Dermatology Flashcards
Ephelius
Clinical features, pathophysiology and treatmen
Freckles on sun exposed areas of light skinned ppl
Increased melanin production especially in summertime, nl melanocyte number
No tx
Vitiligo
Clinical presentation, pathophysiology, dx, treatment
Flat depigmented macule at sites of repeated damage
Autoimmune or idiopathic destruction of melanocytes (dec # and activity)
Montana stains melanin blue (don’t see it in vitiligo)
UVB therapy, PUVA
Albinism
Presentation, pathophysiology, dx, tx
Congenital amelanosis, no pigment, increased risk of skin CA
Decreased or absent prod of melanin with nl # melanocytes
AVOID UV EXPOSURE
Melasma
Patchy tan macules on face and head, worse with sun
M@ take up melanin in superficial dermisfom hormonal stimulation, in pregnancy and OCT
Bx shows lots of pigmented basal cells
Tx remove hormonal stimulation, bleach
Lentigo simplex
Freckles on non-sun-exposed skin especially mucosa in lentiginous ( linear) pattern, increases with age
Melanocytic proliferation in rete ridges
No tx
Solar lentigo
Large brown macules on sun-exposed skin, liver spots, persistent despite sun exposure
Basal hyper pigmentation, elongated rete ridges, slight inc melanocyte but no hyper pigmentation of melanocytes
Mimics melanoma, no tx
Common acquired melanocytic nevi
Round macules or papules, symmetric, homogenous, well defined
Migrating neuralcrest melanoblasts
-jnx-proliferation of Nevus cells nonconfluent along jnx but at tips of rete
-compound- dermal and epidermal involvement and at jnx, smaller nests as base of lesion with collagen bundles (maturation feature)
-intrDermal- no epidermal involvement, polyploid looking, dome shape, no jnx involvement
Tx: remove if changing or irritating,
Melanoma
Atypical hyperpigmentated lesions, ABCDEs,
Basal melanocyte proliferation ( large, pleomorphic, macronucleoli, pigmented) usually nests, spreading horizontally then vertically
The deeper/thick the tumor, the worse prognosis(top of granular layer to base of lesion)
Tx: remove and chemo if deep
CTCL- mycoises fungoides
Clinical presentation
Stages
Microscopic evidence
Indolent, fungal looking erythematous scales, scaly patchy
Patch–> plaque–>tumor (deadly); lymphocytes and miroabscesses (malignancy t lymphocytes), atypical cells with cerebriform nuclei at superficial epidermis
Urticaria
Allergic hives, type 1
Pruritic Wheals
mast cells use IgE receptors to crosslink leading to degranulation of histamine and TNFalpha;
Dx: interstitial neutrophils and eosinophils, spongiosis; vascular margination(neutrophils )
Leukocytoclastic vasculitis- clinical presentation
Types/demonstrations
Microscopic evidence
Palpable purpura, 2 demonstrations
Wegeners granulomatosis (type 2)
- ANCA ag, necrotizing vasculitis w/ granuloma, GN
- livedo reticularis, ENT and acral palpable purpura superficial and deep
LCV: type 3
-ICD, drugs, infection, chemicals, assoc. ds, foreign proteins
-neutrophilic infiltrate into small vessels–> fibrinoid deposition, endothelial damage, leukocytoclasis;
-eroded/ blistering
Henoch-schlonlein purpura
Type 3; ICD w/ IgA
Children purpuric rash on legs, hematuria, athritis, URI, (require follow up for renal ds)
Erythema multiform
Immune type
Forms
Microscopic evidence
Type 4; DTH, interface pattern
-> jnx keratinocyte epidermal necrosis (+ suprabasal ballooning), lichenoid inflammation, (more severe less inflammatory cells and more epidermal necrosis), vacuolar change in basal layer (blister)
3 types
Ordinary: Herpes, target lesion,
Steven-Johnson: drugs, mucosal sites,
Toxic: epidermal necrolysis, lrd flaccid blisters
Lupus erythematous
Anti DNA type 2, 3, 4 immunity
Discoid rash, annular trunk and arm lesions
-> dermal edema, basal vacuolar change at jnx, lichenoid, thick BM
Psoriasis- immune type and microscopic evidense
Autoimmune, type 2, 3, 4, T cell mediated, chronic
Keratinocyte proliferatio, spongiosis and angiogenesis from tnfalpha and cytokines; alternating ortho and parakeratosis
