Arab Board Dermatology Part 1 key terms

A protein complex that rivets adjacent keratinocytes together at their cell membranes, anchoring intermediate filaments. Its disruption by autoantibodies produces intraepidermal blistering, and inherited defects cause forms of ichthyosis and palmoplantar keratoderma.

A junction that attaches basal keratinocytes to the underlying basement membrane by linking intracellular keratin to laminin and collagen via integrins. Antibodies against its components underlie bullous pemphigoid, and mutations cause junctional epidermolysis bullosa.

The layered interface between epidermis and dermis, comprising the lamina lucida, lamina densa and sublamina densa, held together by hemidesmosomes, anchoring fibrils and collagen IV and VII. It is the target in pemphigoid and epidermolysis bullosa and the level used to classify blistering diseases.

Loss of cohesion between keratinocytes caused by breakdown of desmosomal attachments, leaving rounded detached cells. It is the defining histologic feature of pemphigus vulgaris and also occurs in Hailey-Hailey disease and some viral infections.

A rapid bedside cytologic test in which scrapings from the base of a blister or ulcer are stained to look for acantholytic keratinocytes or multinucleated giant cells. It supports, but does not confirm, a diagnosis of pemphigus or herpesvirus infection.

A test in which a fluorochrome-labelled antibody is applied to the patient's own frozen tissue to detect in-vivo deposition of immunoglobulins or complement. Intercellular epidermal staining indicates pemphigus, linear basement membrane staining indicates pemphigoid, and granular staining at the dermoepidermal junction suggests lupus.

A technique in which perilesional skin is incubated in concentrated salt solution to cleave the basement membrane at the lamina lucida, separating roof from floor. Antibody binding to the blister roof indicates pemphigoid, whereas binding to the floor indicates epidermolysis bullosa acquisita.

Magnified, usually polarized, examination of skin lesions that reveals subsurface structures such as pigment networks, vascular patterns and globules invisible to the naked eye. It improves diagnostic accuracy for melanoma and other tumors and helps identify infestations such as scabies.

A dermoscopic pattern of intersecting pigmented lines corresponding to melanin along rete ridges. A regular, uniform network suggests a benign melanocytic nevus, whereas an atypical, irregular or absent network raises concern for melanoma.

A procedure in which standardized allergens are applied under occlusion to intact skin for 48 hours and read at delayed intervals to identify type IV cell-mediated hypersensitivity. It is the gold standard for diagnosing allergic contact dermatitis.

Intercellular edema between keratinocytes that widens the spaces between cells and stretches desmosomes, producing visible intraepidermal vesicles. It is the hallmark histologic finding of acute eczematous dermatitis.

Retention of nuclei within the stratum corneum, reflecting accelerated epidermal turnover and incomplete keratinocyte maturation. It is characteristic of psoriasis, where it occurs with neutrophils in the horny layer, and of other inflammatory dermatoses.

Pinpoint bleeding that occurs when scale is removed from a lesion, caused by exposure of elongated, dilated dermal papillary capillaries. It is classically described in psoriasis but is neither sensitive nor specific.

The appearance of new lesions of an existing skin disease at sites of trauma, scratching or injury. It is classically seen in psoriasis, lichen planus and vitiligo and helps explain linear lesion patterns.

A chronic immune-mediated papulosquamous disease driven by interleukin-23 and T helper 17 cells, producing well-demarcated erythematous plaques with silvery scale on extensor surfaces. It is associated with arthritis, metabolic syndrome and cardiovascular risk.

A pruritic inflammatory skin reaction pattern with erythema, vesicles, oozing and scaling in the acute phase and lichenification when chronic. It is a descriptive diagnosis encompassing atopic, contact, nummular and other forms.

A chronic relapsing pruritic inflammatory dermatosis arising from skin barrier dysfunction, often filaggrin deficiency, combined with immune dysregulation. It typically begins in childhood with flexural involvement and predisposes to bacterial and viral skin infection.

A delayed type IV hypersensitivity reaction to a hapten contacting the skin, producing pruritic eczematous lesions confined to or spreading from contact sites. Diagnosis is confirmed by patch testing.

Non-immunologic skin inflammation caused by direct cytotoxic damage from chemicals, friction, water or repeated wet work. It requires no prior sensitization and is the commonest form of occupational hand dermatitis.

An idiopathic T-cell-mediated disease affecting skin, mucous membranes, hair and nails, characterized by pruritic violaceous flat-topped polygonal papules with fine white lines. Oral involvement may carry a small risk of squamous cell carcinoma.

Fine white lacy lines visible on the surface of lichen planus papules and on oral mucosal lesions. They reflect focal hypergranulosis and are a helpful clinical clue to the diagnosis.

A structural protein that aggregates keratin filaments and helps maintain the cornified skin barrier and natural moisturizing factor. Loss-of-function mutations are a major risk factor for atopic dermatitis and ichthyosis vulgaris.

An autoimmune blistering disease in which IgG antibodies against desmoglein 3, and later desmoglein 1, cause suprabasal acantholysis. It produces flaccid blisters and painful erosions, often starting in the mouth.

An autoimmune subepidermal blistering disease of older adults caused by IgG and IgE antibodies against hemidesmosomal proteins BP180 and BP230. It presents with tense blisters on urticarial plaques and responds to corticosteroids and immunosuppressants.

Direct immunofluorescence of skin showing a continuous granular band of immunoglobulin and complement along the dermoepidermal junction. It is found in lesional skin of cutaneous lupus and in sun-exposed nonlesional skin of systemic lupus erythematosus.

A multisystem autoimmune disease with autoantibodies to nuclear antigens, causing photosensitive rash, arthritis, cytopenias, nephritis and serositis. Antinuclear antibody testing is sensitive but not specific, and anti-double-stranded DNA and anti-Smith are more specific.

