Posts

ID reaction

ID reaction   Updated: 02/25/2021 © Jun Wang, MD, PhD   General features Also called autoeczematization, eczematous reaction Occurs at a site distant to the location of a prior existing inflammatory rash Generalized acute reaction to variety of stimuli, including infection or inflammation More commonly seen in elder patients who neglected a primary rash Pathogenesis Associated with abnormal immune activity Clinical features Usually 1-2 weeks after primary infection/dermatitis Generalized pruritic, erythematous, morbilliform,or papulovesicular rash Management Treat underlying infection or dermatitis Back to acute inflammatory dermatitis Back to contents

Erythema multiforme

Erythema multiforme, Steven Johnson Syndrome/Toxic Epidermal Necrosis Updated: 02/24/2021 © Jun Wang, MD, PhD General features Uncommon, acute process May be self limited in minor forms, or life threatening Risk factors: Immune abnormalities , including HIV infection, corticosteroid exposure, bone marrow transplant, autoimmune disorders, and inflammatory bowel disease Likely EM and SJS/TEN are two different diseases  EM : slightly more common in young male SJS/TEN : more common in female Diagnosed based on clinical presentations Pathogenesis Type IV hypersensitivity reaction associated with infections, drugs, carcinoma / lymphoma, or collagen vascular disorders Immune complex mediated reaction Erythema multiforme minor and major : more commonly associated with viral infections SJS/TEN : more commonly associated with drug reaction Classifications Erythema multiforme minor : Typical targets or raised, edematous papules distributed acrally Erythema multiforme

Dyshidrotic eczema

Dyshidrotic eczema   Updated: 02/11/2021 © Jun Wang, MD, PhD General features AKA acute palmoplantar eczema Pruritic vesicular eruption on palms, soles and lateral aspects of fingers and toes History of atopic dermatitis or contact dermatitis increases risks Rule out allergic contact dermatitis, using patch testing Secondary bacterial infection of the vesicles/bullae may occur Clinical course ranges from self-limited to chronic, severe Usually clinical diagnosis Pathogenesis Unknown etiology Probably associated with contact allergens, irritants, stress, etc Clinical features Sudden onset Deep seated, pruritic vesicles Management Topical steroid Cold compresses Back to acute inflammatory dermatitis Back to contents

Atopic dermatitis

Atopic dermatitis   Updated: 02/24/2020 © Jun Wang, MD, PhD General features Usually starts in early infancy Higher risk to develop other allergic disorders later in life More common in women, Asians, Blacks, immigrants from developing countries into developed countries Patients tend to have hypersensitive skin Usually with family history of atopic dermatitis Intermittent course with flares and remissions occurring, for unexplained reasons Diagnosis based on clinical features, IgE reactivity and history of allergies Pathogenesis Most likely a combination of skin barrier defects and abnormal immune response Filaggrin or SPINK5 mutation: causing increased epidermal permiability  IgE sensitization Imbalance between T cell subgroups Cutaneous hyper-reactivity to environmental triggers Skin barrier dysfunction worsened by inflammation Clinical features Incessant pruritus Relatively age specific site of involvement Early childhood : Face, extensor sides of ext

Contact dermatitis

Allergic contact dermatitis   Updated: 02/11/2021 © Jun Wang, MD, PhD General features Poison ivy, nickel and rubber gloves common associated factors Persistent or relapsing May get bacterial superinfection (impetiginization) Irritant contact dermatitis : Similar conditions caused by chemical -induced direct damage of the skin, NO prior sensitization With chronic irritation (rubbing or scratching), neurodermatitis (lichen simplex chronicus) may occur Pathogenesis Direct contact of antigens topically Delayed hypersensitivity reaction (Type IV) Activation of Langerhans cells results in CD4+ T-cell sensitization Activation of memory T cells upon re-exposure T-cell mediated response to site of antigen encounter Clinical features Occurs at site of contact Usually develop within a few days of exposure Pruritic papules and vesicles on an erythematous base Lichenified pruritic plaques may indicate a chronic form Pathological findings Extensive spongiosis M

Acute inflammatory dermatosis

Acute inflammatory dermatosis and eczematous dermatosis Updated: 02/11/2021 © Jun Wang, MD, PhD General features Clinical history critical for diagnosis Commonly associated with abnormal immune activity Drug eruption should always be considered Acute eczematous dermatitis A group of spongiotic dermatitis Commonly T-cell mediated type IV hypersensitivity to endogenous or exogenous stimuli A few commonly seen eczematous disorders Contact dermatitis (allergic and irritant) Atopic dermatitis Dyshidrotic eczema Nummular eczema Id reaction Xerotic eczema Others Urticaria Erythema multiforme  Rosacea Practice questions Back to contents

Secondary syphilis

Secondary syphilis   Updated: 02/10/2021 © Jun Wang, MD, PhD General features Infectious disease caused by Treponema pallidum Most common in men who have sex with men Rash in second stage Face and trunk Clinical features Scaly, flesh-color to erythematous papules or annular plaques Serology studies ( VDRL , RPR, TRUST for screening, treponemal tests for confirmation) for diagnosis Pathological features Dense perivascular or diffuse plasma cell infiltrate Silverstain or immunohistochemistrystudy reveals spirochetes Management Penicillin Back to papulosquamous disorders Back to contents