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Melanocytes are ______ derived cells in ___________ layer, secreting melanin.
- Neural crest
- epidermal basal
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Melanin is synthesized in _________ catalysed by _____.
- melanosomes
- tyrosinase
- Tyrosine -> DOPA -> -> melanin
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Dendritic processes extend between keratinocytes. Melanin is transferred from melanocytes to neighboring keratinocytes in melanosomes.
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Innate immune response of skin
- Immediately defense; short lived; no memory.
- Physical barriers - skin and mucosal epithelia.
- Soluble factors - complement, antimicrobial peptides, chemokines, and cytokines.
- Cells such as monocytes/macrophages, dendritic cells, natural killer cells, and neutrophils.
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Adaptive immune response
Has memory; has specificity; long lasting.
Initiated by dendritic antigen-presenting cells.
- ______ cells in epidermis
- _______ dendritic cells in dermis.
Executed by T cells and antibodies produced by B cells and plasma cells.
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________ secret cytokines.
Keratinocytes
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Langerhans cells, antigen presenting cells in the epidermis: Phagocytose antigens; migrate via lymphatics to regional lymph nodes; expresses protein on its surface to T lymphocyte then undergo clonal proliferation. Dermal dendritic cells play similar role in the dermis.
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Natural Killer (NK) cells
survey the body looking for transformed or infected cells; kill cells directly or indirectly via the secretion of cytokines.
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________ - Cutaneous immune surveillance in the dermis. ______ function (also _____): take up pathogens, recognize them, and destroy them.
- Macrophages
- Phagocytic
- neutrophils
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descriptive terms for various types of skin lesions.
- Macule
- Patch
- Papule
- Nodule
- Plaque
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Circumscribed flat lesion
- Macule - 5 mm or smaller in diameter.
- Patch - > 5mm.
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Petechiae
small (1-2mm) red or purple macules due to minor hemorrahage. Do not blanch with pressure.
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Purpura
- 0.3–1cm red or purple macules and patches.
- Do not blanch with pressure
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Papule
- Elevated dome-shaped or flat-topped
- <5 mm
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Plaque
- Elevated flat-topped lesion
- >5 mm
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Vesicle
- Fluid-filled
- raised lesion
- <5 mm
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Bulla
- Fluid-filled .
- raised lesion .
- >5 mm.
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Pustule
- Discrete,
- pus-filled,
- raised lesion.
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Wheal
- Itchy,
- transient,
- elevated lesion,
- +/-erythema.
- Dermal edema
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Scale
- Dry,
- horny,
- plate like excrescence; Imperfect cornification.
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Lichenification
- thickened and rough skin,
- prominent skin markings.
- From Repeated rubbing .
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Ulceration
- Complete loss of the epidermis
- revealing dermis or subcutis.
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Eschar
Dead black slouging skin.
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Onycholysis
Nail separates from nail bed.
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Microscopic terms
- Hyperkeratosis-Thickening of the stratum corneum.
- Basket weave hyperkeratosis
- Compact Hyperkeratosis.
- Parakeratosis-Keratinization with retained nuclei in the stratum corneum.
- Hypergranulosis-Hyperplasia of the stratum granulosum.
- Spongiosis-Intercellular edema of the epidermis.
- Hydropic swelling (ballooning) - Intracellular edema of keratinocytes.
- Acanthosis-Diffuse epidermal hyperplasia with thickening of the malphigian layer.
- Acantholysis-Loss of intercellular cohesion between keratinocytes.
- Dyskeratosis-Premature keratinization of cells below the stratum granulosum..
- Dysplasia-premalignant proliferaton; disorderly, pleomorphic, lacks maturation.
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Eczematous dermatitis, clinical and dermatologic findings
- Acute lesions show erythema and aggregates of tiny pruritic vesicles, which exude clear fluid, and become encrusted.
- Micro - Spongiosis; vesicles - superficial perivascular dermal lymphocytic infiltrate.
- Chronic lesions become scaly and thickened (lichenification) from continued scratching.
- Micro - Acanthosis, hyperkeratosis, dermal scarring.
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Eczematous dermatitis, pathogenesis
Group of disorders of differing etiologies that share similar morphologic and histological features spongioticdermatitis.
