Arab Board Dermatology Clinical key terms

Pinpoint bleeding that appears when a scale is removed from a lesion, caused by exposure of elongated dermal papillary capillaries. It is classically sought in psoriasis but is not specific to it.

Development of new lesions of an existing skin disease along a line of trauma, such as a scratch or surgical scar. Best known in psoriasis, lichen planus, and vitiligo.

Histologic pattern of regular, club-shaped elongation of rete ridges with thinning of suprapapillary plates. It is the microscopic hallmark of psoriasis and is also seen in chronic spongiotic dermatitis.

Intercellular edema within the epidermis that widens spaces between keratinocytes and stretches desmosomes, producing visible intercellular bridges. It is the defining feature of eczematous dermatitis.

Thickening of skin with exaggerated skin markings caused by chronic rubbing or scratching. It reflects epidermal hyperplasia from repeated mechanical trauma and is common in chronic atopic and lichen simplex lesions.

Intensely pruritic papulovesicular eruption on extensor surfaces with granular IgA deposits at the dermal papillary tips. It is the cutaneous manifestation of gluten-sensitive enteropathy.

Technique in which a fluorochrome-labeled antibody is applied to the patient's own tissue to detect in vivo-bound immunoglobulins or complement. It is decisive in classifying autoimmune blistering diseases.

Autoimmune blistering disease caused by IgG against desmoglein 3, producing flaccid bullae and painful oral erosions. Suprabasal acantholysis and intercellular IgG on direct immunofluorescence are characteristic.

Loss of cohesion between epidermal keratinocytes because desmosomal attachments break down. It produces rounded, detached keratinocytes and clefting, and is the key finding in pemphigus and Hailey-Hailey disease.

Separation of the epidermis from the dermis when lateral pressure is applied to apparently normal skin. A positive sign suggests intraepidermal cleavage, as in pemphigus or toxic epidermal necrolysis.

Subepidermal blistering eruption with linear IgA along the basement membrane zone on direct immunofluorescence. Lesions often form annular or jewel-like clusters, and drug-induced cases are well recognized.

Life-threatening mucocutaneous reaction with widespread epidermal detachment, usually drug-triggered, classified with Stevens-Johnson syndrome by body surface area involved. Mortality is high and urgent supportive care is required.

Severe delayed drug hypersensitivity with rash, fever, facial edema, eosinophilia, and internal organ involvement, often with viral reactivation. Onset is typically delayed two to six weeks after starting the culprit drug.

Drug-triggered eruption of numerous sterile, nonfollicular pustules on erythematous skin with fever and neutrophilia. It usually resolves quickly after withdrawal of the causative agent.

Small, circumscribed elevation of skin containing visible purulent material. Pustules may be infectious, follicular, or sterile and drug-related, so the distinction guides evaluation.

Plug of keratin and sebum within a dilated pilosebaceous follicle. Open comedones are dark-topped blackheads; closed comedones are white and are the noninflammatory precursor lesion of acne.

Holocrine gland of the pilosebaceous unit that secretes lipid-rich sebum. Its activity is androgen-dependent and drives acne pathogenesis when combined with follicular hyperkeratinization and bacterial colonization.

Elongated mite that colonizes human pilosebaceous follicles. Overpopulation is associated with papulopustular rosacea and may cause a folliculitis-like eruption, particularly on the face.

Chronic facial inflammatory disorder with flushing, telangiectasia, erythema, and papulopustules, often triggered by heat, sun, and alcohol. It lacks comedones, which helps distinguish it from acne.

Bulbous enlargement of the nose with thickened, nodular skin and prominent follicles, representing a late complication of rosacea. It results from sebaceous gland hyperplasia and fibrosis.

Acquired depigmentation from autoimmune loss of functioning melanocytes, producing well-demarcated chalk-white macules. It can follow Koebner phenomenon and is associated with other autoimmune diseases.

Ultraviolet A light source used to examine skin fluorescence and pigment. It accentuates depigmentation in vitiligo and helps distinguish epidermal from dermal pigmentation.

Acquired symmetrical hyperpigmentation of sun-exposed face, driven by ultraviolet exposure, hormones, and genetic factors. It is more common in darker skin phototypes and often relapses after treatment.

Darkening of skin at sites of prior inflammation or injury, caused by increased melanin production or pigment incontinence. It is more prominent and persistent in darker skin phototypes.

Magnified, usually polarized, examination of skin structures below the surface to aid diagnosis. Recognized patterns improve accuracy for melanocytic lesions, tumors, hair disorders, and infestations.

Dermoscopic grid formed by pigmented rete ridges and lighter dermal papillae. Regular, uniform networks suggest benign nevi, while irregular networks raise concern for melanoma.

Dermoscopic feature of confluent blue-gray pigmentation with a whitish ground-glass appearance overlying it. It suggests dermal pigment combined with epidermal changes and is a melanoma warning sign.

Non-scarring autoimmune hair loss producing well-demarcated smooth patches, sometimes with exclamation-mark hairs. Nail pitting and association with other autoimmune disease may occur.

Short, tapered hair that is narrower proximally and wider distally, seen at the edge of active alopecia areata patches. Its presence supports the diagnosis on trichoscopy.

Dermoscopic examination of scalp hair and follicles used to distinguish non-scarring from scarring alopecia. It reveals features such as hair shaft variability, perifollicular scaling, and empty follicles.

Separation of the nail plate from the nail bed, beginning distally and producing a white or discolored area. Causes include trauma, psoriasis, fungal infection, and thyroid disease.

Fungal infection of the nail unit, most often dermatophyte, causing thickening, discoloration, and crumbling of the plate. Confirmation requires microscopy or culture before prolonged treatment.

Chronic relapsing pruritic eczematous disease with impaired skin barrier and immune dysregulation. Distribution varies with age, and personal or family history of atopy is common.

Genetic disorder of filaggrin deficiency causing fine white scaling, mainly on extensor limbs, with sparing of flexures. It is the most common inherited ichthyosis and often coexists with atopic dermatitis.

Autosomal dominant disorder with café-au-lait macules, axillary freckling, neurofibromas, and Lisch nodules. Diagnosis is clinical using established criteria, and systemic complications require surveillance.

Uniform light-brown macule with sharp borders, present from birth or early childhood. Multiple lesions suggest neurofibromatosis type 1 or other neurocutaneous syndromes.

Staged excision in which the entire surgical margin is examined histologically while the patient waits. It offers high cure rates with maximal tissue conservation for selected skin cancers.

Locally invasive keratinocyte cancer with pearly papules, telangiectasia, and ulceration, rarely metastasizing. It is the most common skin cancer and is linked to ultraviolet exposure.

Acute eruption of target lesions, often triggered by herpes simplex infection. Mucosal involvement may occur, but it is distinct from Stevens-Johnson syndrome in cause and prognosis.