An idiopathic inflammatory myopathy with characteristic skin signs including heliotrope rash, Gottron papules and periungual telangiectasia, plus proximal muscle weakness. Myositis-specific antibodies such as anti-Mi-2 and anti-TIF1-gamma help classify subtypes and predict malignancy risk.

Violaceous to erythematous scaly papules overlying the knuckles and other bony prominences, a hallmark cutaneous sign of dermatomyositis. They are usually asymptomatic and may persist after muscle disease resolves.

Small-vessel vasculitis in which immune complex deposition damages vessel walls, recruiting neutrophils whose nuclear debris (leukocytoclasia) accumulates around vessels. It presents as palpable purpura, most often on the lower legs.

Raised, non-blanching purplish lesions caused by extravasation of red cells from inflamed dermal vessels. It is the cardinal sign of cutaneous small-vessel vasculitis and warrants investigation for systemic involvement.

A malignant tumor of melanocytes that may arise de novo or from a nevus, showing asymmetry, border irregularity, color variation, diameter over 6 mm and evolution. Breslow thickness is the strongest prognostic factor.

The measured depth of melanoma invasion from the granular layer of the epidermis to the deepest tumor cell, expressed in millimeters. It drives T staging and determines sentinel node biopsy eligibility and prognosis.

The commonest skin cancer, arising from basal keratinocytes of sun-exposed skin and locally destructive but rarely metastasizing. It presents as a pearly papule with telangiectasia, a rodent ulcer or a superficial plaque.

A UV-induced intraepidermal keratinocyte dysplasia appearing as rough, scaly erythematous macules on chronically sun-damaged skin. It is a precursor lesion for squamous cell carcinoma and is treated by cryotherapy, topical agents or field therapy.

A malignant tumor of keratinocytes, usually on sun-exposed or chronically damaged skin, that can metastasize. Risk is increased by immunosuppression, chronic ulcers, scarring and human papillomavirus infection.

An acquired autoimmune depigmentation disorder in which melanocytes are destroyed, producing sharply demarcated depigmented macules. It is associated with thyroid disease and other autoimmune conditions and may show the Koebner phenomenon.

Patterned hair loss driven by androgen-mediated miniaturization of genetically susceptible scalp follicles, producing bitemporal recession and vertex thinning in men and diffuse crown thinning in women. Treatment includes topical minoxidil and oral antiandrogens or finasteride.

Diffuse, usually reversible hair shedding caused by a trigger such as illness, childbirth, surgery, severe dieting or drugs that pushes many follicles into the resting phase. Shedding typically begins weeks to months after the trigger.

Disseminated herpes simplex virus infection complicating pre-existing skin disease, most often atopic dermatitis, producing monomorphic punched-out erosions with fever. It is a medical emergency requiring prompt systemic antiviral therapy.

A double-stranded DNA herpesvirus causing grouped vesicles on an erythematous base, with type 1 typically orofacial and type 2 genital. It establishes latency in sensory ganglia and reactivates, and can cause severe disease in immunocompromised hosts.

An infestation by the mite Sarcoptes scabiei var. hominis causing intense nocturnal pruritus, burrows and a papular eruption, often with involvement of web spaces and genitals. It spreads by prolonged skin contact and is treated with topical permethrin or oral ivermectin, including contacts.

An inherited disorder of keratinization, usually autosomal dominant with filaggrin loss, causing fine white scaling on extensor surfaces with sparing of flexures. It often coexists with atopic dermatitis and improves in warm humid weather.

An autosomal dominant genodermatosis caused by NF1 mutations, featuring cafe-au-lait macules, axillary freckling, neurofibromas, Lisch nodules and optic glioma. Diagnosis uses established clinical criteria and requires surveillance for associated tumors.

An autosomal dominant disorder of TSC1 or TSC2 mutations causing hamartomas in multiple organs, with facial angiofibromas, ash-leaf macules, shagreen patch and subungual fibromas. It is associated with seizures, renal angiomyolipomas and cardiac rhabdomyomas.

A treatment in which a photosensitizing porphyrin precursor is applied to skin and activated by light of an appropriate wavelength, generating reactive oxygen species that destroy dysplastic cells. It is used for actinic keratoses and superficial skin cancers.

A tissue-sparing technique in which tumor is excised and the entire peripheral and deep margin is examined on frozen sections during the same visit, with staged re-excision until clear. It offers high cure rates for high-risk basal and squamous cell carcinoma and some melanomas.

A severe mucocutaneous reaction, usually drug-induced, with epidermal detachment affecting less than ten percent of body surface area plus at least two mucosal sites. It lies on a spectrum with toxic epidermal necrolysis and requires urgent withdrawal of the culprit drug and supportive care.

The most severe drug-induced mucocutaneous reaction, with epidermal detachment exceeding thirty percent of body surface area and widespread full-thickness epidermal necrosis. Mortality is high and management centers on drug withdrawal, supportive care and sometimes immunomodulation.

A severe delayed drug hypersensitivity with rash, fever, eosinophilia and internal organ involvement such as hepatitis, typically arising two to six weeks after starting an aromatic anticonvulsant, allopurinol or sulfonamide. Reactivation of herpesviruses contributes and relapse after withdrawal is common.

An antifolate immunosuppressant used for psoriasis, eczematous disorders and some connective tissue diseases. It requires folic acid supplementation and monitoring of blood counts, liver enzymes and renal function, and is contraindicated in pregnancy.

Treatment using engineered antibodies or fusion proteins that block specific immune pathways, such as tumor necrosis factor, interleukin-17, interleukin-23 or IgE. Biologics are used for moderate-to-severe psoriasis, atopic dermatitis and chronic urticaria and require infection screening before use.