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54 Cards in this Set
- Front
- Back
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Vesicle
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serous fluid filled, small, raised, 1 cm diameter, thin walled
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Bullae
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large vesicle
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Acneform
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inflammatory follicular sac like lesion that is papular or pustular. Involves pillow sebaceous units. Problem with sebum production.*
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Bullous pemphigoid
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sub epidermal blister formation that results from a cascade of events involving complement activation and recruitment of inflammatory mediators
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Clinical presentation of bullous pemphigoid
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Lesions appear on extremities first then the trunk- flexor surfaces. There is a prodromal non bullous phase and bullous phase.
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Description of non-bullous phase of bullous pemphigoid
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mild to severe pruritis, excoriated, eczematous, papular uticarial lesions.
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Description of bullous phase of bullous pemphigoid
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vesicles and bullae on erythematous skin. Blisters are 1-4 cm in diameter filled with clear/blood tinged fluids. Will crust. *DO NOT EASILY RUPTURE, RARELY ON MUCOSA.
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Etiology of bullous pemphigoid
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Drug induced. In pts with genetic susceptibility by modifying immune response. Caused by diuretics, analegesics, antibiotics. In pts> 60
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Dx of bullous pemphigoid
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Clinical- confirmed by histopathology/immunopathology. Immunofluorescence = IgG and complement C3. IgE in serum, light microscopy of lesions reveals incresed eosinophils, neutrophils, lymphocytes.
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Differentials of bullous pemphigoid
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erythema multiforme, drug eruptions, dermatitis herpetiformis
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Complications of bullous pemphigoid
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secondary infx, dehydration. Chronic disease with exacerbations and remission.
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Management of bullous pemphigoid
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Systemic glucocorticoids, topical steroids.
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Pemphigus Vulgaris
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IgG anitbodies agains cell surface of keratinocytes at desmosomes. Results in a loss of cell to cell adhesion btw keratinocytes-- blister formation. Middle aged & elderly. Can be due to rxn to meds.
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Clinical manifestations of Pemphigus Vulgaris
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Pain, flaccid blister with clear serous flid that arises on normal skin on erythematous base. EASILY BREAK BLISTERS- BLEED. Mucosal lesions precede cutaneous lesions - buccal or palatine erosions.
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Dx of pemphigus vulgaris
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Nikolsky's sign positive. Asboe-Hansen sign: force fluids away from point of pressure. Acantholysis. IgG and C3 in lesions. Tzanck smear = ancantholytic cells.
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Differentials of pemphigus vulgaris
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acute herpetic stomatitis, apthyous stomatitis, erythema multiforme, bullous lichen planus, bullous pemphigoid.
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Complications of pemphigus vulgaris
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secondary infx, dehydration due to loss of fluid, fatal if not treated with immunosuppressive agents.
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Management of pemphigus vulgaris
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treat dehydration if necessary, glucocorticoids, immunosuppressive therapy- azathioprine, methotrexate, cyclophosphamide
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Pilosebaceous unit
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hair follicle, sebaceous gland and erector pili muscle.
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Sebum
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lipid, cholesterol, wax. Bacteriocidal, lubricant for hair follicle. Production related to size of sebaceous gland, rate of cell proliferation and androgens.
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Where are s. epidermidis and propionibacterium found on the skin?
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in lipid rich areas such as sebaceous glands.
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Acne Vulgaris
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Comedones and inflammatory lesions. Primarily disorder of adolescents. Androgens cause overactive sebaceous glands. Bacteria secrete lipase--> converts lipids to fatty acids--> inflammatory response. Papules, pustules, scarring result from follicular rupture and inflammation.
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How do comedones form?
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hyperkeritnization in lining of follicle and plugging of follicle.
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Clinical manifestation of acne vulgaris
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non-inflammatory: open and closed comedones.
inflammatory: expands to form papules, pustules, nodules, and cysts of varying severity. 1-5mm filled with sterile pus. Face, neck, upper trunk. |
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Dx of acne vulgaris
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hormone studies will rule out other categories.