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Eczematous dermatitis, approach to management
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Eczematous dermatitis includes
- •Dyshidrotic eczyma
- •Atopic dermatitis
- •Nummular dermatitis
- •Contact dermatitis
- •Photoallergic dermatitis
- •Drug eruptions.
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contact dermatitis, clinical and dermatologic findings
contact dermatitis, approach to management
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contact dermatitis, pathogenesis
- generic term applied to acute or chronic inflammatory reactions to substances contacting the skin.
- Two variants:
- Allergic contact dermatitis - idiosyncratic immunological reaction to an environmental allergen.
- •Cell-mediated, delayed (type IV) hypersensitivity
- - reaction mediated by Langerhanscells and t cells.
- •Ex: Poison ivy; nickel; chromates; synthetic rubber; primula; topical creams.
- Irritant contact dermatitis follows exposure to physical or chemical substances capable of direct damage to the skin.
- - Mechanisms include keratin denaturation, removal of surface lipids and water, damage to cell membranes, and direct cytotoxic effects.
- - Ex: Soaps, detergents, acids and alkalis , industrial solvents.
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atopic dermatitis, clinical and dermatologic findings
- Chronic, relapsing eczematous rash.
- •Often begins in infancy; Any age.
- •Infants -head, face, neck, diaper area, and extensor aspects.
- •Childhood -flexural aspects.
- •Pruritus is intense -scratching leads to lichenification
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atopic dermatitis, pathogenesis
- Multifactorial disease.
- •Genetic susceptibility
- •Abnormal skin barrier function
- •Abnormal immune system activity
- •Environmental factors
- Personal or family history of asthma or allergies.
- •75% have a family history of atopy.
- •50% have associated asthma or hay fever.
- Associated with dry skin (xerosis); Worsens in the winter months.
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atopic dermatitis, approach to management
- Risk of secondary bacterial, dermatophyteand viral infections.
- The disease improves during childhood; > 50%, clears by teens.
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KNOW THIS seborrheic dermatitis, clinical and dermatologic findings
- A very common chronic dermatosis characterized by redness and scaling where the sebaceous glands are most active: face, scalp, presternal area, body folds.
- Skin Findings: erythematous or yellowish patches, covered by a greasy scale.
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seborrheic dermatitis, pathogenesis
- Unknown
- Presents in infants; Second peak in adults.
- Male predominance; Often a family history.
- Linked with the yeast Malessezia, immunologic abnormalities, sebaceous activity, stress, neurological disorders, and AIDS.
- Course: Self-limited with a good prognosis in infants: Chronic and relapsing in adults
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KNOW THIS erythema multiforme, clinical and dermatologic findings
- An acute, self-limited, usually mild, often relapsing mucocutaneoussyndrome characterized by presence of target-shaped plaques with or without central blisters, predominantly on face and extremities.
- Skin Findings:
- Target lesions, macules, papules, vesicles, bullae.
- •Symmetric; extremities, arms, legs, hands, feet, anywhere.
- •Half have oral or vermillion border lesions.
- •EM minor -No mucosal involvement.
- •EM major -Mucosal involvemenet.
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erythema multiforme, pathogenesis
- Cell-mediated cytotoxic reaction.
- •Immunologic response, most often, to a recurrent herpes simplex virus infection.
- •Begins a week after a recurrence of herpes.
- •Also M. pneumoniae, other infections, drugs, neoplasia.
- Any age, peaks in 20-40s ; children.
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Stevens-Johnson syndrome/toxic epidermal necrolysis, clinical and dermatologic findings
- Acute, life-threatening skin and mucous membrane reaction characterized by extensive necrosis and detachment of the epidermis.
- •Previously considered severe variants of erythema multiformenow considered a separate entity.
- SJS and TEN same process; Vary in % of involved surface area.
- •Stevens-johnsonsyndrome -involved area < 10% body surface.
- •SJS/TEN overlap 10% -30%;
- •Toxic epidermal necrolysis> 30%;
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Stevens-Johnson syndrome/toxic epidermal necrolysis, pathogenesis
Stevens-Johnson syndrome/toxic epidermal necrolysis, approach to management
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lichen planus,
- clinical and dermatologic findings
- pathogenesis
- approach to management
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psoriasis.
- clinical and dermatologic findings
- pathogenesis
- approach to management
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