Iran Specialty Board Dermatology key terms

Intercellular edema of the epidermis that widens the spaces between keratinocytes and stretches desmosomal attachments, producing visible intraepidermal vesicles in acute eczema and other inflammatory dermatoses.

Loss of cohesion between keratinocytes caused by dissolution or disruption of desmosomal attachments, creating rounded intraepidermal clefts and acantholytic cells on cytology.

Pattern of interface dermatitis in which lymphocytes obscure the dermoepidermal junction and damage basal keratinocytes, leading to pigment incontinence and saw-tooth rete ridges.

Granular IgA deposits at the dermal papillary tips causing intensely pruritic grouped vesicles on extensor surfaces, associated with gluten-sensitive enteropathy and celiac disease.

Autoimmune blistering disease with IgG antibodies against desmoglein 3, producing flaccid blisters, mucosal erosions, and suprabasal acantholysis with a tombstone row of basal cells.

Subepidermal blistering disease defined by linear IgA deposition along the basement membrane zone, causing grouped tense vesicles often in an annular or jewel-like arrangement.

Technique using fluorochrome-labeled antibodies on the patient's own frozen skin biopsy to detect in vivo bound immunoglobulins and complement, essential for classifying immunobullous diseases.

Direct immunofluorescence finding of granular immunoglobulin and complement deposition along the dermoepidermal junction of lesional or sun-exposed nonlesional skin, supporting a diagnosis of systemic lupus erythematosus.

Inflammatory pattern concentrated at the dermoepidermal junction with basal vacuolar change or lichenoid infiltrate, seen in lupus, lichen planus, and drug eruptions.

Pinpoint bleeding elicited by removing scale from a psoriatic plaque, reflecting the elongation of dermal papillae and thinning of the suprapapillary epidermis.

Development of new lesions of a skin disease at the site of trauma or injury, classically seen in psoriasis, lichen planus, and vitiligo.

Chronic immune-mediated papulosquamous disorder driven by IL-23 and Th17 pathways, producing sharply demarcated erythematous plaques with silvery scale on extensor surfaces.

Acquired depigmentation from autoimmune destruction of melanocytes, producing sharply demarcated milky-white macules that fluoresce brightly under Wood lamp examination.

Ultraviolet A light source filtered to around 365 nanometers used to accentuate pigmentary changes and detect fluorescence from organisms such as Microsporum and Corynebacterium minutissimum.

Magnified surface examination with polarized or nonpolarized light that reveals subsurface pigment patterns and vascular structures, improving diagnostic accuracy for melanocytic and nonmelanocytic lesions.

Maximum vertical depth of melanoma invasion measured in millimeters from the granular layer to the deepest tumor cell, the strongest predictor of survival and staging driver.

Selective removal and histologic examination of the first draining lymph node from a tumor bed, used for melanoma staging when thickness or other risk features warrant it.

Most common cutaneous T-cell lymphoma, presenting as patches, plaques, or tumors with epidermotropic atypical lymphocytes and clonal T-cell receptor gene rearrangement.

Leukemic variant of cutaneous T-cell lymphoma defined by erythroderma, generalized lymphadenopathy, and circulating atypical T cells with cerebriform nuclei.

Intraepidermal cluster of atypical lymphocytes surrounding a Langerhans cell, a hallmark histologic feature of mycosis fungoides.

Variant of Lynch syndrome with sebaceous adenomas, sebaceous carcinomas, or keratoacanthomas plus internal malignancy, usually from mismatch repair gene mutations.

Autosomal dominant disorder from PTCH1 mutations causing multiple basal cell carcinomas, palmar pits, jaw keratocysts, and skeletal anomalies.

Autosomal dominant neurocutaneous disorder from NF1 mutation, characterized by cafe-au-lait macules, neurofibromas, axillary freckling, and Lisch nodules.

Autosomal dominant disorder of TSC1 or TSC2 mutations causing facial angiofibromas, ash-leaf macules, shagreen patches, seizures, and renal angiomyolipomas.

Heterogeneous group of inherited mechanobullous disorders from mutations in structural skin proteins, classified by cleavage level as simplex, junctional, dystrophic, or Kindler type.

Separation of the epidermis with gentle lateral pressure on perilesional skin, indicating loss of keratinocyte cohesion in pemphigus, toxic epidermal necrolysis, and staphylococcal scalded skin syndrome.

Life-threatening mucocutaneous reaction, usually drug-induced, causing widespread epidermal necrosis and detachment of more than 30 percent of body surface area.

Severe mucocutaneous hypersensitivity reaction with epidermal detachment of less than 10 percent of body surface area, distinguished from toxic epidermal necrolysis mainly by extent.

Human leukocyte antigen allele strongly associated with abacavir hypersensitivity syndrome, used for pretreatment screening to prevent a severe systemic drug reaction.

Allele prevalent in some Asian populations that markedly increases risk of carbamazepine-induced Stevens-Johnson syndrome and toxic epidermal necrolysis, guiding drug selection.

Epicutaneous provocation test applying standardized allergens under occlusion for 48 hours with delayed readings, the gold standard for diagnosing allergic contact dermatitis.

Delayed-type hypersensitivity reaction to a hapten that has penetrated the skin, producing pruritic eczematous plaques confined to contact sites and often spreading.

Nonimmunologic skin inflammation caused by direct cytotoxic or barrier-disrupting effects of chemicals, friction, or moisture, without prior sensitization.

Variant of patch testing in which duplicate allergen strips are applied and one set is irradiated with ultraviolet A to identify photoallergic contact reactions.

Exaggerated sunburn-like skin response to ultraviolet or visible light in the presence of a chemical or drug, occurring without immunologic sensitization and dose-dependent.

Immunologically mediated delayed hypersensitivity reaction triggered when a chemical is converted by ultraviolet light into an antigenic hapten, producing eczematous eruptions in sun-exposed areas.

Treatment using engineered antibodies or fusion proteins that block specific cytokines or receptors, such as TNF inhibitors or IL-17 and IL-23 antagonists, in psoriasis and other inflammatory diseases.

Smallest dose of ultraviolet radiation that produces perceptible erythema in a defined time after exposure, used to individualize phototherapy dosing and assess photosensitivity.

Combined therapy using oral or topical psoralen followed by ultraviolet A irradiation, which intercalates DNA and cross-links strands, used for psoriasis and vitiligo.

Phototherapy using ultraviolet B around 311 to 313 nanometers, the standard office treatment for widespread psoriasis and other inflammatory dermatoses with fewer psoralen-related risks.