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Differentials of acne vulgaris
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folliculitis, steroid folliculitis
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Complications of acne vulgaris
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abscess formation, severe infx, scarring
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Management of acne vulgaris
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comedolytics- topical tretonin
sebum suppressive meds, topical/systemic antibx, benzoyl peroxide. Severe cases- accutane, dermabrasion. |
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Rosacea
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Most common in fair skinned. 30s-40s = MC, Assoc w/ parkinson's, possible assoc w/ h. pylori, related to vascular hyperactivity (repeated episodes of vasodilation). Erythema and telangiectasis.
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Clinical manifestations of rosacea
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Complaint of reddening of face with heat, hot fluids, spicy foods and EtOH. Rhinophyma caused by sebaceous hyperplasia (largening of nose) Blepharophyma (swelling of eyelid), Metrophyma (swelling of forehead)
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Types of Rosacea
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1. vascular: flushing and persistent central facial erythema with or without telangiectasia.
2. papulopustular: central facial erythema with transient papules and pustules. 3. sebaceous hyperplasia: thickening skin, irregular surface nodularities, enlargement. 4. ocular: foregin body sensation in eyes- photosensitivity, periorbital edema, telangiectasia of sclera. |
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Dx of rosacea
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Clinical- vascular ectasia and mild edema, perivascular and perifollicular lymphocytotic inflitrate
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Differentials of rosacea
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Acne vulgaris, perioral dermatitis, seborrheic dermatitis, systemic lupus erythematosus
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Management of rosacea
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Avoid environmental and dietary triggers. Topical metonidazole (inflammation/erythema). Tetracycline, Retinoids, Clonidine (decrease redness), NO potent topical fluorinated steroids on the face!
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Hypersensitivity Vasculitis (serum sickness)
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Immune complex mediated inflammation of small vessels such as arteriole, capillaries, and venules. Immune response due to drug, infx, or autoantibodies.
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Clinical manifestations of hypersensistivity vasculitis
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Pruritis, burning, pain, palpable purpura, localized to lower 1/3 of legs/ankles. Lesions are scattered, discrete, confluent. Can form papules and ulcers (lack of blood supply)
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Dx of hypersensitivity vasculitis
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confirmed by skin biopsy (vascular and pervascular infiltration of broken up leukocytes
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Complications of hypersensitivity vasculitis
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Systemic vascular involvement, necrosis, irreversible damage to kidneys
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Differentials of hypersensitivity vasculitis
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thrombocytopenia purpura, disseminated intravascular coagulation, rocky mountain spotted fever, Steven Johnson Syndrome
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Management of hypersensitivity vasculitis
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antibx, if skin is involved: use colchicine or Dapsone (decrease inflammation and necrotic activity), if visceral involvement : use steroids
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Xerosis
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Dehydration of the corneum. Can be natural occurence sometimes associated with contact dermatitis, exogenous etiolgoy such as dry climate, or excessive exposure to water.
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Clinical manifestations of xerosis
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Pruritis. Involves back, abdomen, extremities. Rough, dry, scaly skin. Cracking and fissure formation.
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Dx of xerosis
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histological findings include compact irregular stratum corneum
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Differential dx for xerosis
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eczema, contact dermatitis, scabies (pruritis)
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Management of xerosis
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Moisturising agents, occlusives which reduce water loss by epidermis.
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What type of vesicular bullae is this?
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Bullous pemphigoid
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What kind of vesicular bullae is this?
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Pemphigus vulgaris
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What kind of vesicular bullae is this?
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Pemphigus vulgaris
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What type of vesicular bullae is this?
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Acne vulgaris
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What type of vesicular bullae is this?
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Acne vulgaris
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What kind of vesicular bullae is this?
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Rosacea
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What kind of vesicular bullae is this?
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Hydradenitis suppurativa
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What kind of vesicular bullae is this?
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hypersensitivity vasculitis (Henoch-Scholein Purpura)
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What kind of vesicular bullae is this?
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Xerosis
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