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44 Cards in this Set
- Front
- Back
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Macule
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Cercumscribed flat alteration in color <1cm
Not palpable |
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Patch
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circumscribed flat alteration in the skin > (=) 1 cm
not palpable |
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Papule
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circumscribed elevation of skin <1 Cm
palpable |
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Plaque
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circumscribe elevation of skin >1cm
Palpable |
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Nodule
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circumscribed mass 1-2cm
palpable Not necessarily raised because it could be in dermis or subcutis subcutaeneous indurated quality |
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Vesicle
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sharply circumscribed lesion
< 1cm contains transparent free fluid |
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Bulae
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sharply circumscribed lesion
>1cm contains transparent free fluid |
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Pustule
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circumscribed lesion
<1cm >1cm : lakes of pus vesicle with pus |
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Wheal
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(hive)
transient circumscribed elevated edematous lesion appears and disappears relatively rapidly - dermatographism: stroke the skin and you will get a wheal where you stroked. no permanent skin change |
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Telangiectasia
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-Dilated superficial capillaries
-Capillaries are in the dermis -Corticosteroid would cause this |
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Crust
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-Dried exudate, may have been serous, purulent, or hemorrhagic
-If the pt scratches something oozes, it will form a crust |
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excoration
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-Hemorrhagic excavation of the skin resulting from scratching
-May be shallow or deep, linear or punctate -Many people will just scratch at their skin if they have anything raised. |
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lichenification
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-thickening of the skin
-exagerated skin creases -Hyperpigmentation in darker patients and dyspigmentation in everyone else. |
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Lichenoid
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flat topped papules
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Necrosis
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death of the skin
black in color necrolysis: superficial necrosis |
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Scar
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Destructive natural process that has involved the dermis
two types A)hypertrophic thick and raised B)Atrophic pitting |
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eschar
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-Plaque covering an ulcer. Like a crust but a lot thicker.
-Black, strap-like tissue. -Occurs when abscess is deep. This takes a lot longer to lift off because the underlying tissue must heal. -implies underlying extensive tissue necrosis, infarcts, deep burns, or gangrene. |
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scale
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flat plate or flake of stratum corneum
Fine (pityriasiform) Thick (micaceious) (psoriasis) |
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exfoliation
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splitting off of stratum corneum in fine scales or sheets
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Fissure
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linear split or gap in the skin surface
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Poikiloderma
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Triad of hypo/hyperpigmentation, atrophy, and telangiectasias
Will also have erythema |
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vegetative
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proliferation of close set papillomatous masses
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Erosion
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partial break in the epidermis
heals without scarring follows a blister |
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Ulcer
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full thickness loss of the epidermis
heals with scarring |
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Atrophy
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thinning and transparency of the skin
caused by diminution wrinkling and translucency of skin with loss of markings |
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sclerosis
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circumscribed or diffuse hardening of the skin
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Comedo
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Keratin, sebum,microorganisms and epithelial cells debris within a dilated folicular opening
Open vs Closed |
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Burrow
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tunnel made in the skin by parasite or larva
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Sinus Tract
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elongated opening to a surface at one end an terminating in a blind sac
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Fistula
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elongated channel which communicated between two surfaces
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Cyst
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sac containing fluid or semisolid material wit an epithelial lining
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Abscess
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localized collection of pus larger than a pustule
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Petechia/ Ecchymosis
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Non-blanching extravasated blood
macules<3mm petechia macules>3mm ecchymosis |
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Hematoma
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extravasation of blood of such a size as to cause a visible swelling
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Approach to a dermatologic patient
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-Symptoms (fever, pain, pruritus)
