies? |
highly contagious infection by the mite, Sarcoptes Scabiei
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What is the etiology of scabies? |
Direct contact or fomite. Female mite burrows into skin and lays eggs. Hatch into larvae in few days. Inflammation and itch can be 30-60 days after initial contact. |
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What are four clinical manifestations of scabies? |
(1)intense pruritis (worse at night), (2)Excoriation -- bacterial infection, (3)burrow – linear ridge w/ vesicle at end, (4)between digits, wrist crease, axilla, waist, nipples, genitals, umbilicus |
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What is the diagnosis and treatment of scabies? |
Dx: excavation of mite with needle or scalpel Tx: scabicide lotion / cream or oral therapy |
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What is pediculosis? |
louse infection (pedicures humans) of head, body, genital. person-person direct transmission or shared items (not pets) |
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What are two risk factors of pediculosis? |
(1)overcrowding (esp school children), (2)Poor hygiene |
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What are four clinical manifestations of pediculosis? |
(1)Severe itching, (2)Small nits attached to hair shaft (Pediculus capitis), (3)Severe excoriations from scratching and found in seams of clothes (Pediculus corporis), (4)Pediculus pubis transmitted by sexual contact or clothing/towels |
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How is pediculosis treated? |
Treat w/ insecticide (lindane) shampoo / soap or just use vinegar, cut hair |