-Duration (acute, subacute, chronic, intermittent) -Basic morphology (macules, patches, papules, plaques, vesicles, pustules) -Secondary morphologies and arrangements (solitary, generalized, annular, linear) -Distribution (arms, feet, etc) -Color (be specific... not just "red") -Lab findings (not set in stone... they have to match what you see) |
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Subacute eruptions
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-Appear gradually
-Don't persist after treatment (may require maintenance) -May become chronic *parasitic infestation (scabies/pediculosis) *some neoplasms *some infections (dermatophytosis, tinea versicolor) *acne vulgaris *rosacea |
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Chronic eruptions
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-Usually a gradual appearance
-May persist for long periods despite treatment -may have a subacute phase and then it will persist. |
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Acute Eruptions
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-sudden onset (days to hrs)
-often resides after short time *contact dermatitis *urticaria *infection *bites/stings *drug eruptions *vasculitis |
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Intermittent eruptions
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-resolve and then recur later
*urticaria (chronic form) *atopic dermatitis *erythema multiforme |
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Keratoderma
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-hyperkeratotic thickening of keratin layer
-can be congenital or mechanical -example: people that write a lot can form it on their finger. |
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Acne Vulgaris
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*Common (adolescents, 30-85%)
*impact on self image *management not always optimal (Myths, trivialized, undertreated) Common pitfalls: *lesion types not properly identified *severity not graded *treatment not properly correlated Appropriate follow-up and documentation (initial benefit = 4-8 wks, peak benefit = 3-4 months) Age Correlations: Preteen: Location-centrofacial, pattern - comedonal Teens: Location - face, trunk, pattern - mixed Adult Females: Location- perioral, chin jawline, upper neck, Pattern: Inflammatory Acne Pathophysiology: *excess sebum production *comedogenesis *p.acnes proliferation *inflammation Acne Pathogenesis: *Microcomedones *comedone (open/closed) *superficial inflammation (papules/pustules) *Deep inflammation (cysts/nodules) *Repair (normal skin, pigmentation, scarring) Ductal Hyperproliferation leads to Inflammatory Cascade. (slide 10) |
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Acne Therapy
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Efficacy Triad:
*Prevent comedogenesis *Reduce inflammation *Reduce P. Acne's impact Topical Therapy Selection -Anti-inflammatory therapy: Benzoyl peroxide, topical antibiotics, topical retinoids (additive benefit - lesion reduction, P. acnes suppression, reduced development of resistant P. acne strain) Anti-comedonal Therapy: Topical Retinoids *half of the backbone of the therapy. Initial maintenance therapy and it reduces inflammatory lesions. *2-8 wks for initial visible benefit *peak effect at 3-4 months (important patient education) Choice and Preference of drugs is based on efficacy, tolerability, and skin type Anti-Inflammatory: Benzoyl peroxide *Half of the backbone *Most potent anti-biotic *Reduction in inflammatory lesions *Prevents development of resistant strains *Prevents continued emergence and proliferation of already existent P. acnes strains Topical anti-biotics: *Direct anti-inflammatory effect *used only in combination therapy Oral Anti-biotic therapy (Acne and Rosacea) Erythromycin** - GI upset, drug-drug interactions, no routine labs Tetracycline - food-drug interactions, photosensitivity, pseudo tumor with all, no routine labs Doxycycline** - Photosensitivity, esophageal irritation, hypersensitivity (rare) Minocycline - dizzy, pigmentation, systemic reactions (rare), hypersensitivity (acute), autoimmune (chronic) Combination Therapy: Morning - benzoyl peroxid/antibiotic Evening - Topical Retinoids Reasons for treatment failure: *Poor compliance *P. acne resistance *Drug interactions *Underlying endocrinopathy *Exogenous Factors Oral Isotretinoin Therapy: *Candidate selection (refractory nodulocystic acne) *Prescribed course (20 wks) *baseline patient education and screening (hyperlipidemia, pregnancy, psychological/psychosocial) *Lab tests *Potential adverse reaction and warnings Hormonal Therapy: *use in women with androgen excess and normal serum *Oral contraceptives: ovarian suppression of androgen production *Spironolactone, Flutamide, Cypoterone acetate: androgen receptor blockage Corticosteroids: adrenal suppression of androgen production |
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Rosacea
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-Common in adulthood, all races/both sexes (Celtic skin type)
-Chronic-recurrent -idiopathic -Worsened by topical corticosteroids Four Components: -Vascular: erythema and telangiectasia -Ocular: Blepharitis, conjunctivitis, keratitis -Sebaceous: Phymas -Inflammatory: erythema, papules, pustules Therapy: Agents reduce lesion counts, reduce erythema, and decrease associated symptoms. Agents: sulfacetamide (sulfur), metronidazole (cream, lotion, gel), Azelaic acid gel, Clindamycin and erythromycin (based on skin type) Clinical Features: Presentation: central facial erythema, papules, pustules, telangiectasias, absence of comedones. (variable intensity) Therapy: Efficacy Triad: avoid flare factors, clear current disease, maintain remission Leave on formulas, therapeutic cleansers, non-medicated cleansers/emollients. Systemic therapy: oral antibiotic agents **No cure! Long-term control Flare factors: heat, alcohol, topical corticosteroids. Therapy Tier: Mild-Moderate: topical metronidazole, azelaic acid, sulfacetamide/sulfur Moderate-Severe: Add oral antibiotic, subantimicrobial dose doxycycline *antibiotic tapered, long-term with topical therapy Expectations: reduce papules/pustules, reduce erythema, no effect on telangiectasias Duration: 2-3 months for initial benefit + chronic maintenance |
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Perioral Dermatitis
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-iodiopathic, young females, topical corticosteroids
Presentation: *confluent or broken ring (pink erythema), small papules, pervermillion sparing, may be perinasal or periocular Treatment: *avoid irritants *it's not acne (no benzoyl peroxide or topical retinoids) *It's not contact dermatitis (no corticosteroid) *Topical therapy: clindamycin phosphate (gel/lotion), sulfacetamide (lotion/cream) *Systemic therapy: Oral tetracycline/doxycycline/minocycline (full dose x 2-3 wks and then half dose x 2-3 wks) *May recur in some cases - restart topical Rx first |
